Publications by authors named "Ai-Ping Wang"

69 Publications

Development and Evaluation of the Psychosocial Adaptation Questionnaire among Patients with Chronic Skin Disease.

Dermatology 2021 Mar 2:1-8. Epub 2021 Mar 2.

Department of Dermatology, The First Affiliated Hospital of China Medical University, Shenyang, China,

Background/objective: Chronic skin disease (CSD) often has physiological, psychological, and social impacts, which requires the patient to adjust to achieve psychosocial adaptation (PSA). As a standardized assessment instrument was lacking, we developed a PSA questionnaire for patients with CSD (PSAQ-CSD).

Methods: According to the steps of questionnaire development, a systematic process of scoping review, qualitative research, content validity expert review, testing in a sample of 321 adults, item analysis, and classical test theory methods were applied.

Results: Following item analysis and exploratory factor analyses, 18 items were eventually entered into the model of confirmatory factor analyses, with a cumulative contribution of 65.435%. Three subscales were developed: emotional, self-cognitive, and social dimensions. Item analysis, exploratory factor analyses, and content validity expert review narrowed the subscales to 8, 6, and 4 items, respectively.

Conclusions: The 18-item PSAQ-CSD has been confirmed to have good internal consistency reliability and convergent and discriminant validity. It may be a useful tool to evaluate the PSA among patients with CSD and provide a basis for further research.
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http://dx.doi.org/10.1159/000514306DOI Listing
March 2021

Exploring psychosocial adaptation among people with chronic skin disease: A grounded theory study.

Nurs Open 2021 Feb 25. Epub 2021 Feb 25.

Department of Nursing, The First Affiliated Hospital of China Medical University, Shenyang, China.

Aim: Chronic skin disease (CSD) often has devastating effects on the physiological, psychological and social aspects of patients, who must adapt to them. However, it is not clear how patients adapt, especially with regard to their psychosocial adaptation (PSA). This research explored a theoretical model of PSA among people with CSD.

Design: Following constructivist grounded theory methodology, a qualitative study was undertaken between August 2018 and June 2019.

Methods: Observation and semi-structured interview were conducted with included participants (n=19). Data were iteratively coded and analyzed by constant comparison following the key stages of initial, focused, axial and theoretical coding until saturation was achieved.

Results: When individuals face the impacts of disease, they try to adjust to adapt it. The findings showed the core category (self-cognitive) and the contributing categories (impacts of chronic skin disease, contextual factors, physiological experiences, psychological experiences, social experiences, and positive and negative psychosocial adaptations) of the PSA among people with CSD. The process of PSA among people with CSD was not linear throughout the disease and was instead entwined within a set of complexes (contextual factors-experience) interactions. The consequences of PSA included positive and negative aspects. The theoretical model of PSA among people with CSD will provide us with information needed to develop accurate assessment and effective intervention strategies. Understanding that PSA among people with CSD is a complex, dynamic, and interactional process may provide evidence for further assessing and meeting the needs of people.
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http://dx.doi.org/10.1002/nop2.823DOI Listing
February 2021

Risk prediction using the National Early Warning Score and the Worthing Physiological Scoring System in patients who were transported to the Intensive Care Unit from the Emergency Department: A cohort study.

Intensive Crit Care Nurs 2021 Feb 18:103015. Epub 2021 Feb 18.

Emergency Department, Beijing Tongren Hospital, Capital Medical University, Beijing, China.

Objectives: The aim of this study was to assess the value of the National Early Warning Score and Worthing Physiological Scoring System for predicting changes in the condition of critical cases during transfer from the emergency department to the intensive care unit.

Methods: This prospective single-centre study was conducted at a 1759-bed hospital in Beijing. We recorded the vital signs in the cases before leaving the emergency department and their changes in condition during transit.

Results: A total of 258 critically ill cases were included. Forty-four cases (17.05%) exhibited changes in their condition during transit. Compared with cases with NEWS ≤ 5, cases with NEWS > 5 were more likely to experience changes with an OR of 5.744 (95% CI 2.888-11.426). Compared with cases with WPS ≤ 2, cases with WPS > 2 were more likely to experience changes with an OR of 7.217 (95% CI 3.575-14.569). The difference between the areas under the curve of the NEWS (0.751 ± 0.045) and the WPS (0.736 ± 0.045) was not statistically significant (P = 0.4518).

Conclusion: In our study, the Worthing Physiological Scoring System and National Early Warning Score both exhibited good discriminatory power, but the Worthing Physiological Scoring System is simpler to use and more suitable for use in a busy emergency department.
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http://dx.doi.org/10.1016/j.iccn.2021.103015DOI Listing
February 2021

Aetiology of superficial fungal infections of the foot in urban outpatients in mainland China: A multicentre, prospective case study.

Mycoses 2020 Nov 9;63(11):1235-1243. Epub 2020 Sep 9.

Department of Dermatology and Venerology, Peking University First Hospital, Beijing, China.

Background: In China, the prevalence of superficial fungal infections of the foot is high and recurrence is common. However, a prospective, large-scale and multicentre study on the aetiology of superficial fungal infections of the foot is still lacking.

Objectives: To study the epidemiology of aetiological agents of superficial fungal infections of the foot in urban outpatients in mainland China, as well as to understand the aetiology features of the pathogenic agent.

Methods: The study was designed as a multicentre, prospective epidemiological survey. A total of 1704 subjects were enrolled from seven geographical areas in mainland China. For each subject, one mycological sample and one bacterial sample were collected. KOH wet mount examination and culture were performed at local laboratories. The bacterial results were only reported in those with positive mycology. Further morphological identification and, if necessary, molecular biological identification were conducted in a central laboratory.

Results: Of 1704 enrolled subjects, 1327 (77.9%) subjects had positive fungal culture results. The incidence of dermatophytes, yeasts and moulds was 90.1%, 8.1% and 1.1%, respectively. The most frequently isolated aetiological agent (fungus) was Trichophyton rubrum. Moccasin form was the most commonly reported clinical diagnosis of superficial fungal infections. The most frequently isolated bacterial genus in patients was Staphylococcus.

Conclusion: This study prospectively investigated the clinical and mycological features of human dermatophytosis in mainland China. T rubrum was the most frequently isolated fungus, and moccasin form was the most commonly reported clinical diagnosis of superficial fungal infections.
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http://dx.doi.org/10.1111/myc.13168DOI Listing
November 2020

Microglia-associated neuroinflammation is a potential therapeutic target for ischemic stroke.

Neural Regen Res 2021 Jan;16(1):6-11

Institute of Clinical Research, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan Province, China.

