Publications by authors named "Qing-Tao Meng"

53 Publications

Corrigendum: Mechanism and Management of Fentanyl-Induced Cough.

Front Pharmacol 2020 11;11:629157. Epub 2020 Dec 11.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.

[This corrects the article DOI: 10.3389/fphar.2020.584177.].
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http://dx.doi.org/10.3389/fphar.2020.629157DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7760133PMC
December 2020

Mechanism and Management of Fentanyl-Induced Cough.

Front Pharmacol 2020 28;11:584177. Epub 2020 Oct 28.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.

Fentanyl-induced cough (FIC) often occurs after intravenous bolus administration of fentanyl analogs during induction of general anesthesia and analgesia procedure. The cough is generally benign, but sometimes it causes undesirable side effects, including elevated intra-abdominal, intracranial or intraocular pressure. Therefore, understanding the related mechanisms and influencing factors are of great significance to prevent and treat the cough. This paper reviews the molecular mechanism, influencing factors and preventive administration of FIC, focusing on the efficacy and side effects of various drugs in inhibiting FIC to provide some medical reference for anesthesiologists.
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http://dx.doi.org/10.3389/fphar.2020.584177DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7723435PMC
October 2020

Gastrointestinal Symptoms Associated With Unfavorable Prognosis of COVID-19 Patients: A Retrospective Study.

Front Med (Lausanne) 2020 11;7:608259. Epub 2020 Nov 11.

Division Anaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, Chelsea and Westminster Hospital, London, United Kingdom.

The global pandemic of COVID-19 has posed an enormous threat to the economy and people's lives across various countries. Patients with COVID-19 most commonly present with respiratory symptoms. However, gastrointestinal (GI) symptoms can also occur. We aimed to study the relationship between GI symptoms and disease prognosis in patients with COVID-19. In a single-center and retrospective cohort study, the outcomes in COVID-19 patients with or without GI symptoms were compared. The propensity score is a conditional probability of having a particular exposure (COVID-19 patients with GI symptoms vs. without GI symptoms) given a set of baseline measured covariates. Survival was estimated using the Kaplan-Meier method, and any differences in survival were evaluated with a stratified log-rank-test. To explore the GI symptoms associated with ARDS, non-invasive ventilator treatment, tracheal intubation, tracheotomy, and CRRT, univariable and multivariable COX regression models were used. Among 1,113 eligible patients, 359 patients with GI symptoms and 718 without GI symptoms had similar propensity scores and were included in the analyses. Patients with GI symptoms, as compared with those without GI symptoms, were associated with a similar risk of death, but with higher risks of ARDS, non-invasive mechanical ventilation in COVID-19 patients, respectively. The presence of GI symptoms was associated with a high risk of ARDS, non-invasive mechanical ventilation and tracheal intubation in patients with COVID-19 but not mortality.
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http://dx.doi.org/10.3389/fmed.2020.608259DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7686879PMC
November 2020

Epigenetic modulation of the MAPK pathway prevents isoflurane-induced neuronal apoptosis and cognitive decline in aged rats.

Exp Ther Med 2020 Nov 1;20(5):35. Epub 2020 Sep 1.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

Isoflurane is a broadly used inhalation anesthetic that causes cognitive impairment in rodent models as well as humans. Although previous studies suggested an association between isoflurane exposure and neuro-inflammation, apoptosis and mitochondrial dysfunction, the pathogenesis of isoflurane-induced cognitive decline remains elusive. In the present study, 22-month-old male Sprague-Dawley male rats (n=96) were divided into three groups: Control (Cont), isoflurane (ISO) and MS-275 pre-treated groups. The rats were sacrificed following exposure to isoflurane and a cognitive test. The hippocampus of each animal was harvested for quantitative PCR, TUNEL staining and western blot analysis. Histone deacetylases (HDAC)-1, -2 and -3 exhibited a significant increase at the gene and protein expression levels, whereas negligible mRNA expressions were observed for genes HDAC 4-11 (P>0.05; compared with Cont). Pre-treatment with the HDAC inhibitor MS-275 significantly inhibited the increase in TUNEL-positive cells induced by isoflurane exposure (70.72% decrease; P<0.001; compared with ISO). Furthermore, MS-275 significantly decreased caspase-3 and Bax expression levels while increasing Bcl-2 protein expression. The isoflurane-induced changes in the MAPK pathway signaling proteins ERK1/2, JNK and p38 were also reversed with MS-275 pre-treatment. Finally, in a Morris water maze test, the time to find a hidden platform was reduced in MS-275 pre-treated rats, compared with the ISO group. Therefore, the present study provided insight into the effect of isoflurane exposure on neuronal apoptosis pathways, as well as cognitive decline via epigenetic programming of MAPK signaling in aged rats.
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http://dx.doi.org/10.3892/etm.2020.9162DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7480129PMC
November 2020

Aggravated intestinal ischemia‑reperfusion injury is associated with activated mitochondrial autophagy in a mouse model of diabetes.

Mol Med Rep 2020 Sep 24;22(3):1892-1900. Epub 2020 Jun 24.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

Numerous studies have reported that diabetes is associated with an increased susceptibility to cardiac ischemia‑ reperfusion injury; however, the mechanism underlying the role of diabetes during intestinal ischemia‑reperfusion (IIR) has yet to be elucidated. The present study evaluated the intestinal pathological alterations and possible underlying mechanisms in a mouse model of type 1 diabetes mellitus with IIR. The effects of diabetes were investigated by assessing the histopathology, oxidative stress, inflammatory cytokine levels in intestine tissues and blood plasma, and protein expression levels of phosphatase and tensin homolog‑induced putative kinase (PINK1), Parkin and the ratio of light chain 3B (LC3B) II/I. The results demonstrated that diabetes increased the Chiu's intestinal injury score, concentration of interleukin (IL)‑1β, IL‑6 and tumor necrosis factor (TNF)‑α, and levels of oxidative stress. Furthermore, the alterations were more pronounced in the diabetes with IIR group. The expression levels of PINK1 and Parkin, as well as the ratio of LC3BII/I, were significantly upregulated in the IIR group compared with the Sham group. Diabetes activated PINK1 and Parkin, and increased the expression of LC3BII. Furthermore, transmission electron microscopy revealed that mitochondrial destruction and the number of autophagosomes was increased in the diabetic groups compared with the non‑diabetic groups. Collectively, the results of the present study suggest that diabetes increased intestinal vulnerability to IIR by enhancing inflammation and oxidative stress. Furthermore, IIR was associated with overactivation of mitochondrial autophagy; therefore, the increased vulnerability to IIR‑induced intestine damage due to diabetes may be associated with PINK1/Parkin‑regulated mitochondrial autophagy.
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http://dx.doi.org/10.3892/mmr.2020.11270DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7411361PMC
September 2020

