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| 温阳益气活血汤上调Calumenin干预内质网应激治疗阿霉素诱 导性心肌病的作用机制研究 |
| Wenyang Yiqi Huoxue Decoction improves Adriamycin-induced myocardial injury by Calumenin intervention of endoplasmic reticulum stress |
| 投稿时间：2025-09-29 修订日期：2026-03-31 |
| DOI： |
| 中文关键词: 温阳益气活血汤 钙网蛋白 内质网应激 阿霉素 心肌损伤 |
| 英文关键词:Wenyang Yiqi Huoxue decoction Calumenin endoplasmic reticulum stress Adriamycin myocardial damage |
| 基金项目:浙江省基础公益研究计划项目（LGF22H020018）；浙江省中医药科学研究基金项目（A 类），2022ZA036；国家优势专科建设项目--老年病科，浙江省立同德医院（项目编号：[2024]90662）, |
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| 中文摘要: |
| 背景:阿霉素(Adriamycin, DOX)因其心脏毒性而限制了临床应用。因此,本研究旨在探讨温阳益气活血汤调控 DOX 所致心肌损伤的机制,以期减轻 DOX 在癌症治疗中的副作用。方法:本研究建立DOX 诱导的心肌损伤模型,采用 TUNEL 检测心肌组织细胞凋亡情况,并通过超声心动图评估损伤后心脏功能的变化。采用 Western blot 分析检测 DOX 和 温阳益气活血汤处理后心肌组织中 Bax、Bcl-2 及内质网应激相关蛋白 GRP78 和 Chop 的表达变化。通过 CCK-8 检测温阳益气活血汤 在 H9C2 细胞中的最佳作用浓度；并在 siRNA 与温阳益气活血汤联合处理后,从转录与翻译水平检测钙网蛋白(Calumenin)、Chop 和 GRP78 的表达变化。结果:在体内实验中,DOX 可导致心肌组织损伤与细胞凋亡,而 温阳益气活血汤治疗后,细胞凋亡减少,GRP78、Chop 和钙网蛋白表达受到抑制。CCK-8 结果显示,5 μmol/L DOX 可抑制约 50% H9C2 细胞活力,而在 DOX 诱导的 H9C2 细胞中,1.5 mg/ml 温阳益气活血汤处理下的细胞活力最高。进一步研究发现,DOX 诱导的 H9C2 细胞经温阳益气活血汤处理后,细胞凋亡率下降,Bcl-2/Bax 比值显著升高,内质网应激水平受到干预。而 siCalumenin 处理则削弱了温阳益气活血汤对心肌细胞的保护作用。结论:温阳益气活血汤可能通过上调钙网蛋白表达并介导内质网应激,从而改善 DOX 所致心肌损伤。 |
| 英文摘要: |
| Background: Adriamycin (DOX) has limited clinical application due to its cardiotoxicity. Therefore, the aim of this study is to investigate the mechanism of Wenyang Yiqi Huoxue decoction (WYYQ) in regulating DOX-induced myocardial injury in order to alleviate the side effects of DOX in the treatment of cancer. Method: In this study, we established a DOX-induced myocardial injury model, and used TUNEL assay and echocardiography to detect cell apoptosis in myocardial tissue and changes in cardiac function after injury. Western blot analysis was used to detect the expression changes of Bax, Bcl-2 and ER stress-related proteins GRP78 and Chop in DOX and WYYQ treated myocardial tissues. CCK-8 assay was used to find the optimal concentration of WYYQ in H9C2 cells in vitro. , The expression changes of Calumenin, Chop and GRP78 were detected at the transcription and translation levels following treatment with siRNA and WYYQ. Results: In the in vivo study, DOX was found to induce myocardial tissue injury and cell apoptosis. After WYYQ treatment, the reduction of apoptosis inhibited GRP78, Chop and Calumenin expression. The results of CCK-8 assay showed that 5μmol/L DOX inhibited the viability of H9C2 cells by about 50%. In DOX-induced H9C2 cells, 1.5mg/ml MYYQ treatment had the highest cell viability. After DOX-induced H9C2 cells were treated with WYYQ, the apoptosis rate was decreased, the Bcl2/Bax ratio was significantly increased, and the level of endoplasmic reticulum stress was interfered. siCalumenin treatment attenuated the protective effect of WYYQ on cardiomyocytes. Conclusion: WYYQ has the potential to improve DOX-induced myocardial injury by upregulating Calumenin expression and mediating endoplasmic reticulum stress. |
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