Microglia-associated neuroinflammation plays an important role in the pathophysiology of ischemic stroke. Microglial activation and polarization, and the inflammatory response mediated by these cells play important roles in the development, progression and outcome of brain injury after ischemic stroke. Currently, there is no effective strategy for treating ischemic stroke in clinical practice. Therefore, it is clinically important to study the role and regulation of microglia in stroke. In this review, we discuss the involvement of microglia in the neuroinflammatory process in ischemic stroke, with the aim of providing a better understanding of the relationship between ischemic stroke and microglia.
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http://dx.doi.org/10.4103/1673-5374.286954DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7818879PMC
January 2021

Low expression of miR‑532‑3p contributes to cerebral ischemia/reperfusion oxidative stress injury by directly targeting NOX2.

Mol Med Rep 2020 Sep 10;22(3):2415-2423. Epub 2020 Jul 10.

Office of Good Clinical Practice, The Affiliated Changsha Hospital of Hunan, Normal University, Changsha, Hunan 410006, P.R. China.

NADPH oxidase 2 (NOX2) is a major subtype of NOX and is responsible for the generation of reactive oxygen species (ROS) in brain tissues. MicroRNAs (miRNAs/miRs) are important epigenetic regulators of NOX2. The present study aimed to identify the role of NOX2 miRNA‑targets in ischemic stroke (IS). A rat cerebral ischemia/reperfusion (CI/R) injury model and a SH‑SY5Y cell hypoxia/reoxygenation (H/R) model were used to simulate IS. Gene expression levels, ROS production and apoptosis in tissue or cells were determined, and bioinformatic analysis was conducted for target prediction of miRNA. In vitro experiments, including function‑gain and luciferase activity assays, were also performed to assess the roles of miRNAs. The results indicated that NOX2 was significantly increased in brain tissues subjected to I/R and in SH‑SY5Y cells subjected to H/R, while the expression of miR‑532‑3p (putative target of NOX2) was significantly decreased in brain tissues and plasma. Overexpression of miR‑532‑3p significantly suppressed NOX2 expression and ROS generation in SH‑SY5Y cells subjected to H/R, as well as reduced the relative luciferase activity of cells transfected with a reporter gene plasmid. Collectively, these data indicated that miR‑532‑3p may be a target of NOX2 and a biomarker for CI/R injury. Thus, the present study may provide a novel target for drug development and IS therapy.
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http://dx.doi.org/10.3892/mmr.2020.11325DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7411405PMC
September 2020

Apelin-13 attenuates high glucose-induced calcification of MOVAS cells by regulating MAPKs and PI3K/AKT pathways and ROS-mediated signals.

Biomed Pharmacother 2020 Aug 22;128:110271. Epub 2020 May 22.

College of Veterinary Medicine, Shandong Agricultural University, Taian, Shandong 271018, China. Electronic address:

Vascular calcification (VC) is an inducement of many cardiovascular diseases. Clinic evidences have confirmed that diabetes was the independent risk factor for VC, and the mechanism has not been well explored. Apelin as a ligand molecule is widely found in the cardiovascular system and showed potential in inhibiting VC, but the inhibitory effect and mechanism of apelin-13 against high glucose-induced VC have not been investigated yet. Herein, apelin-13 was employed to inhibit high glucose-induced VC in mouse aortic vascular smooth muscle cells (MOVAS), and the underlying mechanism was explored. The results showed that apelin-13 significantly inhibited high glucose-induced cells proliferation, migration and invasion of MOVAS cells. Apelin-13 also effectively attenuated high glucose-induced calcification by inhibiting alkaline phosphatase (ALP) activity and expression. Further investigation revealed that apelin-13 dramatically suppressed high glucose-induced DNA damage through inhibiting reactive oxide species (ROS) generation. Moreover, apelin-13 also effectively improved high glucose-induced dysfunction of MAPKs and PI3K/AKT. Inhibition of ERK by inhibitor (U0126) significantly blocked high glucose-induced calcification, which further confirmed the significance of MAPKs. Taken together, these results suggested that apelin-13 had the potential to attenuate high glucose-induced calcification of MOVAS cells by inhibiting ROS-mediated DNA damage and regulating MAPKs and PI3K/AKT pathways. Our findings validated the strategy of using apelin-13 maybe a novel way in treating high glucose-mediated VC.
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http://dx.doi.org/10.1016/j.biopha.2020.110271DOI Listing
August 2020

[Vasovagal syncope or postural orthostatic tachycardia syndrome in children with neurological symptoms at disease onset: a clinical analysis of 88 cases].

Zhongguo Dang Dai Er Ke Za Zhi 2020 May;22(5):488-493

Department of Pediatrics, Second Xiangya Hospital of Central South University, Changsha 410011, China.

Objective: To study the clinical features of vasovagal syncope (VVS) and postural orthostatic tachycardia syndrome (POTS) in children with neurological symptoms at disease onset.

Methods: A retrospective analysis was performed on the medical data of 88 children with the initial symptoms of the nervous system, such as transient loss of consciousness, dizziness, headache, and convulsion, who were finally diagnosed with VVS or POTS.

Results: Of the 88 children, there were 35 boys (40%) and 53 girls (60%), with an age of 4-15 years. The peak age of onset was between 10 and 13 years. All the children had the initial symptoms of transient loss of consciousness, dizziness, headache, and convulsion. Nervous system diseases were excluded by electroencephalography, cerebrospinal fluid examination, and cranial MRI. Of the 88 children, 53 (60%) were confirmed with VVS, and 35 (40%) with POTS, according to the results of head-up tilt test (HUTT). Five children with the initial symptom of transient loss of consciousness were misdiagnosed with epilepsy. Predisposing factors were determined for 59 children (67%), and prolonged standing was the most common factor, followed by change in body position and strenuous exercise. Premonitory symptoms were observed in 66 children (75%), among which chest discomfort was the most common symptom, followed by gastrointestinal symptoms (nausea, vomiting, and abdominal pain) and pale complexion. All 88 children received health education and exercise for autonomic nerve function, among whom 53 children with VVS were given oral rehydration salts and 35 children with POTS were given oral rehydration salts and metoprolol. All 88 children were followed up for 18 months, and the response rates to the above treatment at 3, 6, 12, and 18 months of follow-up were 87%, 93%, 93%, and 90% respectively.

Conclusions: In addition to nervous system diseases, functional cardiovascular diseases including VVS and POTS should be considered for children with the initial symptoms of transient loss of consciousness, dizziness, headache, and convulsion. HUTT can be used to make a confirmed diagnosis, and the early treatment can achieve a good outcome.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7389402PMC
May 2020

Maggot excretions/secretions promote diabetic wound angiogenesis via miR18a/19a - TSP-1 axis.

Diabetes Res Clin Pract 2020 Jul 8;165:108140. Epub 2020 Apr 8.