Ischemic postconditioning attenuates acute kidney injury following intestinal ischemia-reperfusion through Nrf2-regulated autophagy, anti-oxidation, and anti-inflammation in mice.

FASEB J 2020 07 10;34(7):8887-8901. Epub 2020 Jun 10.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.

Intestinal ischemia-reperfusion (IIR) often occurs during and following major cardiovascular or gut surgery and causes significant organ including kidney injuries. This study was to investigate the protective effect of intestinal ischemic postconditioning (IPo) on IIR-induced acute kidney injury (AKI) and the underling cellular signaling mechanisms with focus on the Nrf2/HO-1. Adult C57BL/6J mice were subjected to IIR with or without IPo. IIR was established by clamping the superior mesenteric artery (SMA) for 45 minutes followed by 120 minutes reperfusion. Outcome measures were: (i) Intestinal and renal histopathology; (ii) Renal function; (iii) Cellular signaling changes; (iv) Oxidative stress and inflammatory responses. IPo significantly attenuated IIR-induced kidney injury. Furthermore, IPo significantly increased both nuclear Nrf2 and HO-1 expression in the kidney, upregulated autophagic flux, inhibited IIR-induced inflammation and reduced oxidative stress. The protective effect of IPo was abolished by the administration of Nrf2 inhibitor (Brusatol) or Nrf2 siRNA. Conversely, a Nrf2 activator t-BHQ has a similar protective effect to that of IPo. Our data indicate that IPo protects the kidney injury induced by IIR, which was likely mediated through the Nrf2/HO-1 cellular signaling activation.
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http://dx.doi.org/10.1096/fj.202000274RDOI Listing
July 2020

Avoiding health worker infection and containing the coronavirus disease 2019 pandemic: Perspectives from the frontline in Wuhan.

Int J Surg 2020 Jul 23;79:120-124. Epub 2020 May 23.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China; Department of Anesthesiology, East Hospital, Renmin Hospital of Wuhan University, Wuhan, 430060, China. Electronic address:

Coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused great public concern worldwide due to its high rates of infectivity and pathogenicity. The Chinese government responded in a timely manner, alleviated the dilemma, achieved a huge victory and lockdown has now been lifted in Wuhan. However, the outbreak has occurred in more than 200 other countries. Globally, as of 9:56 am CEST on 19 May 2020, there have been 4,696,849 confirmed cases of COVID-19, including 315,131 deaths, reported to Word Health Organization (WHO). The spread of COVID-19 overwhelmed the healthcare systems of many countries and even crashed the fragile healthcare systems of some. Although the situation in each country is different, health workers play a critical role in the fight against COVID-19. In this review, we highlight the status of health worker infections in China and other countries, especially the causes of infection in China and the standardised protocol to protect health workers from the perspective of an anaesthesiologist, in the hope of providing references to reduce medical infections and contain the COVID-19 epidemic.
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http://dx.doi.org/10.1016/j.ijsu.2020.05.060DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7245215PMC
July 2020

In reply: Spinal anesthesia for Cesarean delivery in women with COVID-19 infection: questions regarding the cause of hypotension.

Can J Anaesth 2020 08 27;67(8):1099-1100. Epub 2020 Apr 27.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.

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http://dx.doi.org/10.1007/s12630-020-01664-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7184817PMC
August 2020

Ischemic Postconditioning Alleviates Intestinal Ischemia-Reperfusion Injury by Enhancing Autophagy and Suppressing Oxidative Stress through the Akt/GSK-3/Nrf2 Pathway in Mice.

Oxid Med Cell Longev 2020 14;2020:6954764. Epub 2020 Mar 14.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.

Aims: Ischemic postconditioning (IPO) has a strong protective effect against intestinal ischemia-reperfusion (IIR) injury that is partly related to autophagy. However, the precise mechanisms involved are unknown.

Methods: C57BL/6J mice were subjected to unilateral IIR with or without IPO. After 45 min ischemia and 120 min reperfusion, intestinal tissues and blood were collected for examination. HE staining and Chiu's score were used to evaluate pathologic injury. We test markers of intestinal barrier function and oxidative stress. Finally, we used WB to detect the expression of key proteins of autophagy and the Akt/GSK-3/Nrf2 pathway.

Results: IPO significantly attenuated IIR injury. Expression levels of LC3 II/I, Beclin-1, and p62 were altered during IIR, indicating that IPO enhanced autophagy. IPO also activated Akt, inhibited GSK-3/Nrf2 pathway.

Conclusion: Our study indicates that IPO can ameliorate IIR injury by evoking autophagy, activating Akt, inactivating GSK-3, and activating Nrf2. These findings may provide novel insights for the alleviation of IIR injury./Nrf2 pathway.
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http://dx.doi.org/10.1155/2020/6954764DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102478PMC
December 2020

In reply: Uncertainty in using chest computed tomography in early coronavirus disease (COVID-19).

Can J Anaesth 2020 07 2;67(7):898-899. Epub 2020 Apr 2.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.

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http://dx.doi.org/10.1007/s12630-020-01640-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7117879PMC
July 2020

Role of adiponectin in diabetes myocardial ischemia-reperfusion injury and ischemic postconditioning.

