Publications by authors named "Zhishan Liang"

11 Publications

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Interleukin-9 deficiency affects lipopolysaccharide-induced macrophage-related oxidative stress and myocardial cell apoptosis via the Nrf2 pathway both in vivo and in vitro.

Biofactors 2021 May 12. Epub 2021 May 12.

Department of Cardiology, the People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.

Previous studies showed that interleukin-9 (IL-9) is involved in cardiovascular diseases, including hypertension and cardiac fibrosis. This study aimed to investigate the role of IL-9 in lipopolysaccharide (LPS)-induced myocardial cell (MC) apoptosis. Mice were treated with LPS, and IL-9 expression was measured and the results showed that compared with WT mice, LPS-treated mice exhibited increased cardiac Mø-derived IL-9. Additionally, the effects of IL-9 deficiency (IL-9-/-) on macrophage (Mø)-related oxidative stress and MC apoptosis were evaluated, the results showed that IL-9 knockout significantly exacerbated cardiac dysfunction, inhibited Nrf2 nuclear transfer, promoted an imbalance in M1 and M2 Møs, and exacerbated oxidative stress and MC apoptosis in LPS-treated mice. Treatment with ML385, a specific nuclear factor erythroid-2 related factor 2 (Nrf2) pathway inhibitor significantly alleviated the above effects in LPS-treated IL-9-/- mice. Bone marrow-derived Møs from wild-type (WT) mice and IL-9-/- mice were treated with LPS, and the differentiation and oxidative stress levels of Møs were measured. The effect of Mø differentiation on mouse MC apoptosis was also analyzed in vitro. The results showed that LPS-induced M1 Mø/M2 Mø imbalance and Mø-related oxidative stress were alleviated by IL-9 knockout but were exacerbated by ML385 treatment. The protective effects of IL-9 deficiency on the MC apoptosis mediated by LPS-treated Møs were reversed by ML-385. Our results suggest that deletion of IL-9 decreased the nuclear translocation of Nrf2 in Møs, which further aggravated Mø-related oxidative stress and MC apoptosis. IL-9 may be a target for the prevention of LPS-induced cardiac injury.
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http://dx.doi.org/10.1002/biof.1754DOI Listing
May 2021

Anti-Interleukin-16-Neutralizing Antibody Attenuates Cardiac Inflammation and Protects against Cardiac Injury in Doxorubicin-Treated Mice.

Mediators Inflamm 2021 17;2021:6611085. Epub 2021 Apr 17.

Department of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.

Background: Interleukin-16 (IL-16) is an important inflammatory regulator and has been shown to have a powerful effect on the regulation of the inflammatory response. Cardiac inflammation has been reported to be closely related to doxorubicin- (DOX-) induced cardiac injury. In this study, the role of IL-16 in DOX-induced cardiac injury and the possible mechanisms were examined.

Methods: Cardiac IL-16 levels were first measured in DOX- or saline-treated mice. Additionally, mice were pretreated with the anti-IL-16-neutralizing antibody (nAb) or isotype IgG for 1 day and further administered DOX or saline for 5 days. Then, cardiac injury, cardiac M1 macrophage levels, and cardiomyocyte apoptosis were analyzed. The effects of the anti-IL-16 nAb on macrophage differentiation and cardiomyocyte apoptosis were also investigated in vitro.

Results: DOX administration increased IL-16 expression in cardiac macrophages compared with that of saline treatment. The anti-IL-16 nAb significantly decreased serum levels of lactate dehydrogenase (LDH), myocardial-bound creatine kinase (CK-MB), and cardiac troponin T (cTnT) and elevated cardiac function in DOX-induced mice. Treatment with the anti-IL-16 nAb also reduced p65 pathway activation, decreased M1 macrophage-related marker and cytokine expression, and protected against cardiomyocyte apoptosis in DOX-induced mice. In cell studies, the anti-IL-16 nAb also reduced DOX-induced M1 macrophage differentiation and alleviated apoptosis in cardiomyocytes cocultured with macrophages.

Conclusions: The anti-IL-16 nAb protects against DOX-induced cardiac injury by reducing cardiac inflammation, and IL-16 may be a promising target to prevent DOX-related cardiac injury.
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http://dx.doi.org/10.1155/2021/6611085DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8075660PMC
April 2021

Novel strategy of natural antioxidant nutrition quality evaluation in food: Oxidation resistance mechanism and synergistic effects investigation.

Food Chem 2021 Oct 24;359:129768. Epub 2021 Apr 24.

Center for Advanced Analytical Science, School of Chemistry and Chemical Engineering c/o School of Civil Engineering, Guangzhou University, Guangzhou 510006, PR China; State Key Laboratory of Electroanalytical Chemistry, c/o Engineering Laboratory for Modern Analytical Techniques, CAS Center for Excellence in Nanoscience, Changchun Institute of Applied Chemistry, Changchun 130022, PR China; University of Chinese Academy of Sciences, Beijing 100039, PR China.