Endocrinology Department, Air Force Hospital of Eastern Theater Command, No.1 Malu Road, Nanjing 210002, China. Electronic address:

Aims: The impaired angiogenesis is one of the main factors affecting the healing of diabetic foot ulcer (DFU) wounds. Maggot debridement therapy (MDT) promotes granulation tissue growth and angiogenesis during DFU wound healing. Non-coding microRNAs can also promote local angiogenesis in DFU wounds by regulating wound repairing related gene expression. The purpose of this study was to investigate the mechanism of microRNAs in MDT promoting DFU wound angiogenesis.

Methods: In this study, we applied MDT to treat DFU wound tissue and detect the expression of the miR-17-92 cluster. In vitro experiments, human umbilical vein endothelial cells (HUVECs) were treated with maggot excretions/secretions (ES), the miR-17-92 cluster and the predicted target gene expression were measured. Tube formation assay and cell scratch assay were performed when inhibition of miR-18a/19a or overexpression of thrombospondin-1 (TSP-1) were used in this study.

Results: miR-18a/19a transcription significantly up-regulated and TSP-1 expression down-regulated in patients wound tissue and in HUVECs. Inhibition of miR-18a/19a or overexpression of TSP-1 partially blocked the migration and tube formation ability stimulated by ES.

Conclusion: Targeted activation of miR-18a/19a transcription levels and subsequent regulation of TSP-1 expression may be a novel therapeutic strategy for DFU.
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http://dx.doi.org/10.1016/j.diabres.2020.108140DOI Listing
July 2020

Adherence status to Adjuvant Endocrine Therapy in Chinese Women with Early Breast Cancer and its influencing factors: A cross-sectional survey.

Cancer Med 2020 06 1;9(11):3703-3713. Epub 2020 Apr 1.

The First Affiliated Hospital of China Medical University, Shenyang, China.

Objective: Despite the proven benefits of adjuvant endocrine therapy, adherence to oral endocrine therapy in breast cancer treatment is a substantial problem. The aim of this study was to assess adherence to adjuvant endocrine therapy by women in China for the first 5 years, and to identify its influencing factors.

Methods: Stratified sampling method was adopted to select 1875 cases of breast cancer patients for cross-sectional telephone follow-up. Compliance to medications was assessed using the Morisky Medication Adherence Scale. Status of endocrine therapy was assessed using nine additional questions. Binomial regression was used when assessing the factors associated with persistence, multinomial regression models were used to assess factors associated with compliance.

Results: Of 888 patients who started adjuvant endocrine therapy, 769(86.6%) persisted and 119 (13.4%) discontinued. 760 patients who completed Morisky Medication Adherence Scale, the compliance was 7.4% low, 42% medium, and 50.6% high. The type of medication, duration of medication and side effects had an impact both on persistence and compliance. Age, history of radiotherapy and caregivers only had an impact on persistence.

Conclusions: Medication adherence was affected by many factors. Special attention and interventions should be given to women taking tamoxifen in the 2nd to 3rd year of medication, and aromatase inhibitors in the 1st to 2nd year. Further prospective design studies are needed to explore effective measures to improve medication adherence of women with breast cancer treated by endocrine therapy.
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http://dx.doi.org/10.1002/cam4.3017DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7286448PMC
June 2020

miR-652 protects rats from cerebral ischemia/reperfusion oxidative stress injury by directly targeting NOX2.

Biomed Pharmacother 2020 Apr 27;124:109860. Epub 2020 Jan 27.

Office of Good Clinical Practice, The Affiliated Changsha Hospital of Hunan Normal University, Changsha, 410006, Hunan, China; Institute of Emergency and Critical Care Medicine of Changsha, Changsha, China. Electronic address:

Ischemic stroke is a devastating central nervous disease associated with oxidative stress and NOX2 is the main source of ROS responsible for brain tissue. miRNAs are a class of negative regulator of genes in mammals and involves the pathogenesis of ischemic stroke. This study aims to observe the role of target miRNA(miR-652) of NOX2 in ischemic stroke. A rat cerebral ischemia/reperfusion (CI/R) injury model and an SH-SY5Y cell hypoxia/reoxygenation(H/R) model were used to simulate ischemic stroke, and corresponding gene expression, biochemical indicators and pathophysiological indicators were measured to observe the role of miR-652. NOX2 significantly increased in brain tissues subjected to I/R or in SH-SY5Y cells subjected to H/R, while the expression level of miR-652(potential target of NOX2) significantly decreased in both brain tissues and plasma. Overexpression of miR-652 significantly suppressed NOX2 expression and ROS generation in H/R treated SH-SY5Y cells and reduced the relative luciferase activity of cells transfected with plasmid NOX2-WT (reporter gene plasmid). MiR-652 agomir significantly decreased the expression of NOX2 and ROS generation in brain tissues of CIR rats, as well as tissue injury. These data indicated that miR-652 protected rats from cerebral ischemia reperfusion injury by directly targeting NOX2, is a novel target for ischemic stroke therapy.
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http://dx.doi.org/10.1016/j.biopha.2020.109860DOI Listing
April 2020

CXCL2, a new critical factor and therapeutic target for cardiovascular diseases.

Clin Exp Hypertens 2020 Jul 21;42(5):428-437. Epub 2019 Nov 21.

Institute of Clinical Medicine, Nanhua Affiliated Hospital, University of South China, Hengyang, Hunan, P.R. China.

Cardiovascular diseases (CVDs) are the leading cause of death worldwide. Previous studies have shown that inflammatory chemokines are involved in the physiological functions of cytoskeletal reorganization, cell migration, adhesion and immune responses. However, in the past decade, there have been studies showing that inflammatory chemokines play a key role in CVD. Importantly, CXC motif chemokine ligand 2 (CXCL2) has been shown to be involved in the pathogenesis of cardiovascular disease. CXCL2 exerts its effects on the cardiovascular system by mediating inflammatory responses, but the specific signaling pathways by which CXCL2 exerts its effects in CVD remain unknown and need to be further investigated. This review aims to investigate the expression changes of CXCL2 in acute myocardial infarction (AMI), atherosclerosis (AS), obesity, diabetes and ischemic stroke (IS) and its potential key role in cardiovascular disease in order to provide new ideas for the prevention and treatment of cardiovascular diseases.
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http://dx.doi.org/10.1080/10641963.2019.1693585DOI Listing
July 2020

The psychosocial adaptation of patients with skin disease: a scoping review.

BMC Public Health 2019 Oct 29;19(1):1404. Epub 2019 Oct 29.

Department of Nursing, The First affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.

Background: Skin disease is a global public health problem that often has physiological, psychological and social impacts. However, it is not very clear how to adapt to these impacts, especially psychosocial adaptation of patients with skin disease.