Acta Cir Bras 2020 23;35(1):e202000107. Epub 2020 Mar 23.

PhD, Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China. Scientific and intellectual content of the study, statistical analysis, final approval.

Purpose: Patients with diabetes are vulnerable to myocardial I/R (ischaemia/reperfusion) injury, but are not responsive to IPO (ischaemic post-conditioning). We hypothesized that decreased cardiac Adiponectin (APN) is responsible for the loss of diabetic heart sensitivity to IPO cardioprotecton.

Methods: Diabetic rats were subjected to I/R injury (30 min of LAD occlusion followed by 120 min of reperfusion). Myocardial infarct area was determined by TTC staining. Cardiac function was monitored by a microcatheter. ANP, 15-F2t-isoprostane, nitrotyrosine and MDA were measured by assay kits. Levels of p-Akt, total-Akt and GAPDH were determined by Western Blot.

Results: Diabetic rats subjected to myocardial IR exhibited severe myocardial infarction and oxidative stress injury, lower APN in the plasma and cardiac p-Akt expression ( P <0.05). IPO significantly attenuated myocardial injury and up-regulated plasma APN content and cardiac p-Akt expression in non-diabetic rats but not in diabetic rats. Linear correlation analysis showed that the expression of adiponectin was positively correlated with p-Akt and negatively correlated with myocardial infarction area ( P <0.01).

Conclusion: Protective effect of IPO was tightly correlated with the expression of adiponectin, exacerbation of I/R injury and ineffectiveness of IPO was partially due to the decline of adiponectin and inactivation of Akt in diabetes mellitus.
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http://dx.doi.org/10.1590/s0102-865020200010000007DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7092667PMC
May 2020

Safety and efficacy of different anesthetic regimens for parturients with COVID-19 undergoing Cesarean delivery: a case series of 17 patients.

Can J Anaesth 2020 06 16;67(6):655-663. Epub 2020 Mar 16.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.

Purpose: To assess the management and safety of epidural or general anesthesia for Cesarean delivery in parturients with coronavirus disease (COVID-19) and their newborns, and to evaluate the standardized procedures for protecting medical staff.

Methods: We retrospectively reviewed the cases of parturients diagnosed with severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection disease (COVID-19). Their epidemiologic history, chest computed tomography scans, laboratory measurements, and SARS-CoV-2 nucleic acid positivity were evaluated. We also recorded the patients' demographic and clinical characteristics, anesthesia and surgery-related data, maternal and neonatal complications, as well as the health status of the involved medical staff.

Results: The clinical characteristics of 17 pregnant women infected with SARS-CoV-2 were similar to those previously reported in non-pregnant adult patients. All of the 17 patients underwent Cesarean delivery with anesthesia performed according to standardized anesthesia/surgery procedures. Fourteen of the patients underwent continuous epidural anesthesia with 12 experiencing significant intraoperative hypotension. Three patients received general anesthesia with tracheal intubation because emergency surgery was needed. Three of the parturients are still recovering from their Cesarean delivery and are receiving in-hospital treatment for COVID-19. Three neonates were born prematurely. There were no deaths or serious neonatal asphyxia events. All neonatal SARS-CoV-2 nucleic acid tests were negative. No medical staff were infected throughout the patient care period.

Conclusions: Both epidural and general anesthesia were safely used for Cesarean delivery in the parturients with COVID-19. Nevertheless, the incidence of hypotension during epidural anesthesia appeared excessive. Proper patient transfer, medical staff access procedures, and effective biosafety precautions are important to protect medical staff from COVID-19.
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http://dx.doi.org/10.1007/s12630-020-01630-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7090434PMC
June 2020

Chest computed tomography images of early coronavirus disease (COVID-19).

Can J Anaesth 2020 06 11;67(6):754-755. Epub 2020 Mar 11.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.

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http://dx.doi.org/10.1007/s12630-020-01625-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7091470PMC
June 2020

Pri-miR-34b/c rs4938723 Polymorphism is Associated with Decreased Risk and Better Prognosis for Colorectal Cancer Patients.

Arch Med Res 2019 02 12;50(2):55-62. Epub 2019 Jun 12.

Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing, China; Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou, China. Electronic address:

Background: Colorectal cancer (CRC) is a major cause of cancer-related deaths worldwide. miR-34 induces changes of its downstream genes and plays a key role in altering the apoptotic cycle and pathways of downstream cells and therefore influences carcinogenesis.

Objective: The present study investigated whether the single nucleotide polymorphism rs4938723T > C in the promoter of region of miR-34b/c may increase the risk of CRC and influence outcome in patients with CRC.

Methods: We enrolled 1078 CRC patients and 1175 cancer-free controls subjects from the Chinese population. miR-34b/c rs4938723T > C polymorphisms were genotyped using a TaqMan PCR method.

Results: We found that subjects carrying rs4938723CT/CC genotypes have significantly decreased risk of CRC (adjusted odds ratios (AOR) = 0.75, 95% CI (0.63-0.90) for CT vs.TT; AOR = 0.61, 95% CI (0.46-0.83) for CC vs. TT and AOR = 0.73,95% CI (0.61-0.86) for CT/CC vs. TT) and a significant increased median survival time (MST) compared with those with TT genotypes (MST = 96.500; 75.883 and 71.370 months for CT, CC and CT/CC respectively vs. MST = 54.300 months for TT, p <0.0001). Stratified analysis by both life style and clinicopathological risks revealed that subjects carrying rs4938723CT/CC genotypes were remained significantly associated with increased survival and low risk of CRC compared with those with TT genotypes in all subgroup (all p <0.05). Similar observation was also reported for the prognostic value of rs4938723TC/CC genotypes across all subgroups.

Conclusion: These findings indicate that the miR-34b/c rs4938723T > C polymorphism is an independent variable and associated with a decreased risk of CRC in Chinese population. This study provides evidence of the protective effects of rs4938723CT/CC genotypes in the development of CRC.
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http://dx.doi.org/10.1016/j.arcmed.2019.05.008DOI Listing
February 2019

Propofol alleviates oxidative stress via upregulating lncRNA-TUG1/Brg1 pathway in hypoxia/reoxygenation hepatic cells.

