| 引用本文: | 刘晓萍,李靖璇,柯权英,罗润琪,江晟,张仙映,赖丽嫦.冬凌草甲素抑制棕榈酸诱导的心肌细胞凋亡[J].中国现代应用药学,2026,43(5):15-22. |
| Liu Xiaoping,Li Jingxuan,Ke quanying,Luo Runqi,Jiang Sheng,Zhang Xianying,Lai Lichang.Oridonin Alleviates Palmitate Acid-induced Cardiomyocyte Apoptosis[J].Chin J Mod Appl Pharm(中国现代应用药学),2026,43(5):15-22. |
|
| 摘要: |
| 目的：探讨冬凌草甲素(Oridonin,Ori)对棕榈酸(palmitate acid, PA)诱导H9C2细胞凋亡的影响及作用机制。方法：以PA处理H9C2细胞24h,MTT法检测细胞存活率；Western blotting法检测Cleaved Caspase 3、Nrf2、NQO1、HO1的蛋白表达水平；DHE荧光探针检测超氧阴离子数量；TUNEL法检测心肌细胞凋亡。结果：以200μM.L-1 PA处理H9C2 24h,与对照组比较,细胞存活率明显下降；凋亡相关蛋白Cleaved Caspase 3水平和心肌细胞凋亡阳性数目(红色)显著升高；超氧阴离子数量显著增加,Nrf2/ARE信号通路关键蛋白Nrf2、NQO1、HO1蛋白显著下调(P<0.05)；给予Ori处理后,与PA组比较,细胞存活率显著增加,Cleaved Caspase 3蛋白表达水平和心肌细胞凋亡阳性数目(红色)显著降低；超氧阴离子数量显著降低,Nrf2、NQO1、HO1蛋白表达水平显著上升(P<0.05),而给予Nrf2抑制剂则逆转上述改变。结论：冬凌草甲素通过激活Nrf2/ARE信号通路,减轻PA诱导的H9C2心肌细胞凋亡。 |
| 关键词: 冬凌草甲素 棕榈酸 Nrf2/ARE 细胞凋亡 |
| DOI： |
| 分类号: |
| 基金项目:国家自然科学基金项目（青年基金） |
|
| Oridonin Alleviates Palmitate Acid-induced Cardiomyocyte Apoptosis |
|
Liu Xiaoping, Li Jingxuan, Ke quanying, Luo Runqi, Jiang Sheng, Zhang Xianying, Lai Lichang
|
|
The Affiliated Qingyuan Hospital（Qingyuan People’s Hospital），Guangzhou Medical University
|
| Abstract: |
| ABSTRACT OBJECTIVE: To investigate the effect of Oridonin (Ori) on the apoptosis of H9C2 induced by palmitate acid (PA) and its mechanism. METHODS: H9C2 were treated with PA for 24h.The survival rate was detected by MTT. The protein expression levels of Cleaved Caspase 3、Nrf2、NQO1 and HO1were detected by Western blotting. The quantity of superoxide anion was detected by DHE. The apoptosis was detected by TUNEL. RESULTS: Compared with the control group, the survival rate which treated with 200μM·L-1 PA for 24h was decreased significantly. The protein expression level of Cleaved Caspase 3 was significant increased, and positive apoptosis was significantly increased. The number of superoxide anions was significantly increased, and the protein expression levels of Nrf2, NQO1 and HO1 were significantly down-regulated (P<0.05). After Ori treatment, compared with PA group, the cell survival rate was significantly increased, The protein expression level of Cleaved Caspase 3 and the positive apoptosis was significantly decreased. The number of superoxide anions was significantly decreased, and the protein expression levels of Nrf2, NQO1 and HO1 were significantly increased (P<0.05). While Nrf2 inhibitor treatment reversed the above changes. CONCLUSION: Oridonin alleviates PA-induced cardiomyocyte apoptosis by activating Nrf2/ARE signaling. |
| Key words: Oridonin Palmitic acid Nrf2/ARE Apoptosis |