Methods: We searched EMBASE, PubMed, CINAHL and PsycINFO from 2009 to 2018. The following themes were extracted from the included articles: the concepts, related factors, and interventions for psychosocial adaptation of patients with skin disease. Two reviewers independently screened and analyzed.

Results: From 2261 initial records, 69 studies were identified and analyzed. The concept of psychosocial adaptation in patients with skin disease was referred to under an assortment of descriptions. The related factors for psychosocial adaptation in patients with skin disease included the following: demographic factors (sex, age, education level, ethnicity, BMI, sleep quality, marital status, exercise amount, family history, the use of topical treatment only, personality and history of smoking); disease-related factors (disease severity, clinical symptoms, localization and duration); psychological factors (anxiety/depression, self-esteem, body image, stigma and suicidal ideation); and social factors (social support, social interaction, sexual life, economic burden and social acceptance). Despite being limited in quantity, several studies have clarified the benefits of adjuvant care in the form of cognitive behavioral training, educational training and self-help programs, all of which have become common methods for dealing with the psychosocial impacts.

Conclusions: Based on the previous literatures, we constructed a protocol of care model for psychosocial adaptation in patients with skin disease. It not only provided the direction for developing new instruments that could assess psychosocial adaptation statue, but also a basis for helping patients adjust to changes in skin disease.
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http://dx.doi.org/10.1186/s12889-019-7775-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6819547PMC
October 2019

Factors influencing medication-taking behaviour with adjuvant endocrine therapy in women with breast cancer: A qualitative systematic review.

J Adv Nurs 2020 Feb 13;76(2):445-458. Epub 2019 Nov 13.

Department of Nursing, The First Affiliated Hospital of China Medical University, Shenyang, China.

Aims: To explore the experience and feelings associated with the endocrine therapy treatment trajectory in women with breast cancer and what affects medication taking behaviour.

Design: Qualitative systematic review.

Data Sources: Qualitative studies were extracted from PubMed, EMBASE, CINAHL, PsycINFO from inception of each database until February 2019.

Review Methods: The systematic search method SPIDER (sample, phenomenon of interest, design, evaluation, research type) was used. Thematic synthesis of the qualitative data was used.

Results: A total of 478 were identified in the initial search. Only 17 articles met inclusion criteria and were included in this review. Five analytical themes and 17 descriptive subthemes were identified.

Conclusions: The systematic review highlights knowledge, balancing the scales, self-efficacy and support influence medication taking behaviour to women with breast cancer.

Impact: The medication taking behaviour of breast cancer women can be classified into four types: acceptance/persistence, bearing/suffering, hesitation/adjustment, refusing/abandoning. The four types can switch from one to another. Medication taking behaviour is affected by knowledge, balancing the scales, self-efficacy, and support. The medical institutions, communities, and families can gain knowledge of the treatment experiences of women to better understand medication taking behaviour and those at risk for non-adherence. Women wanted different types and amounts of information. Healthcare providers should be aware of patient preferences and take targeted interventions to help them receive treatment.
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http://dx.doi.org/10.1111/jan.14253DOI Listing
February 2020

Berberine inhibits adipocyte differentiation, proliferation and adiposity through down-regulating galectin-3.

Sci Rep 2019 09 16;9(1):13415. Epub 2019 Sep 16.

State Key Laboratory of Bioactive Natural Products and Function, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

This study is designed to investigate the effects of berberine (BBR) on galectin-3 (Gal-3) and the relationships to its suppressive activities on adipocyte differentiation, proliferation and adiposity. Our results showed that BBR greatly suppressed the differentiation and proliferation of mouse primary preadipocytes isolated from epididymal white adipose tissue (eWAT), during which the expression level of Gal-3 was down-regulated significantly. Overexpression of Gal-3 totally abolished the suppressive activities of BBR on Gal-3 expression, preadipocyte differentiation and proliferation. BBR reduced Gal-3 promoter activity, destabilized its mRNA and inhibited firefly luciferase activity of a recombinant plasmid containing the Gal-3 3' untranslated region (UTR). Furthermore, BBR up-regulated microRNA (miRNA) let-7d expression and the suppressive activity on Gal-3 3'UTR was abolished by point mutation on the let-7d binding site. In mice fed a high-fat diet (HFD), BBR up-regulated let-7d and down-regulated Gal-3 expression in eWAT; it also suppressed adipocyte differentiation and proliferation and reduced adiposity greatly. In summary, our study proves that BBR inhibits the differentiation and proliferation of adipocytes through down-regulating Gal-3, which is closely associated with its anti-obesity effect. Our results may support the future clinical application of BBR for the treatment of obesity or related diseases.
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http://dx.doi.org/10.1038/s41598-019-50103-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6746795PMC
September 2019

Oxymatrine ameliorates insulin resistance in rats with type 2 diabetes by regulating the expression of KSRP, PETN, and AKT in the liver.

J Cell Biochem 2019 09 14;120(9):16185-16194. Epub 2019 May 14.

Office of Good Clinical Practice, The Affiliated Changsha Hospital of Hunan Normal University, Changsha, Hunan, China.

Insulin resistance plays a key role in the development and progression of type 2 diabetes mellitus (T2DM). Recent studies found that insulin resistance was associated with the dysfunction of KH-type splicing regulatory protein (KSRP) expression and AKT pathway, and that oxymatrine possesses an antidiabetic effect. The aim of the present study was to investigate whether the protection of oxymatrine against T2DM was associated with the modulation of the KSRP expression and AKT pathway. Sprague-Dawley rats were fed a high-fat diet and injected with streptozotocin intraperitoneally to induce T2DM, which led to an increase in blood glucose levels and insulin resistance, and a decrease in insulin sensitivity and glycogen synthesis concomitant with KSRP downregulation, PTEN upregulation, and AKT phosphorylation deficiency. The administration of oxymatrine decreased blood glucose levels and insulin resistance, increased insulin sensitivity, and improved glycogen synthesis in the liver of T2DM rats, through a reversal in the expression of KSRP, PTEN, and AKT. On the basis of these observations, we concluded that oxymatrine can protect T2DM rats from insulin resistance through the regulation of the KSRP, PETN, and AKT expression in the liver.
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http://dx.doi.org/10.1002/jcb.28898DOI Listing
September 2019

Prevalence and clinical characteristics of hypertension and metabolic syndrome in newly diagnosed patients with ketosis-onset diabetes: a cross-sectional study.

Diabetol Metab Syndr 2019 25;11:31. Epub 2019 Apr 25.

1Department of Endocrinology and Metabolism, Shanghai Clinical Center for Diabetes, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Key Clinical Center for Metabolic Disease, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road, Shanghai, 200233 China.