J Biochem 2019 Nov;166(5):415-421

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.

Reducing oxidative stress is an effective method to prevent hepatic ischaemia/reperfusion injury (HIRI). This study focuses on the role of propofol on the oxidative stress of hepatic cells and the involved lncRNA-TUG1/Brahma-related gene 1 (Brg1) pathway in HIRI mice. The mouse HIRI model was established and was intraperitoneally injected with propofol postconditioning. Hepatic injury indexes were used to evaluate HIRI. The oxidative stress was indicated by increasing 8-isoprostane concentration. Mouse hepatic cell line AML12 was treated with hypoxia and subsequent reoxygenation (H/R). The targeted regulation of lncRNA-TUG1 on Brg1 was proved by RNA pull-down, RIP (RNA-binding protein immunoprecipitation) and the expression level of Brg1 responds to silencing or overexpression of lncRNA-TUG1. Propofol alleviates HIRI and induces the upregulation of lncRNA-TUG1 in the mouse HIRI model. Propofol increases cell viability and lncRNA-TUG1 expression level in H/R-treated hepatic cells. In H/R plus propofol-treated hepatic cells, lncRNA-TUG1 silencing reduces cell viability and increased oxidative stress. LncRNA-TUG1 interacts with Brg1 protein and keeps its level via inhibiting its degradation. Brg1 overexpression reverses lncRNA-TUG1 induced the reduction of cell viability and the increase in oxidative stress. LncRNA-TUG1 silencing abrogates the protective role of propofol against HIRI in the mouse HIRI model. LncRNA-TUG1 has a targeted regulation of Brg1, and thereby affects the oxidative stress induced by HIRI. This pathway mediates the protective effect of propofol against HIRI of hepatic cell.
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http://dx.doi.org/10.1093/jb/mvz054DOI Listing
November 2019

The Pathway of Let-7a-1/2-3p and HMGB1 Mediated Dexmedetomidine Inhibiting Microglia Activation in Spinal Cord Ischemia-Reperfusion Injury Mice.

J Mol Neurosci 2019 Sep 12;69(1):106-114. Epub 2019 Jun 12.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei Province, People's Republic of China.

Microglial cell activation after spinal cord ischemia-reperfusion injury (SCIRI) commonly causes the secondary nerve motion function injury. This study aims to study the mechanism by which the drug dexmedetomidine (DEX) inhibits microglial cell activation and improves motion function of SCIRI mice. Mice SCIRI model was established, and microglia from spinal cord were isolated and cultured for subsequent molecule analysis of let-7a-1-3p, let-7a-2-3p, HMGB1, TNF-α, and IL-6. DEX was given by intraperitoneal injection. Mice motion function was evaluated by Basso mouse score. In vitro microglial cells were subjected to oxygen and glucose deprivation/reoxygenation (OGD/R) to imitate ischemia-reperfusion injury stimulation. DEX injection improves the mouse motion function in SCIRI model and upregulates let-7a-1/2-3p expression in the isolated activated microglia from SCIRI mice. In OGD/R-stimulated microglia, DEX treatment also caused the inactivation of cells, the upregulation of let-7a-1/2-3p expression, and the downregulation of HMGB1 expression. While the co-silencing of let-7a-1/2-3p in microglia in addition to DEX treatment restored the activation of microglia. HMGB1 is a targeted gene for let-7a-1/2-3p and negatively regulated by them. HMGB1 knockdown abrogates the pro-activation impact on microglial cell by let-7a-1/2-3p silencing. DEX inhibits the activation of microglial cell in the spinal cord of SCIRI mice, mediated by the let-7a-1/2-3p/HMGB1 pathway.
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http://dx.doi.org/10.1007/s12031-019-01338-4DOI Listing
September 2019

[Dexmedetomidine preconditioning protects against lung injury in hemorrhagic shock rats].

Rev Bras Anestesiol 2019 Mar - Apr;69(2):160-167. Epub 2019 Jan 14.

Wuhan University, Renmin Hospital, Department of Anesthesiology, Wuhan, China; Wuhan University, Renmin Hospital, Laboratory of Anesthesiology and Critical Care Medicine, Wuhan, China. Electronic address:

Background And Objectives: Dexmedetomidine has demonstrated protective effects against lung injury in vitro. Here, we investigated whether dexmedetomidine preconditioning protected against lung injury in hemorrhagic shock rats.

Methods: Male Sprague-Dawley rats were randomly divided into four groups (n=8): control group, hemorrhagic shock group, 5ug.kg dexmedetomidine (DEX1) group, and 10ug.kg dexmedetomidine (DEX2) group. Saline or dexmedetomidine were administered over 20min. 30min after injection, hemorrhage was initiated in the hemorrhagic shock, DEX1 and DEX2 group. Four hours after resuscitation, protein and cellular content in bronchoalveolar lavage fluid, and the lung histopathology were measured. The malondialdehyde, superoxide dismutase, Bcl-2, Bax and caspase-3 were also tested in the lung tissue.

Results: Compare with hemorrhagic shock group, 5ug.kg dexmedetomidine pretreatment reduced the apoptosis (2.25±0.24 vs. 4.12±0.42%, p<0.05), histological score (1.06±0.12 vs. 1.68±0.15, p<0.05) and protein (1.92±0.38 vs. 3.95±0.42mg.mL, p<0.05) and WBC (0.42±0.11 vs. 0.92±0.13×10/L, p<0.05) in bronchoalveolar lavage fluid. Which is correlated with increased superoxide dismutase activity (8.35±0.68 vs. 4.73±0.44U.mg protein, p<0.05) and decreased malondialdehyde (2.18±0.19 vs. 3.28±0.27nmoL.mg protein, p<0.05). Dexmedetomidine preconditioning also increased the Bcl-2 level (0.55±0.04 vs. 0.34±0.05, p<0.05) and decreased the level of Bax (0.46±0.03 vs. 0.68±0.04, p<0.05), caspase-3 (0.49±0.03 vs. 0.69±0.04, p<0.05). However, we did not observe any difference between the DEX1 and DEX2 groups for these (p>0.05).