Effective evaluation methods for assessing the nutritional quality of foods that eliminate free radicals (i.e., foods that are classified as antioxidants) have long attracted the attention of scientists and the populace. In this case, constructing a corresponding photoelectrochemical sensor that has the advantages of being intuitive, rapid, and capable of accurate assessment for global antioxidant capacity is of profound significance. In this study, a novel g-CN/NiS/TiO photoelectric sensitive platform was constructed and afforded the possibility of a synergistic/antagonistic effect for estimating intrinsic antioxidant ingredients in food. Further investigation revealed that the internal influences of the compound structure, such as the redox potential and type of groups on the molecular benzene ring should be the main internal reasons for antioxidant synergistic behaviors. The photochemical strategy of concern is expected to provide benefits for on-site foods nutrition assays that should become a guide for health care diets.
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http://dx.doi.org/10.1016/j.foodchem.2021.129768DOI Listing
October 2021

Anti-Interleukin-16 Neutralizing Antibody Treatment Alleviates Sepsis-Induced Cardiac Injury and Dysfunction via the Nuclear Factor Erythroid-2 Related Factor 2 Pathway in Mice.

Oxid Med Cell Longev 2021 13;2021:6616422. Epub 2021 Feb 13.

Department of Cardiology, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.

Several interleukin (IL) members have been reported to participate in sepsis. In this study, the effects of IL-16 on sepsis-induced cardiac injury and dysfunction were examined, and the related mechanisms were detected. IL-16 expression in septic mice was first measured, and the results showed that both cardiac and serum IL-16 expression levels were increased in mice with sepsis induced by LPS or cecal ligation and puncture (CLP) compared with control mice. Then, IL-16 was neutralized, and the effects on lipopolysaccharide- (LPS-) induced cardiac injury were detected. The results showed that an anti-IL-16 neutralizing antibody (nAb) significantly reduced mortality and increased serum lactate dehydrogenase (LDH), creatine kinase myocardial bound (CK-MB), and cardiac troponin T (cTnT) levels while improving cardiac function in mice with LPS-induced sepsis. Neutralization of IL-16 also increased the activation of antioxidant pathways and the expression of antioxidant factors in septic mice while decreasing the activation of prooxidant pathways and the expression of prooxidants. Treatment with the anti-IL-16 nAb increased mitochondrial apoptosis-inducing factor (AIF) expression, decreased nuclear AIF and cleaved poly-ADP-ribose polymerase (PARP) expression, and decreased TUNEL-positive cell percentages in LPS-treated mice. Additionally, treatment with CPUY192018, the nuclear factor erythroid-2 related factor 2 (Nrf2) pathway, significantly increased mortality and reversed the above effects in mice treated with LPS and the anti-IL-16 nAb. Our results showed that the anti-IL-16 nAb regulates oxidative stress through the Nrf2 pathway and participates in the regulation of cardiac injury in septic mice. Neutralization of IL-16 may be a beneficial strategy for the prevention of cardiac injury and dysfunction in sepsis patients.
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http://dx.doi.org/10.1155/2021/6616422DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7896865PMC
February 2021

Molecularly imprinted photo-electrochemical sensor for hemoglobin detection based on titanium dioxide nanotube arrays loaded with CdS quantum dots.

Talanta 2021 Mar 28;224:121924. Epub 2020 Nov 28.

Center for Advanced Analytical Science, School of Chemistry and Chemical Engineering c/o School of Civil Engineering, Guangzhou University, Guangzhou, 510006, China; State Key Laboratory of Electroanalytical Chemistry, c/o Engineering Laboratory for Modern Analytical Techniques, CAS Center for Excellence in Nanoscience, Changchun Institute of Applied Chemistry, Changchun, 130022, China; University of Chinese Academy of Sciences, Beijing, 100039, China.

A novel molecularly imprinted photo-electrochemical sensor based on CdS/TiO nanocomposites was constructed for precisely detection of hemoglobin under visible light irradiation. CdS quantum dots were decorated on the surface of TiO nanorod arrays to form a heterojunction, which could enhance the charge-transfer efficiency for visible light and further increase the photo-generated current of the sensor. The molecularly imprinted polymer film assembled by dopamine monomer had achieved excellent performance for specifically binding with human hemoglobin. The hemoglobin bound on the sensor could catalyze the oxidation reaction of 4-chloro-1-naphthol by HO, generating insoluble product on the sensor surface and triggering an obviously decrease on photocurrent. The molecularly imprinted photo-electrochemical sensor exhibited excellent sensitivity, selectivity and stability for the detection of human hemoglobin. The sensor had a linear range from 0.01 to 100 ng mL with a detection limit of 0.53 pg/mL (S/N = 3). Furthermore, the sensor was successfully applied on the analysis of human hemoglobin in the urine samples.
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http://dx.doi.org/10.1016/j.talanta.2020.121924DOI Listing
March 2021

CdS/TiO Nanocomposite-Based Photoelectrochemical Sensor for a Sensitive Determination of Nitrite in Principle of Etching Reaction.