Background: To investigate the prevalence and clinical characteristics of hypertension (HTN) and metabolic syndrome (MetS) in newly diagnosed diabetes with ketosis-onset.

Methods: A cross-sectional study was adopted in 734 newly diagnosed diabetics including 83 type 1 diabetics with positive islet-associated autoantibodies, 279 ketosis-onset diabetics without islet-associated autoantibodies and 372 non-ketotic type 2 diabetics. The clinical characteristics of HTN and MetS were compared across the three groups, and the risk factors of them were appraised in each group.

Results: The prevalence of HTN and MetS were substantially higher in the ketosis-onset diabetics (34.4% for HTN and 58.8% for MetS) than in the type 1 diabetics (15.7% for HTN, = 0.004; 25.3% for MetS, < 0.001), but showed no remarkable difference compared with the type 2 diabetics (42.7% for HTN, = 0.496; 72.3% for MetS, = 0.079). Furthermore, the risk factors for both HTN and MetS in the ketosis-onset diabetics resembled those in the type 2 diabetics, but significantly different from those in the type 1 diabetics.

Conclusions: The prevalence of HTN and MetS in the ketosis-onset diabetics were magnificently higher than in the type 1 diabetics but showed no difference in comparison to the type 2 diabetics. Likewise, the clinical features and risk factors of HTN and MetS in the ketosis-onset diabetes resembled those in the type 2 diabetes but differed from those in the type 1 diabetes. Our findings indicate that ketosis-onset diabetes should be classified into type 2 diabetes rather than idiopathic type 1 diabetes.
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http://dx.doi.org/10.1186/s13098-019-0426-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6482555PMC
April 2019

Comparative toxicity and toxicokinetic studies of oxiracetam and (S)-oxiracetam in dogs.

Xenobiotica 2019 Sep 4;49(9):1054-1062. Epub 2019 Jan 4.

a New Drug Safety Evaluation Center, Institute of Materia Medica , Chinese Academy of Medical Sciences and Peking Union Medical College , Beijing , China.

Oxiracetam (ORT) is known as a derivative of piracetam in the family of nootropics for treating memory impairment and cognition disorders. Given the chiral toxicological concerns surrounding ORT and the absence studies of (S)-ORT, the toxicity and toxicokinetics of (S)-ORT, and comparative toxicology of oxiracetam were systematically investigated in dogs following acute and 13-week repeated oral dosing. The animal toxicity mainly manifested as loose stools in both the acute and the 13-week studies. The no-observed-adverse-effect level is proposed to be 100 mg/kg. The 13-week toxicokinetics study indicated that, in the (S)-ORT group, the time to peak concentration was delayed, elimination half-life extended, and apparent volume of distribution increased compared with the ORT group. The clearance rate increased at low- and mid-doses, but decreased in the high-dose group and was accompanied by drug accumulation. Compared with the same dose of ORT, (S)-ORT had a lower clearance rate and longer elimination half-life.
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http://dx.doi.org/10.1080/00498254.2018.1528027DOI Listing
September 2019

Genotoxicity and Embryotoxicity Study of Bicyclol Methyl Ether, Main Impurity in Bicyclol.

Chin J Integr Med 2019 Oct 22;25(10):743-749. Epub 2018 Sep 22.

New Drug Safety Evaluation Center, Institute of Materia Medica, Chinese Academy of Medical Sciences, Beijing, 100050, China.

Objective: To assess the genotoxicity and embryotoxicity of bicyclol methyl ether (BME), the main impurity in bicyclol.

Methods: Five concentrations of BME (0.5, 5, 50, 500 and 5000 μg/plate) were used in the Ames test to detect gene mutation. In the chromosome aberration test, Chinese hamster lung cells were used to detect chromosomal aberration of BME (15, 30, 60, 120 μg/mL) with or without S9 mixture. Embryotoxicity test was also conducted to determine any embryotoxicity of BME (7.5, 22.5, 67.5 μg/L) using zebrafish embryos.

Results: No significant differences were observed in the Ames test and the chromosome aberration test in the BME groups compared with the vehicle control group. The zebrafish embryos toxicity test also showed no embryo development toxicity of BME, including hatching rate, body length, pericardial area and yolk sac area.

Conclusions: Bicyclol methyl ether has no genotoxicity in vitro and embryotoxicity in zebrafish embryos, and the impurity in bicyclol is qualified.
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http://dx.doi.org/10.1007/s11655-018-2553-xDOI Listing
October 2019

Hydrogen Sulfide Antagonizes Chronic Restraint Stress-Induced Depressive-Like Behaviors via Upregulation of Adiponectin.

Front Psychiatry 2018 31;9:399. Epub 2018 Aug 31.

Institute of Neuroscience, Medical College, University of South China, Hengyang, China.

Chronic restraint stress (CRS) induces depressive-like behaviors in rodents, which involves dysregulation of hippocampal synapse formation and excessive autophagy. Adiponectin has antidepressant activity. Hydrogen sulfide (HS) is a novel gasotransmitter. The present work was to investigate whether HS antagonizes CRS-induced depressive-like behaviors in rats and to explore whether its potential mechanism involves ameliorated synaptic and autophagic dysregulation by upregulation of adiponectin. Depressive-like behavior was analyzed by the tail suspension test (TST), novelty suppressed feeding test (NSFT), and open field test (OFT). The structure of autophagy was observed under transmission electron microscopy. The expressions of adiponectin, beclin1, and sequestosome 1 (p62/SQSTMI) protein in hippocampus were measured by Western blot. The levels of synapsin1 (SYN1) in the hippocampus were calculated by Western blot and immunofluorescence technique. The behavior experiments, including TST, NSFT, and OFT, showed that NaHS (a donor of HS) reduced CRS-induced depressive-like behaviors. NaHS decreased the loss of hippocampal synapse as evidenced by increased the level of SYN1 in the hippocampus of CRS-exposed rats. NaHS rescued CRS-induced excessive hippocampal autophagy as evidenced by declines in the number of autophagosomes and the expression of beclin1 as well as increase in the expression of P62 in the hippocampus of CRS-exposed rats. NaHS upregulated hippocampal adiponectin expression in the CRS-exposed rats. Furthermore, neutralizing adiponectin by Anti-acrp30 reversed the protective response of NaHS to CRS-produced depressive-like behaviors as well as hippocampal synaptic disruption and excessive autophagy. HS mitigates CRS-induced depressive behavior via upregulation of adiponectin, which in turn results in amelioration in hippocampal synapse formation dysfunction and excessive autophagy.
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http://dx.doi.org/10.3389/fpsyt.2018.00399DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6127318PMC
August 2018

Role of ALK5/SMAD2/3 signaling in the regulation of NOX expression in cerebral ischemia/reperfusion injury.