Conclusion: Dexmedetomidine preconditioning has a protective effect against lung injury caused by hemorrhagic shock in rats. The potential mechanisms involved are the inhibition of cell death and improvement of antioxidation. But did not show a dose-dependent effect.
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http://dx.doi.org/10.1016/j.bjan.2018.09.011DOI Listing
August 2019

Non-canonical Opioid Signaling Inhibits Itch Transmission in the Spinal Cord of Mice.

Cell Rep 2018 Apr;23(3):866-877

Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address:

Chronic itch or pruritus is a debilitating disorder that is refractory to conventional anti-histamine treatment. Kappa opioid receptor (KOR) agonists have been used to treat chronic itch, but the underlying mechanism remains elusive. Here, we find that KOR and gastrin-releasing peptide receptor (GRPR) overlap in the spinal cord, and KOR activation attenuated GRPR-mediated histamine-independent acute and chronic itch in mice. Notably, canonical KOR-mediated G signaling is not required for desensitizing GRPR function. In vivo and in vitro studies suggest that KOR activation results in the translocation of Ca-independent protein kinase C (PKC)δ from the cytosol to the plasma membrane, which in turn phosphorylates and inhibits GRPR activity. A blockade of phospholipase C (PLC) in HEK293 cells prevented KOR-agonist-induced PKCδ translocation and GRPR phosphorylation, suggesting a role of PLC signaling in KOR-mediated GRPR desensitization. These data suggest that a KOR-PLC-PKCδ-GRPR signaling pathway in the spinal cord may underlie KOR-agonists-induced anti-pruritus therapies.
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http://dx.doi.org/10.1016/j.celrep.2018.03.087DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5937707PMC
April 2018

Penehyclidine hydrochloride inhibits TLR4 signaling and inflammation, and attenuates blunt chest trauma and hemorrhagic shock-induced acute lung injury in rats.

Mol Med Rep 2018 May 27;17(5):6327-6336. Epub 2018 Feb 27.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

Blunt chest trauma with hemorrhagic shock (THS) frequently induces pulmonary inflammation that leads to acute lung injury (ALI). Penehyclidine hydrochloride (PHC) possesses anti‑inflammatory properties that may attenuate the systemic inflammatory response. The present study aimed to evaluate the molecular mechanism of PHC in modifying THS‑induced ALI in rats. Rats underwent either THS or a sham procedure. At 6 h subsequent to blunt chest trauma, arterial blood was drawn for blood gas and pro‑inflammatory factors analyses, and lung tissue samples were collected to examine pulmonary histopathological alterations, the wet/dry weight ratio, myeloperoxidase activity, and the protein expression levels of Toll-like receptor 4 (TLR4), phosphorylated (p‑)p38 mitogen‑activated protein kinase (MAPK), nuclear factor (NF)‑κB and activator protein‑1 (AP‑1). THS caused significant reductions in heart rate and mean arterial blood pressure, and was associated with significant increases in tumor necrosis factor‑α, interleukin (IL)‑6, IL‑1β, p‑p38MAPK, NF‑κB and AP‑1 activation, in addition to TLR4 expression, in the lung. PHC effectively attenuated THS‑induced ALI, and inhibited TLR4 expression, reduced the activation of p‑p38MAPK, NF‑κB and AP‑1, and downregulated the expression of pro‑inflammatory mediators. In conclusion, the results of the present study demonstrated that PHC may exert an anti‑inflammatory effect and attenuate THS‑induced ALI by inhibiting the TLR4 signaling pathway. These preclinical findings may offer a novel therapeutic strategy to restrict TLR4 overactivation in ALI.
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http://dx.doi.org/10.3892/mmr.2018.8644DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5928610PMC
May 2018

Involvement of poly(ADP-ribose) polymerase-1 in development of spinal cord injury in Chinese individuals: a Chinese clinical study.

Drug Des Devel Ther 2017 6;11:3491-3495. Epub 2017 Dec 6.

Department of Spine Surgery, The Third People's Hospital of Dalian, Dalian, People's Republic of China.

Objective: We aimed to evaluate whether the polymorphism of poly(ADP-ribose) polymerase-1 (PARP-1) is involved as potential risk factor in the development of spinal cord injury (SCI) among Chinese individuals.

Patients And Methods: Patients with a confirmed diagnosis of SCI (other than traumatic injury) and healthy individuals with no clinical symptoms of SCI were enrolled at Spinal Cord Injury Care Center, The Third People's Hospital of Dalian, China. Genetic polymorphisms were studied in plasma samples by polymerase chain reaction-restriction fragment length polymorphism assay.

Results: A total of 130 Chinese patients with SCI and 130 healthy Chinese individuals were included. We found that patients with the GG genotype (odds ratio [OR]: 4.09, 95% confidence interval [CI] 2.42-6.90, <0.001) and carriers of the G allele (OR 3.96, 95% CI 2.33-6.74, <0.0001) were at high risk of developing SCI. A del/ins polymorphism of the NF-κB1 gene (OR 3.32, 95% CI 1.96-5.61, <0.001) was also found to be associated with SCI.

Conclusion: Our study suggests that PARP-1 polymorphisms are involved in the development of SCI in Chinese individuals. Thus, PARP-1 polymorphisms can be considered as one of the potential risk factors for developing SCI.
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http://dx.doi.org/10.2147/DDDT.S142005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5723107PMC
July 2018

Distinct roles of NMB and GRP in itch transmission.

Sci Rep 2017 11 13;7(1):15466. Epub 2017 Nov 13.

Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, 63110, USA.

