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Protective Effect And Mechanism Of Salidroside On Stress Hyperglycemia In H9c2 Cardiomyocytes

Posted on:2020-03-11Degree:MasterType:Thesis
Country:ChinaCandidate:Y MaFull Text:PDF
GTID:2404330572480534Subject:Integrative Chinese and Western medicine
Abstract/Summary:PDF Full Text Request
Objective:To investigate the protective effects of Salidroside in H9c2 cardiomyocytes under Stress hyperglycemiaMethods:H9c2 cardiomyocytes were divided into five groups:?the control group(the cells treated with normal glucose,5.5mmol/L),?the high glucose group(the cells treated with high glucose,33.3mmol/L),?the H2O2 group(the cells treated with H2O2 at concentrations of 100umol/L for 2 hours),?the high glucose+H2O2 group(the cells treated with H2O2 and high glucose),?the high glucose+H2O2+Salidroside group(the cells treated with H2O2 and high glucose,salidroside at concentrations of 0.4mg/ml).A ctivity of H9c2 cardiomyocytes was detected by cell counting kit(CCK-8).The rate of apoptotic cells were detected by flow cytometry.Mitochondria membrane potentials were measured by JC-1 kit.The expression of OPA1 and Drpl protein in mitochondria was determined by Western blot.Results:1.Compared with the control group,the expression of Drpl in H9c2 cells in high glucose group was significantly increased(P<0.01).The expression level of OPA1 protein was significantly decreased(P<0.01),Mitochondrial membrane potential decreased significantly(P<0.05),the rate of apoptotic cells increased(P<0.05);Compared with the control group,the expression of Drpl in H9c2 cells in H2O2 group,high glucose+H2O2 group was significantly higher(P<0.01),the expression of OPA1 protein was significantly decreased(P<0.01),Mitochondrial membrane potential decreased significantly(P<0.01).the rate of apoptotic cells increased(P<0.01)2.Compared with the high glucose+H2O2 group,the expression of OPA1 cells increased(P<0.01),the expression of Drpl cells decreased(P<0.01),accompanied by increased mitochondrial membrane potential and the rate of apoptotic cells were were decreased(P<0.01)in salidroside+high glucose+H2O2 group.Conclusions:1.Stress hyperglycemia can reduce mitochondrial membrane potential,increases the rate of apoptotic H9c2 cardiomyocytes,and thus damages H9c2 cardiomyocytes by inhibiting mitochondrial dynamic balance of H9c2 cardiomyocytes.2.Salidroside can alleviate injury from stress hyperglycemia of H9c2 cardiomyocytes,reduce cardiomyocyte apoptosis and protect mitochondrial function.
Keywords/Search Tags:H9c2 cardiomyocytes, Salidroside, Stress hyperglycemia, Mitochondrial dynamics, Apoptosis
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