Anal Chem 2021 01 15;93(2):820-827. Epub 2020 Dec 15.

Center for Advanced Analytical Science, School of Chemistry and Chemical Engineering c/o School of Civil Engineering, Guangzhou University, Guangzhou 510006, P. R. China.

The CdS/TiO nanocomposite (NC) photoelectrochemical (PEC) sensor was constructed based on a new sensing strategy for nitrite assay. The CdS etching process caused by nitrite-in-acid solution was confirmed and applied to nitrite sensing. The CdS etching phenomenon occurring on the sensor led to an obvious reduction in the photocurrent response under visible-light irradiation, which responded to the nitrite concentration. The CdS/TiO NC-based PEC sensor exhibited excellent performance on nitrite detection. The linear range for nitrite determination was from 1-100 and 100-500 μM, and the sensitivity of the PEC sensor was 2.91 and 0.186 μA μM cm, respectively. The detection limit of the sensor was 0.56 μM (S/N = 3). In addition, the PEC sensor was also equipped with advantages such as good selectivity, excellent stability, low background, and recyclability. Satisfying results were obtained for the nitrite assay in real samples by such a PEC sensor. In summary, this work contributed a fresh idea to precisely determinate nitrite through PEC sensing.
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http://dx.doi.org/10.1021/acs.analchem.0c03315DOI Listing
January 2021

LncRNA MCM3AP-AS1 inhibits cell proliferation in cervical squamous cell carcinoma by down-regulating miRNA-93.

Biosci Rep 2020 02;40(2)

Department of Radiotheragy, Guangzhou Red Cross Hospital, Medical College, Jinan University, Guangzhou, Guangdong 510220, P.R. China.

Background: MCM3AP antisense RNA 1 (MCM3AP-AS1) is characterized as an oncogenic lncRNA in hepatocellular carcinoma and glioblastoma. We analyzed TCGA dataset and observed the down-regulation of MCM3AP-AS1 in cervical squamous cell carcinoma (CSCC). The present study was therefore performed to investigate the role of MCM3AP-AS1 in CSCC.

Methods: A total of 64 female patients with CSCC (38-68 years old; mean age: 53.1 ± 6.5 years old) were enrolled in the present study. RT-qPCR was performed to evaluate gene expression. Methylation specific PCR (MSP) was performed to assess the methylation of miR-93 gene after the overexpression and silencing of MCM3AP-AS1. Cell transfections were performed to investigate the interactions between MCM3AP-AS1 and miR-93. Cell proliferation was assessed by CCK-8 assay.

Results: The results showed that MCM3AP-AS1 was down-regulated in CSCC and predicted poor survival. The expression levels of MCM3AP-AS1 were inversely correlated with the expression levels of miR-93. Overexpression of MCM3AP-AS1 led to down-regulation of miR-93, while silencing of MCM3AP-AS1 played an opposite role in CSCC cells. Methylation-specific PCR revealed that MCM3AP-AS1 could positively regulate the methylation of miR-93 gene. Cell proliferation analysis showed that overexpression of MCM3AP-AS1 led to reduced proliferation rate of CSCC cells. Silencing of MCM3AP-AS1 played an opposite role and overexpression of miR-93 reduced the effects of overexpressing MCM3AP-AS1.

Conclusions: Therefore, MCM3AP-AS1 may inhibit cell proliferation in CSCC by down-regulating miRNA-93.
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http://dx.doi.org/10.1042/BSR20193794DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7007402PMC
February 2020

IL-37 inhibits the maturation of dendritic cells through the IL-1R8-TLR4-NF-κB pathway.

Biochim Biophys Acta Mol Cell Biol Lipids 2019 10 21;1864(10):1338-1349. Epub 2019 May 21.