A key question in our understanding of itch coding mechanisms is whether itch is relayed by dedicated molecular and neuronal pathways. Previous studies suggested that gastrin-releasing peptide (GRP) is an itch-specific neurotransmitter. Neuromedin B (NMB) is a mammalian member of the bombesin family of peptides closely related to GRP, but its role in itch is unclear. Here, we show that itch deficits in mice lacking NMB or GRP are non-redundant and Nmb/Grp double KO (DKO) mice displayed additive deficits. Furthermore, both Nmb/Grp and Nmbr/Grpr DKO mice responded normally to a wide array of noxious stimuli. Ablation of NMBR neurons partially attenuated peripherally induced itch without compromising nociceptive processing. Importantly, electrophysiological studies suggested that GRPR neurons receive glutamatergic input from NMBR neurons. Thus, we propose that NMB and GRP may transmit discrete itch information and NMBR neurons are an integral part of neural circuits for itch in the spinal cord.
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http://dx.doi.org/10.1038/s41598-017-15756-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5684337PMC
November 2017

Mechanism of myocardial ischemia/reperfusion-induced acute kidney injury through DJ-1/Nrf2 pathway in diabetic rats.

Exp Ther Med 2017 Nov 1;14(5):4201-4207. Epub 2017 Sep 1.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

The objective of the present study was to investigate acute kidney injury (AKI) induced by myocardial ischemia/reperfusion (MIR) in diabetic rats and elucidate its underlying mechanism. A rat model of MIR was established by left anterior descending coronary artery occlusion for 30 min, followed by reperfusion for 2 h. Rats were randomly divided into four groups: i) Sham group, ii) sham + MIR group, iii) diabetic group and iv) diabetes + MIR group. Myocardial injury was detected by plasma creatine kinase isoenzyme MB and lactate dehydrogenase assays. AKI induced by MIR in diabetic rats was characterized by increases in cystatin C and β2-microglobulin levels. Oxidative stress injury was accompanied by an increase of malondialdehyde levels and a decrease of total antioxidative capacity in the renal tissues. Immunohistochemistry and western blot analysis demonstrated that the expression of DJ-1 and nuclear factor erythroid 2-related factor 2 (Nrf2) were significantly increased in the diabetes + MIR group compared with that in the sham + MIR and diabetic groups. Taken together, these results suggested that AKI induced by MIR in diabetic rats may be associated with activation of the DJ-1/Nrf2 pathway.
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http://dx.doi.org/10.3892/etm.2017.5095DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5658721PMC
November 2017

Transcription factors Nrf2 and NF-κB contribute to inflammation and apoptosis induced by intestinal ischemia-reperfusion in mice.

Int J Mol Med 2017 Dec 2;40(6):1731-1740. Epub 2017 Oct 2.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

Intestinal ischemia/reperfusion (IIR) is a common pathological event associated with intestinal injury and apoptosis with high mortality. Nuclear factor (NF)-E2-related factor-2 (Nrf2) is a key transcription factor that interacts with NF-κB and has a vital anti-inflammatory effect. However, whether Nrf2 has a role in IIR-induced apoptosis and the possible underlining mechanisms, such as modulation of the inflammation regulation pathway, have remained to be fully elucidated. In the present study, IIR was identified to cause significant intestinal injury and apoptosis, with high expression levels of inflammatory cytokines, as well as the apoptotic proteins B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax) and caspase-3, while simultaneously decreasing the protein levels of Bcl-2. The effect was more pronounced after pretreatment of the animals with all-trans retinoic acid or brusatol, potent inhibitors of Nrf2. t-Butylhydroquinone, an Nrf2 activator, significantly attenuated IIR-induced intestinal injury and apoptosis, with inhibition of the overexpression of the inflammatory cytokines, Bax and caspase-3 protein and partial restoration of Bcl-2 protein expression. Taken together, these results indicated that increased Nrf2 expression reduced IIR-induced intestinal apoptosis and that the protective function of Nrf2 may be based on its anti-inflammatory effects through the inhibition of the NF-κB pathway.
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http://dx.doi.org/10.3892/ijmm.2017.3170DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5716448PMC
December 2017

[Dexmedetomidine preconditioning protects against lipopolysaccharides-induced injury in the human alveolar epithelial cells].

Rev Bras Anestesiol 2017 Nov - Dec;67(6):600-606. Epub 2017 Aug 18.

Wuhan University, Renmin Hospital, Department of Anesthesiology, Wuhan, Hubei, China; Wuhan University, Renmin Hospital, Laboratory of Anesthesiology and Critical Care Medicine, Wuhan, Hubei, China. Electronic address:

Background And Objectives: Dexmedetomidine (DEX) has demonstrated the preconditioning effect and shown protective effects against organize injury. In this study, using A549 (human alveolar epithelial cell) cell lines, we investigated whether DEX preconditioning protected against acute lung injury (ALI) in vitro.

Methods: A549 were randomly divided into four groups (n=5): control group, DEX group, lipopolysaccharides (LPS) group, and D-LPS (DEX+LPS) group. Phosphate buffer saline (PBS) or DEX were administered. After 2h preconditioning, the medium was refreshed and the cells were challenged with LPS for 24h on the LPS and D-LPS group. Then the malondialdehyde (MDA), superoxide dismutase (SOD), Bcl-2, Bax, caspase-3 and the cytochrome c in the A549 were tested. The apoptosis was also evaluated in the cells.

Results: Compare with LPS group, DEX preconditioning reduced the apoptosis (26.43%±1.05% vs. 33.58%±1.16%, p<0.05) in the A549, which is correlated with decreased MDA (12.84±1.05 vs. 19.16±1.89nmol.mg protein, p<0.05) and increased SOD activity (30.28±2.38 vs. 20.86±2.19U.mg protein, p<0.05). DEX preconditioning also increased the Bcl-2 level (0.53±0.03 vs. 0.32±0.04, p<0.05) and decreased the level of Bax (0.49±0.04 vs. 0.65±0.04, p<0.05), caspase-3 (0.54±0.04 vs. 0.76±0.04, p<0.05) and cytochrome c.

