基础医学与临床 ›› 2019, Vol. 39 ›› Issue (7): 978-982.

• 研究论文 • 上一篇    下一篇

柚皮苷抑制低氧/复氧致大鼠心肌细胞系H9c2损伤

刘丹,费慧芝,金良友,宋红霞,张永慧   

  1. 重庆三峡医药高等专科学校
  • 收稿日期:2019-01-15 修回日期:2019-04-28 出版日期:2019-07-05 发布日期:2019-07-02
  • 通讯作者: 刘丹 E-mail:liudan20042007@126.com
  • 基金资助:
    重庆市卫生计生委中医药科技项目

Naringin inhibits hypoxia/reoxygenation-induced of rat cardiomyocyte cell line H9c2 injury

  • Received:2019-01-15 Revised:2019-04-28 Online:2019-07-05 Published:2019-07-02

摘要: 目的 研究柚皮苷(NAR)对H9c2低氧/复氧(H/R)损伤心肌细胞内质网应激的影响。方法 将H9c2心肌细胞随机分为对照组(C组)、低氧/复氧组(H/R组)低氧4h后复氧24h、柚皮苷10、20和40μg/mL组。于低氧前6h给予柚皮苷培养再行低氧4h后复氧24h。实验后Tunel检测心肌细胞凋亡;Western blot 检测GRP78、ATF6、Bax及Bcl-2蛋白表达。结果 与对照组相比,H/R组细胞凋亡增加,GRP78、ATF6、Bax蛋白表达和Bax/Bcl-2比率显著上调,而Bcl-2蛋白表达显著下调 (P <0.05);与H/R组比较,柚皮苷3个剂量组均可使细胞凋亡减少,GRP78、ATF6、Bax、Bax/Bcl-2比率下调,Bcl-2上调(P <0.05),尤其以柚皮苷20和40μg/mL组作用最显著。结论 柚皮苷预处理可以降低细胞凋亡,其机制可能与抑制内质网应激有关。

关键词: 柚皮苷, GRP78, ATF6, 缺氧/复氧损伤, 凋亡, Bax/Bcl-2

Abstract: Objective To study the effect of naringin (NAR) on endoplasmic reticulum (ER) stress in cardiomyocytes injured by H9c2 hypoxia/reoxygenation (H/R).Methods H9c2 cardiomyocytes were randomly divided into three groups: control group, hypoxia/ reoxygenation group (H/R) for 24 h after hypoxia for 4 h, naringin 10, 20 and 40 μg /mL groups.Naringin was cultured 6 h before hypoxia for 4 h and then reoxygenation for 24 h. TUNEL detects apoptosis of cardiomyocytes after the experiment. Western blot was used to detect the expression of GRP78,ATF6,Bax and Bcl-2.Results Compared with control group, the cell apoptosis was increased, the expression of GRP78, ATF6, Bax protein expression and Bax/Bcl-2 were remarkably up-regulated (P < 0.05), but Bcl-2 protein expression was remarkably down-regulated in H/R group. Compared with the H/R group, the cell apoptosis decreased; the expression of GRP78, ATF6 , Bax and Bax/Bcl-2 were down-regulated (P < 0.05), but Bcl-2 was up-regulated in the groups with naringin three groups,especially naringin 20 and 40μg/mL groups had remarkably effect.Conclusion:The pretreatment of naringin can reduce the apoptosis of myocardial cell. The mechanism may be related to the inhibition of the apoptotic pathway of endoplasmic reticulum stress.

Key words: Naringin, GRP78, ATF6, Hypoxia-Reoxygenation injury , apoptosis, Bax/Bcl-2