Department of Cardiology, the People's Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China; Emergency & Critical Care Center, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung, and Blood Vessel Diseases, Beijing 100029, China. Electronic address:

Mature dendritic cells (DCs) play a pathogenic role in atherosclerosis. Our previous study demonstrated that exogenous interleukin (IL)-37 suppresses the maturation of DCs, induces the T-regulatory (Treg) cell response, and attenuates atherosclerosis in ApoE mice. The aim of the present study was to explore the molecular mechanism of IL-37 on the maturation of DCs throughout the development of atherosclerosis. The expression of interleukin-1 receptor 8 (IL-1R8), which is a single Ig-domain receptor that was recently found to be pivotal for the extracellular function of IL-37, Toll-like receptor (TLR) 4 and p65, was measured in ApoE mice and IL-37 transgenic (IL-37tg) ApoE mice. IL-1R8 was mainly expressed in aortic plaque-infiltrated DCs and at significantly higher levels in IL-37tg atherosclerotic mice, accompanied by lower levels of TLR4 and p65. Furthermore, IL-37 eliminated the maturation of DCs induced by oxidized low-density lipoprotein (oxLDL) and caused marked upregulation of IL-1R8 in vitro and downregulation of TLR4 and p65, which was consistent with the experiments in mice. However, the inhibitory effect of IL-37 on the maturation of DCs in vitro was abolished when IL-37 was used to treat DCs isolated from IL-1R8-deficient and TLR4-deficient mice. Therefore, this study indicated that IL-37 inhibited the maturation of DCs via the IL-1R8-TLR4-NF-κB pathway and attenuated atherosclerosis in ApoE mice.
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http://dx.doi.org/10.1016/j.bbalip.2019.05.009DOI Listing
October 2019

The effect of pravastatin on carotid artery thrombosis in rats under the stimulus of C-reactive protein.

Thromb Res 2016 Aug 28;144:213-4. Epub 2016 Jun 28.

Department of Cardiology, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, China.

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http://dx.doi.org/10.1016/j.thromres.2016.06.024DOI Listing
August 2016

[The elevated levels of plasma chemerin and C-reactive protein in patients with acute coronary syndrome].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2015 Jul;31(7):953-6

Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

Objective: To investigate the plasma levels of chemerin and C-reactive protein (CRP) in the patients with acute coronary syndrome.

Methods: The plasma levels of chemerin and CRP were respectively measured by ELISA and immune luminescence sandwich assay in 40 patients with acute myocardial infarction (AMI), 40 patients with unstable angina (UA), 40 patients with stable angina (SA) and 40 control patients.

Results: The levels of chemerin and CRP were significantly higher in the AMI and UA groups than in the SA and control groups, and the level of chemerin was significantly higher in the AMI group than in the UA group. The level of chemerin was positively correlated with the level of CRP, fasting glucose and left ventricular end-diastolic diameter, but negatively correlated with left ventricular ejection fraction.

Conclusion: The plasma levels of chemerin and CRP are elevated in patients with acute coronary syndrome.
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July 2015

Chemerin is a novel biomarker of acute coronary syndrome but not of stable angina pectoris.

Cardiovasc Diabetol 2014 Nov 1;13:145. Epub 2014 Nov 1.

Background: Recent evidence demonstrated that the circulating adipokines were associated with the onset of acute coronary syndrome (ACS) including unstable angina pectoris (UAP) and acute myocardial infarction (AMI). As a novel adipokine, chemerin has been related to atherosclerosis and the presence of coronary artery disease. However, the plasma levels of chemerin in patients with ACS have yet to be investigated.

Methods: Plasma levels of chemerin and adiponectin were measured by an enzyme-linked immunosorbent assay (ELISA) in 60 patients with stable angina pectoris (SAP), 60 patients with UAP, 60 patients with AMI and 40 control patients. Left ventricular end-diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF) were measured using a GE ViVid E7 ultrasonography machine, and the severity of coronary stenosis in patients was estimated with a Gensini coronary score following coronary angiography.

Results: Plasma chemerin levels were significantly higher in ACS patients than in the control and SAP groups, while plasma adiponectin levels were significantly lower in ACS patients than the control group. A correlation analysis revealed that plasma chemerin levels were positively correlated with the levels of C-reactive protein (CRP) (r = 0.29, P < 0.01) and LVEDD (r = 0.27, P < 0.01) but negatively correlated with LVEF (r = -0.45, P < 0.01) and that plasma adiponectin levels were positively correlated with LVEF (r = 0.53, P < 0.01) but negatively correlated with CRP (r = -0.33, P < 0.01) and LVEDD (r = -0.30, P < 0.01). Although significant correlations between chemerin, adiponectin and BMI or the Gensini coronary score were found in patients with SAP, neither chemerin nor adiponectin was correlated with BMI and the Gensini coronary score in patients with ACS. Furthermore, both chemerin (OR 1.103, 95% CI 1.065 to 1.142; P = 0.001) and adiponectin (OR 0.871, 95% CI 0.776 to 0.970; P = 0.018) were independently associated with the presence of ACS.

Conclusions: Chemerin is a novel biomarker of acute coronary syndrome but not of stable angina pectoris.
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http://dx.doi.org/10.1186/s12933-014-0145-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4229596PMC
November 2014