Conclusion: DEX preconditioning has a protective effect against ALI in vitro. The potential mechanisms involved are the inhibition of cell death and improvement of antioxidation.
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http://dx.doi.org/10.1016/j.bjan.2017.07.003DOI Listing
May 2019

(-)-Epigallocatechin-3-gallate attenuates myocardial injury induced by ischemia/reperfusion in diabetic rats and in H9c2 cells under hyperglycemic conditions.

Int J Mol Med 2017 Aug 8;40(2):389-399. Epub 2017 Jun 8.

Department of Clinical Nutrition, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, P.R. China.

(-)-Epigallocatechin gallate (EGCG) exerts multiple beneficial effects on cardiovascular performance. In this study, we aimed to examine the effects of EGCG on diabetic cardiomyopathy during myocardial ischemia/reperfusion (I/R) injury. EGCG (100 mg/kg/day) was administered at week 6 for 2 weeks to diabetic rats following the induction of type 1 diabetes by streptozotocin (STZ). At the end of week 8, the animals were subjected to myocardial I/R injury. The EGCG-elicited structural and functional effects were analyzed. Additionally, EGCG (20 µM) was administered for 24 h to cultured cardiac H9c2 cells under hyperglycemic conditions (30 mM glucose) prior to hypoxia/reoxygenation (H/R) challenge, and its effects on oxidative stress were compared to H9c2 cells transfecteed with silent information regulator 1 (SIRT1) small interfering RNA (siRNA). In rats with STZ-induced diabetes, EGCG treatment ameliorated post-ischemic cardiac dysfunction, decreased the myocardial infarct size, apoptosis and cardiac fibrosis, and reduced the elevated lactate dehydrogenase (LDH) and malonaldehyde (MDA) levels, and attenuated oxidative stress. Furthermore, EGCG significantly reduced H/R injury in cardiac H9c2 cells exposed to high glucose as evidenced by reduced apoptotic cell death and oxidative stress. The protein expression levels of SIRT1 and manganese superoxide dismutase (MnSOD) were reduced in the diabetic rats and the H9c2 cells under hyperglycemic conditions, compared with the control rats following I/R injury and H9c2 cells under normal glucose conditions. EGCG pre-treatment significantly upregulated the levels of htese proteins in vitro and in vivo. However, treatment with EX527 and SIRT1 siRNA blocked the EGCG-mediated cardioprotective effects. Taken together, our data indicate that SIRT1 plays a critical role in the EGCG-mediated amelioration of I/R injury in diabetic rats, which suggests that EGCG may be a promising dietary supplement for the prevention of diabetic cardiomyopathy.
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http://dx.doi.org/10.3892/ijmm.2017.3014DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5504977PMC
August 2017

Protective effects of SOCS3 overexpression in high glucose‑induced lung epithelial cell injury through the JAK2/STAT3 pathway.

Mol Med Rep 2017 Sep 6;16(3):2668-2674. Epub 2017 Jul 6.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

Previous studies have suggested that the Janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway is involved in hyperglycemia‑induced lung injury. The present study aimed to investigate the roles of suppressor of cytokine signaling3 (SOCS3) in the regulation of JAK2/STAT3 activation following high glucose (HG) treatment in A549 human pulmonary epithelial cells. Cell viability was evaluated using Cell Counting Kit-8 and lactate dehydrogenase assays. HG‑induced inflammatory injury in A549 cells was assessed through the evaluation of interleukin‑6 (IL‑6) and tumor necrosis factor‑α (TNF‑α) levels using ELISA. The protein expression levels of SOCS3, JAK2, STAT3, phosphorylated (p)‑JAK2 and p‑STAT3 were determined using western blot analysis. Cellular viability was significantly decreased, whereas IL‑6 and TNF‑α levels were significantly increased, following HG stimulation of A549 cells. In addition, the protein levels of SOCS3, p‑JAK2 and p‑STAT3 were significantly increased in HG‑treated cells. Treatment with the JAK2/STAT3 inhibitor tyrphostin AG490, or SOCS3 overexpression, appeared to prevent the HG‑induced alterations in protein expression. Furthermore, cellular viability was enhanced, whereas the levels of proinflammatory cytokines were suppressed. These finding suggested the involvement of the SOCS3/JAK2/STAT3 signaling pathway in HG‑induced responses in lung cells. Therefore, it may be hypothesized that the inhibition of the JAK2/STAT3 pathway through SOCS3 overexpression may prevent hyperglycemia‑induced lung injury, and may have therapeutic potential for the treatment of patients with diabetic lung injury.
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http://dx.doi.org/10.3892/mmr.2017.6941DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5547984PMC
September 2017

Propofol protects against hepatic ischemia/reperfusion injury via miR-133a-5p regulating the expression of MAPK6.

Cell Biol Int 2017 May 7;41(5):495-504. Epub 2017 Mar 7.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.

Propofol has been found to play an important role in hepatic ischemia/reperfusion (I/R) injury with the antioxidant effects. However, the molecular mechanism of propofol in hepatic I/R injury has not been fully understood. Male Sprague-Dawley rats were randomly assigned into Sham group, hepatic I/R group, and propofol treatment group. I/R injury was attained by ischemia for 1 h and reperfusion for 2 h. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activity were detected. QSG-7701 cells were cultured in hypoxia condition for 15 h and then in reoxygenation condition for 6 h to imitate hypoxia/reoxygenation (H/R) injury in vitro. Real-time RT-PCR and Western blot were performed to determine the expression of miR-133a-5p and MAPK6. Luciferase reporter assay was used to determine the regulation of miR-133a-5p on MAPK6. Propofol significantly reduced the activities of serum AST and ALT induced by hepatic I/R injury in rats. Propofol increased the level of miR-133a-5p and decreased the expression of MAPK6 in vivo and in vitro. Luciferase reporter assay showed that MAPK6 was a target of miR-133a-5p. Knockdown of miR-133a-5p abrogated the effect of propofol on the upregulation of MAPK6 induced by H/R. MAPK6 overexpression promoted the cell apoptosis induced by H/R which could be attenuated by propofol. Finally, we found that miR-133a-5p reversed the protective effect of propofol in rats with hepatic I/R injury. Propofol showed protective roles for hepatic I/R injury in vivo and H/R injury in vitro, which involved with miR-133a-5p regulating the expression of MAPK6.
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http://dx.doi.org/10.1002/cbin.10745DOI Listing
May 2017

Sudden death due to ventricular double rupture as a complication of inferior acute myocardial infarction: A case report.

