熊果苷缓解脂多糖诱导的H9c2心肌氧化应激、细胞凋亡及炎症反应  

Arbutin relieves lipopolysaccharide-induced oxidative stress,apoptosis and inflammatory response in H9c2 cardiomyocytes

作　　者：梅丽军 周紫微 赵婧莎 潘传亮[1] 刘剑萍[1] 何韵 MEI Lijun;ZHOU Ziwei;ZHAO Jingsha;PAN Chuanliang;LIU Jianping;HE Yun(Health Management Center,Third People’s Hospital of Chengdu,Chengdu 610031,China)

机构地区：[1]成都市第三人民医院健康管理中心,610031

出　　处：《免疫学杂志》2023年第12期1028-1033,共6页Immunological Journal

基　　金：重庆市自然科学基金面上项目(estc2020jcyjmsxmX0029);重庆市渝中区基础研究与前沿探索项目(20190127)

摘　　要：目的探讨熊果苷(Ar)对脂多糖(LPS)诱导的心肌细胞损伤模型中细胞凋亡和炎症因子分泌的影响。方法用CCK-8法检测LPS(0.1μg/ml、0.5μg/ml、1μg/ml、2μg/ml)和Ar(0μmol/L、25μmol/L、50μmol/L、100μmol/L)处理后的H9c2心肌细胞增殖情况,选出最佳药物处理浓度,后续实验组由LPS处理12 h后再经Ar处理12 h。通过DCFH-DA荧光标记法检测心肌细胞中ROS的水平。流式细胞术检测心肌细胞的凋亡情况。Western blot检测心肌细胞中TNF-α、IL-1β和Caspase-3蛋白的表达。结果经Ar处理后,被LPS抑制的H9c2细胞增殖能力有所增强(P<0.05)。LPS诱导心肌细胞产生ROS累积,ROS荧光信号增强,而Ar可以明显抑制LPS诱导的ROS累积(P<0.05)。与对照组相比,LPS组的凋亡细胞数量增加,Ar处理缓解了LPS诱导的细胞凋亡。Western blot结果显示,LPS诱导了炎症因子TNF-α、IL-1β和凋亡蛋白Caspase-3显著升高,Ar可明显抑制上述蛋白表达,发挥其抗炎抗凋亡的作用。结论Ar可在体外脓毒症模型中,通过发挥其抗ROS累积、抗炎和抗凋亡作用,以此抑制LPS造成的心肌损伤。This study was performed to investigate the effects of Arbutin(Ar)on oxidative stress,apoptosis level and inflammatory response of H9c2 cardiomyocytes induced by lipopolysaccharide(LPS).H9c2 cardiomyocytes were randomly divided into blank control group,lipopolysaccharide group(LPS),LPS+Ar(25μmol/L)group,LPS+Ar(50μmol/L)group,LPS+Ar(100μmol/L)group and Ar(50μmol/L)group.CCK-8 was used to detect the cell viability of H9c2 cardiomyocytes after LPS treatment and Ar treatment;DCFH-DA fluorescence labeling was used to detect the ROS levels of H9c2 cardiomyocytes;flow cytometry was applied to detect cell apoptosis rate;Western blot was used to detect the expression of apoptosis-related proteins(Caspase-3)and inflammatory proteins(IL-1β and TNF-α).Data showed that compared with the LPS group,the cell viabilities were recovered after Ar treatment.The level of oxidative stress markers(ROS),apoptosis rate,and inflammatory factor levels(IL-1β and TNF-α)in the LPS+Ar groups were significantly reduced compared with the LPS group(P<0.05).In conclusion,Ar can alleviate the damage,apoptosis,oxidative stress and inflammatory response of LPS-induced H9c2 cardiomyocytes.

关 键 词：熊果苷 脂多糖 心肌损伤 氧化应激 凋亡 炎症 

分 类 号：R541.9[医药卫生—心血管疾病] R631[医药卫生—内科学]