Exp Ther Med 2018 Sep 29;16(3):1671-1678. Epub 2018 Jun 29.

Department of Pharmacy, The Affiliated Changsha Hospital of Hunan Normal University, Changsha, Hunan 410006, P.R. China.

Nicotinamide adenine dinucleotide phosphate oxidase (NOX)-derived reactive oxygen species (ROS) serve an important role in cerebral ischemia/reperfusion (I/R) injury. However, the mechanism by which ROS generation is regulated has not yet been fully elucidated. The present study aimed to explore the role of transforming growth factor-β signaling in ROS generation. Sprague Dawley rats were subjected to I/R injury and PC-12 cells were transfected with small interfering RNA against activin receptor-like kinase (ALK)5 or hypoxia/reoxygenation (H/R). The results indicated that I/R or H/R significantly increased ALK5 expression, SMAD2/3 phosphorylation and NOX2/4 expression and activity, concomitant with ROS generation and apoptosis. In addition, ALK5 knockdown significantly reversed changes induced by H/R treatment in PC-12 cells. These results suggest that ALK5/SMAD2/3 signaling serves a key role in oxidative stress. To the best of our knowledge, this is the first study to demonstrate that ALK5/SMAD2/3 activation is associated with the regulation of NOX2/4 expression and exacerbates I/R injury.
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http://dx.doi.org/10.3892/etm.2018.6377DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6122315PMC
September 2018

Perivascular adipose tissue dysfunction aggravates adventitial remodeling in obese mini pigs via NLRP3 inflammasome/IL-1 signaling pathway.

Acta Pharmacol Sin 2019 Jan 12;40(1):46-54. Epub 2018 Jul 12.

Research Lab of Translational Medicine, Medical School, University of South China, Hengyang, 421001, China.

Perivascular adipose tissue (PVAT), a special type of adipose tissue, closely surrounds vascular adventitia and produces numerous bioactive substances to maintain vascular homeostasis. PVAT dysfunction has a crucial role in regulating vascular remodeling, but the exact mechanisms remain unclear. In this study, we investigated whether and how obesity-induced PVAT dysfunction affected adventitia remodeling in early vascular injury stages. Mini pigs were fed a high sugar and fat diet for 6 months to induce metabolic syndrome and obesity. In the mini pigs, left carotid vascular injury was then generated using balloon dilation. Compared with normal mini pigs, obese mini pigs displayed significantly enhanced vascular injury-induced adventitial responses, evidenced by adventitia fibroblast (AF) proliferation and differentiation, and adventitia fibrosis, as well as exacerbated PVAT dysfunction characterized by increased accumulation of resident macrophages, particularly the M1 pro-inflammatory phenotype, increased expression of leptin and decreased expression of adiponectin, and production of pro-inflammatory cytokines interleukin (IL)-1β and IL-18. Primary AFs cultured in PVAT-conditioned medium from obese mini pigs also showed significantly increased proliferation and differentiation. We further revealed that activated nod-like receptor protein 3 (NLRP3) inflammasome and its downstream products, i.e., IL-1 family members such as IL-1β and IL-18 were upregulated in the PVAT of obese mini pigs; PVAT dysfunction was also demonstrated in preadipocytes treated with palmitic acid. Finally, we showed that pretreatment with IL-1 receptor (IL-1R) antagonist or IL-1R knockdown blocked AF proliferation and differentiation in AFs cultured in PVAT-conditioned medium. These results demonstrate that obesity-induced PVAT dysfunction aggravates adventitial remodeling after early vascular injury with elevated AF proliferation and differentiation via activating the NLRP3/IL-1 signaling pathway.
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http://dx.doi.org/10.1038/s41401-018-0068-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6318288PMC
January 2019

Development of a Quality of Sexual Life Questionnaire for Breast Cancer Survivors in Mainland China.

Med Sci Monit 2018 Jun 16;24:4101-4112. Epub 2018 Jun 16.

Department of Nursing, First Affiliated Hospital of China Medical University, Shenyang, Liaoning, China (mainland).

BACKGROUND There is a great need for a quality of sexual life questionnaire (QVS) in breast cancer survivors (BCSs) based on the Chinese social culture since the imported tools lack localization verification. To develop a QVS in BCSs and determine its validity and reliability. MATERIAL AND METHODS In the qualitative study, a total of 21 BCSs were interviewed by purposive sampling and snowball sampling; and in the quantitative study, a total of 249 BCSs, who were admitted and received outpatient follow-up, were investigated. Regarding construct validity, factor analysis was performed. The female sexual function index (FSFI), self-rating depression scale (SDS), and Locke-Wallace marital adjustment test (LWMAT) were used to evaluate criterion validity. Cronbach's alpha coefficient was used as an index of internal consistency. To evaluate test-retest reliability, 50 patients were re-evaluated after 1 week. RESULTS We put 28 items in the factor analysis model: (1) 5 factors were extracted by exploratory factor analysis (EFA), with a cumulative contribution of 60.37%; (2) the confirmatory factor analysis (CFA) showed that the path coefficients among the factors were all above 0.5, and the standardized load coefficients of the most items were above 0.5; (3) the Cronbach's alpha coefficient was 0.929 for the overall questionnaire, and ranged from 0.571 to 0.869 for the 5 factors; (4) the correlation coefficients between the overall questionnaire and the FSFI, SDS, and LWMAT were 0.582, -0.456 and 0.515, respectively (P<0.01); and (5) the test-retest correlation coefficient was 0.816, and the split-half-reliability coefficient was 0.899. CONCLUSIONS The QVS in BCSs has good reliability and validity, and can be used to assess the quality of sexual life among BCSs in Mainland China.
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http://dx.doi.org/10.12659/MSM.906666DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6035499PMC
June 2018

The zonal pattern of arterial supply to the brachial plexus and its clinical significance.

Surg Radiol Anat 2018 Jul 8;40(7):815-822. Epub 2018 May 8.

Clinical Anatomy & Reproductive Medicine Application Institute, School of Medicine, University of South China, Hengyang, 421001, China.

Purpose: To provide the anatomical basis of blood supply of brachial plexus for the clinical microsurgical treatment of brachial plexus injury.

Methods: Thirteen adult anticorrosive cadaveric specimens (8 males, 5 females) were dissected in this study. 3 fresh cases (2 males, 1 female) were used to observe the zonal pattern of arteries supplying brachial plexus, and 10 cases (6 males, 4 females) were used to observe the source and distribution of the brachial plexus arteries under microscope.

