摘要
目的:探讨6-姜酚(6-G)预处理对心肌细胞的保护作用及作用机制。方法将H9c2大鼠心肌细胞密度调整为5×104/ml,随机分为4组:正常组(Control组)、6-G干预组(6-G组)、H/R组、6-G+H/R组。Control组不加任何药物干预;6-G组给予6-G预处理;H/R组通过将培养的心肌细胞缺氧3h,复氧1 h建立H/R模型;6-G+H/R组在制作H/R模型前24 h给予6-G干预。采用CCK-8法、乳酸脱氢酶释放法和流式细胞术分别检测心肌细胞活力,细胞毒性和凋亡。使用倒置显微镜观察细胞的形态变化,Western blot检测凋亡蛋白Bax、Bcl-2、Cleaved Caspase-3的水平。结果:①与Control组比较,6-G组不存在细胞毒性(P<0.05)。②与H/R组比较.H/R+6-G组细胞存活率增加,且200 fig/ml浓度组细胞存活率最高(P<0.05)。③与H/R组比较,H/R+6-G组细胞形态明显改善。④与H/R组比较,H/R+6-G组caspase-3xBax表达显著降低,Bcl-2表达显著增加(P<0.05)。结论:6-G预处理可减轻H/R导致的心肌细胞损伤,其机制可能与抑制凋亡有关。
Objective:To investigate the protective effect and mechanism of 6・Gingerol(6-G)pretreatment on cardiomyocytes.Methods:H9c2 rat cardiomyocytes(5×104/ml)were randomized into the following 4 groups:the normal group(control group),6-G intervention group(6-G group),H/R group and 6-G plus H/R group.No drug intervention was added into the control group;while 6-G pretreatment was given to the 6-G group,the H/R model was established by hypoxia for 3 h and reoxygenation for 1 h In the H/R group,and the 6-G plus H/R group had received 6-G intervention for 24 hours prior to the making the H/R model.Cardiomyocyte viability,cytotoxicity and apoptosis were detected by the respective CCK-8 method,lactate dehydrogenase release method and flow cytometry.The morphological changes of the cells were observed by inverted microscope,and the levels of Bax,Bcl-2 and Cleaved Caspase-3 were detected by western blot.Results:(1)Compared with the Control group,there existed no cytotoxicity in 6-G group(P<0.05);(2)Compared with the H/R group,the cell viability of the H/R plus 6-G group increased,and the cell viability of the 200ug/ml concentration group was the highest(P<0.05);(3)Compared with H/R group,the cell morphology of H/R plus 6-G group was significantly improved;(4)Compared with H/R group,the expressions of caspase-3 and Bax was significantly decreased,while the expression of Bcl-2 was significantly increased in H/R plus 6-G group(P<0.05).Conclusion:6-G pretreatment can alleviate myocardial cell damage caused by H/R,and its mechanism may be related to the inhibition of apoptosis.
作者
彭丽
吕祥威
赵位昆
PENG Li;LYU Xiangwei;ZHAO Weikun(General Health Care Ward,the Affiliated Hospital of Guilin Medical University,Guilin 541001,China;Ward II of Cardiovascular Department,the Affiliated Hospital of Guilin Medical University,Guilin 541001,China)
出处
《华夏医学》
CAS
2019年第4期1-5,共5页
Acta Medicinae Sinica
基金
国家自然科学基金资助项目(NO:81760861)
广西自然科学基金重点资助项目(2018GXNSFDA281039)
广西自然科学基金资助项目(2018GXNSFAA294096)
桂林医学院中青年教职工科研能力提升资助项目(2018glmcy048)
广西高校中青年教师科研基础能力提升资助项目(2019KY0532)
广西自然科学基金资助项目(2018GXNSFAA050110)。