Medicine (Baltimore) 2016 Dec;95(52):e5757

Department of Cardiology, West China Hospital, Sichuan University, Chengdu, China.

Rationale: Ventricular double rupture (VDR) is a rare but lethal mechanical complication of acute myocardial infarction (AMI). The early identification and timely treatment of VDR remain challenging problems. We present a case of AMI with VDR and briefly review the characteristics and prognosis of this life-threatening disease.

Patient Concerns And Diagnoses: A 77-year-old male presented to our hospital with a 4-day history of severe dizziness, mild chest tightness, and dyspnea. An inferior AMI was diagnosed.

Interventions And Outcomes: On the second hospital day, hypotension and a new cardiac murmur was found. The emergency echocardiographic study disclosed a ventricular septal defect. Soon after that the patient suddenly died of ventricular free-wall rupture.

Lessons: In patients with AMI complicated by a septal perforation in the apical region, close to the septum-free wall junction, special attention should be paid to the great risk of VDR. Other high risk factors included advanced age, delayed reperfusion, and inferior infarction. Sufficient evaluation of the risk factors, close monitoring of vital signs, early identification of the specific symptoms, and timely treatment are the key points for the effective prediction and prevention of VDR.
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http://dx.doi.org/10.1097/MD.0000000000005757DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5207586PMC
December 2016

Long non-coding RNA MALAT1 functions as a mediator in cardioprotective effects of fentanyl in myocardial ischemia-reperfusion injury.

Cell Biol Int 2017 Jan 24;41(1):62-70. Epub 2016 Nov 24.

Department of Anesthesiology, Renmin Hospital of Wuhan University, Hubei Zhang Road, Wu chang District No. 99 Jie fang Road 238, 430060, Wuhan, China.

Long non-coding (lncRNA) MALAT1 can be increased by hypoxia or ischemic limbs. Also, downregulation of MALAT1 contributes to reduction of cardiomyocyte apoptosis. However, the functional involvement of MALAT1 in myocardial ischemia-reperfusion (I/R) injury has not been defined. This study investigated the functional involvement of lncRNA-MALAT1 in cardioprotective effects of fentanyl. HL-1, a cardiac muscle cell line from the AT-1 mouse atrial cardiomyocyte tumor lineage was pre-treated with fentanyl and generated cell model of hypoxia-reoxygenation (H/R). Relative expression of MALAT1, miR-145, and Bnip3 mRNA in cells was determined by quantitative real-time PCR. Cardiomyocyte H/R injury was indicated by lactate dehydrogenase (LDH) release and cell apoptosis. The results showed that fentanyl abrogates expression of responsive gene for H/R and induces downregulation of MALAT1 and Bnip3 and upregulation of miR-145. We found that miR-145/Bnip3 pathway was negatively regulated by MALAT1 in H/R-HL-1 cell with or without fentanyl treatment. Moreover, both MALAT1 overexpression and miR-145 knockdown reverse cardioprotective effects of fentanyl, as indicated by increase in LDH release and cell apoptosis. The reversal effect of MALAT1 for fentanyl is confirmed in cardiac ischemia/reperfusion (I/R) mice. In summary, lncRNA-MALAT1 is sensitive to H/R injury and abrogates cardioprotective effects of Fentanyl by negatively regulating miR-145/Bnip3 pathway.
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http://dx.doi.org/10.1002/cbin.10701DOI Listing
January 2017

Safety and efficacy of etomidate and propofol anesthesia in elderly patients undergoing gastroscopy: A double-blind randomized clinical study.

Exp Ther Med 2016 Sep 24;12(3):1515-1524. Epub 2016 Jun 24.

Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA.

The aim of the present study is to compare the safety, efficacy and cost effectiveness of anesthetic regimens by compound, using etomidate and propofol in elderly patients undergoing gastroscopy. A total of 200 volunteers (65-79 years of age) scheduled for gastroscopy under anesthesia were randomly divided into the following groups: P, propofol (1.5-2.0 mg/kg); E, etomidate (0.15-0.2 mg/kg); P+E, propofol (0.75-1 mg/kg) followed by etomidate (0.075-0.1 mg/kg); and E+P, etomidate (0.075-0.01 mg/kg) followed by propofol (0.75-1 mg/kg). Vital signs and bispectral index were monitored at different time points. Complications, induction and examination time, anesthesia duration, and recovery and discharge time were recorded. At the end of the procedure, the satisfaction of patients, endoscopists and the anesthetist were evaluated. The recovery (6.1±1.2 h) and discharge times (24.8±2.8 h) in group E were significantly longer compared with groups P, P+E and E+P (P<0.05). The occurrence of injection pain in group P+E was significantly higher compared with the other three groups (P<0.05). In addition, the incidence of myoclonus and post-operative nausea and vomiting were significantly higher in group P+E compared with the other three groups (P<0.05). There was no statistical difference among the four groups with regards to the patients' immediate, post-procedure satisfaction (P>0.05). Furthermore, there was no difference in the satisfaction of anesthesia, as evaluated by the anesthetist and endoscopist, among the four groups (P>0.05). The present study demonstrates that anesthesia for gastroscopy in elderly patients can be safely and effectively accomplished using a drug regimen that combines propofol with etomidate. The combined use of propofol and etomidate has unique characteristics which improve hemodynamic stability, cause minimal respiratory depression and less side effects, provide rapid return to full activity and result in high levels of satisfaction.
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http://dx.doi.org/10.3892/etm.2016.3475DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4998221PMC
September 2016