Results: The brachial plexus is supplied by branches of the subclavian-axillary axis (SAA), and these branches anastomose each other. According to distribution feature, blood supply of the brachial plexus could be divided into three zones. The first zone was from the nerve roots of intervertebral foramina to its proximal trunks, which was supplied by the vertebral artery and the deep cervical artery. The second zone was from the distal nerve trunks of the brachial plexus, encompassing the divisions to its proximal cords, which was supplied by direct branches of the subclavian artery or by branches originating from the dorsal scapular artery. The third zone was from the distal portion of the cords to terminal branches of the brachial plexus, which was supplied by direct branches of the axillary artery.

Conclusions: The zonal pattern of arterial supply to the brachial plexus is a systematic and comprehensive modality to improve anatomical basis for the clinical microsurgical treatment for brachial plexus injury.
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http://dx.doi.org/10.1007/s00276-018-2024-2DOI Listing
July 2018

Upregulation of NOX2 and NOX4 Mediated by TGF-β Signaling Pathway Exacerbates Cerebral Ischemia/Reperfusion Oxidative Stress Injury.

Cell Physiol Biochem 2018 28;46(5):2103-2113. Epub 2018 Apr 28.

The Affiliated Changsha Hospital of Hunan Normal University, Changsha, China.

Background/aims: Ischemic stroke is still one of the leading debilitating diseases with high morbidity and mortality. NADPH oxidase (NOX)-derived reactive oxygen species (ROS) play an important role in cerebral ischemia/reperfusion (I/R) injury. However, the mechanism underlying the regulation of ROS generation is still not fully elucidated. This study aims to explore the role of transforming growth beta (TGF-β) signals in ROS generation.

Methods: Sprague-Dawley rats were subjected to I/R injury, and PC-12 cells were challenged by hypoxia/reoxygenation (H/R) and/or treated with activin receptor-like kinase (ALK5) inhibitor Sb505124 or siRNA against ALK5. Brain damage was evaluated using neurological scoring, triphenyl tetrazolium chloride staining, hematoxylin and eosin staining, infarct volume measurement, TUNEL staining, and caspase-3 activity measurement. Expression of TGF-β and oxidative stress-related genes was analyzed by real-time polymerase chain reaction and Western blot; NOX activity and ROS level were measured using spectrophotometry and fluorescence microscopy, respectively.

Results: I/R contributed to severe brain damage (impaired neurological function, brain infarction, tissue edema, apoptosis), TGF-β signaling activation (upregulation of ALK5, phosphorylation of SMAD2/3) and oxidative stress (upregulation of NOX2/4, rapid release of ROS [oxidative burst]). However, Sb505124 significantly reversed these alterations and protected rats against I/R injury. As in the animal results, H/R also contributed to TGF-β signaling activation and oxidative stress. Likewise, the inhibition of ALK5 or ALK5 knockdown significantly reversed these alterations in PC-12 cells. Other than ALK5 knockdown, ALK5 inhibition had no effect on the expression of ALK5 in PC-12 cells.

Conclusions: Our studies demonstrated that TGF-β signaling activation is involved in the regulation of NOX2/NOX4 expression and exacerbates cerebral I/R injury.
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http://dx.doi.org/10.1159/000489450DOI Listing
August 2018

Spermidine prevents high glucose-induced senescence in HT-22 cells by upregulation of CB1 receptor.

Clin Exp Pharmacol Physiol 2018 08 5;45(8):832-840. Epub 2018 Jun 5.

Institute of Neuroscience, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, Hunan, China.

Hyperglycaemia-induced neurotoxicity involved in the pathogenesis of diabetic encephalopathy and neuronal senescence is one of the worst effects of hyperglyceamic neurotoxicity. Cannabinoid receptor type 1 (CB1) has neuroprotective function in a series of neuropathy. Spermidine (Spd) has anti-aging function in many tissues. However, the role of Spd in hyperglyceamia-induced neuronal senescence remains unexplored. Therefore, we used high glucose (HG)-treated HT-22 cell as vitro model to investigate whether Spd protects neurons against hyperglyceamia-induced senescence and the mediatory role of CB1 receptor. The HT-22 cells were cultured in HG condition in the presence of different dose of Spd. Then, the viability of cells was measured by Cell Counting Kit-8 (CCK-8) assay. The senescence of cells was detected by Senescence-associated β-galactosidase (SA-β-Gal) staining. The expressions of p16 , p21 and CB1 receptor were measured by western blot. We found that Spd inhibited HG-induced neurotoxicity (the loss of cell viability) and senescence (the increase of SA-β-Gal positive cells, the upregulation of p16 and p21 ) in HT-22 cells. Also, Spd prevented HG-induced downregulation of CB1 receptor in HT-22 cells. Furthermore, we demonstrated that AM251 (a specific inhibitor of the CB1 receptor) reversed the protective effects of Spd on HG-induced neurotoxicity and senescence. These results indicated that Spd prevents HG-induced neurotoxicity and senescence via the upregulation of CB1 receptor. Our findings provide a promising future of Spd-based preventions and therapies for diabetic encephalopathy.
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http://dx.doi.org/10.1111/1440-1681.12955DOI Listing
August 2018

A novel variant in MITF in a child from Yunnan-Guizhou Plateau with autosomal dominant inheritance of nonsyndromic hearing loss: A case report.

Mol Med Rep 2018 Apr 22;17(4):6054-6058. Epub 2018 Feb 22.

Department of Human Anatomy, Zhongshan School of Medicine, Sun Yat‑Sen University, Guangzhou, Guangdong 510080, P.R. China.

Deafness and hearing loss may have functional, economic, social and emotional impacts on humans, including the ability of an individual to communicate with others, feelings of isolation and frustration, and health sector costs. The World Health Organization reported that there are 32 million children worldwide with hearing loss. In order to investigate genetic mutations in children of 26 nationalities with hearing loss in Yunnan, Sanger sequencing was employed to screen for mutations in four of the most common pathological genes, including gap junction protein β2 and 3, solute carrier family 26 member 4 and mitochondrial DNA. Whole exome sequencing was used to detect the mutation in the proband of a family in which these four genes were normal. Subsequently, the mutation was identified by Sanger sequencing. The present study reports a novel mutation, c.718C>G; p. (Arg240Gly) in the melanogenesis associated transcription factor gene, in Han people with hearing loss. The results of the present study may provide parents and children an accurate diagnosis, which may allow physicians to how to rehabilitate children's hearing.
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http://dx.doi.org/10.3892/mmr.2018.8627DOI Listing
April 2018

Role of silent information regulator 1 in the protective effect of hydrogen sulfide on homocysteine-induced cognitive dysfunction: Involving reduction of hippocampal ER stress.

Behav Brain Res 2018 04 4;342:35-42. Epub 2018 Jan 4.

Institute of Neuroscience, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Medical College, University of South China, Hengyang, 421001, Hunan, PR China; Department of Physiology, Medical College, University of South China, Hengyang, 421001, Hunan, PR China; Department of Neurology, Nanhua Affiliated Hospital, University of South China, Hengyang, 421001, Hunan, PR China. Electronic address:

Homocysteine (Hcy) causes cognitive deficits and hippocampal endoplasmic reticulum (ER) stress. Our previous study has confirmed that Hydrogen sulfide (HS) attenuates Hcy-induced cognitive dysfunction and hippocampal ER stress. Silent information regulator 1 (Sirt-1) is indispensable in the formation of learning and memory. Therefore, the aim of this study was to explore the role of Sirt-1 in the protective effect of HS against Hcy-induced cognitive dysfunction. We found that NaHS (a donor of HS) markedly up-regulated the expression of Sirt-1 in the hippocampus of Hcy-exposed rats. Sirtinol, a specific inhibitor of Sirt-1, reversed the improving role of NaHS in the cognitive function of Hcy-exposed rats, as evidenced by that sirtinol increased the escape latency and the swim distance in the acquisition trial of morris water maze (MWM) test, decreased the times crossed through and the time spent in the target quadrant in the probe trail of MWM test, and reduced the discrimination index in the novel object recognition test (NORT) in the rats cotreated with NaHS and Hcy. We also found that sirtinol reversed the protection of NaHS against Hcy-induced hippocampal ER-stress, as evidenced by up-regulating the expressions of GRP78, CHOP, and cleaved caspase-12 in the hippocampus of rats cotreated with NaHS and Hcy. These results suggested the contribution of upregulation of hippocampal Sirt-1 to the improving role of HS in the cognitive function of Hcy-exposed rats, which involves suppression of hippocampal ER stress. Our finding provides a new insight into the mechanism underlying the inhibitory role of HS in Hcy-induced cognitive dysfunction.
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http://dx.doi.org/10.1016/j.bbr.2017.12.040DOI Listing
April 2018

Anti-Psoriasis Effects and Mechanisms of Α-(8-Quinolinoxy) Zinc Phthalocyanine-Mediated Photodynamic Therapy.

Cell Physiol Biochem 2017 9;44(1):200-214. Epub 2017 Nov 9.

Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.

Background/aims: The aim of this study was to determine the anti-psoriasis effects of α-(8-quinolinoxy) zinc phthalocyanine (ZnPc-F7)-mediated photodynamic therapy (PDT) and to reveal its mechanisms.

Methods: HaCaT cells were used to observe the influence of ZnPc-F7-PDT on cell proliferation in vitro. The in vivo anti-psoriasis effects of ZnPc-F7-PDT were evaluated using a mouse vagina model, a propranolol-induced cavy psoriasis model and an imiquimod (IMQ)-induced nude mouse psoriasis model. Flow cytometry was carried out to determine T lymphocyte levels. Western blotting was performed to determine protein expression, and a reverse transcription-polymerase chain reaction test was performed to determine mRNA expression.

Results: The results showed that ZnPc-F7-PDT significantly inhibited the proliferation of HaCaT cells in vitro; when the light doses were fixed, changing the irradiation time or output power had little influence on the inhibition rate. ZnPc-F7-PDT significantly inhibited the hyperproliferation of mouse vaginal epithelium induced by diethylstilbestrol and improved propranolol- and IMQ-induced psoriasis-like symptoms. ZnPc-F7-PDT inhibited IMQ-induced splenomegaly and T lymphocyte abnormalities. ZnPc-F7-PDT did not appear to change T lymphocytes in the mouse vagina model. ZnPc-F7-PDT down-regulated the expression of proliferating cell nuclear antigen (PCNA), B-cell lymphoma-2 (Bcl-2), interleukin (IL)-17A mRNA and IL-17F mRNA, and up-regulated the expression of Bax.

Conclusion: In conclusion, ZnPc-F7-PDT exhibited therapeutic effects in psoriasis both in vitro and in vivo and is a potential approach in the treatment of psoriasis. Potential mechanisms of these effects included the inhibition of hyperproliferation; regulation of PCNA, Bcl-2, Bax, IL-17A mRNA and IL-17F mRNA expression; and immune regulation.
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http://dx.doi.org/10.1159/000484647DOI Listing
March 2018

Time-response characteristic and potential biomarker identification of heavy metal induced toxicity in zebrafish.

Fish Shellfish Immunol 2018 Jan 28;72:309-317. Epub 2017 Oct 28.

Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, No. 1 Xian Nong Tan Street, Postal Code 100050, Beijing, China. Electronic address:

The present work aims to explore the time-response (from 24 h to 96 h) characteristic and identify early potential sensitive biomarkers of copper (Cu) (as copper chloride dihydrate), cadmium (Cd) (as cadmium acetate), lead (Pb) (as lead nitrate) and chromium (Cr) (as potassium dichromate) exposure in adult zebrafish, focusing on reactive oxygen species (ROS), SOD activity, lipid peroxidation and gene expression related to oxidative stress and inflammatory response. Furthermore, the survival rate decreased apparently by a concentration-dependent manner after Cu, Cr, Cd and Pb exposure, and we selected non-lethal concentrations 0.05 mg/L for Cu, 15 mg/L for Cr, 3 mg/L for Cd and 93.75μg/L for Pb to test the effect on the following biological indicators. Under non-lethal concentration, the four heavy metals have no apparent histological change in adult zebrafish gills. Similar trends in ROS production, MDA level and SOD activity were up-regulated by the four heavy metals, while MDA level responded more sensitive to Pb by time-dependent manner than the other three heavy metals. In addition, mRNA levels related to antioxidant system (SOD1, SOD2 and Nrf2) were up-regulated by non-lethal concentration Cu, Cr, Cd and Pb exposure. MDA level and SOD1 gene have a more delayed response to heavy metals. Genes related to immunotoxicity were increased significantly after heavy metals exposure at non-lethal concentrations. TNF-α and IL-1β gene have similar sensibility to the four heavy metals, while IL-8 gene was more responsive to Cr, Cd and Pb exposure at 48 h groups and IFN-γ gene showed more sensitivity to Cu at 48 h groups than the other heavy metals. In conclusion, the present works have suggested that the IFN-γ gene may applied as early sensitive biomarker to identify Cu-induced toxicity, while MDA content and IL-8 gene may use as early sensitive biomarkers for evaluating the risk of Pb exposure. Moreover, IL-8 and IFN-γ gene were more responsive to heavy metals, which may become early sensitive and potential biomarkers for evaluating inflammatory response induced by heavy metals. This work reinforces the concept of the usefulness of gene expression assays in the evaluation of chemicals effects and helps to establish a background data as well as contributes to evaluate early environmental risk for chemicals, even predicting toxicity.
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http://dx.doi.org/10.1016/j.fsi.2017.10.047DOI Listing
January 2018