Wei Wenjuan, Li Caiyan, Zhang Baoyong, Huang Deyun, Li Zheming, Gao Jiaer
Department of Cardiology, The First People's Hospital of Xiaoshan District, No. 199, Shixin Nan Road, Xiaoshan District, Hangzhou, 311200, Zhejiang, China.
College of Pharmacy, Hangzhou Medical College, No. 481, Binwen Road, Binjiang District, Hangzhou, 310053, Zhejiang, China.
J Cardiovasc Transl Res. 2024 Apr;17(2):388-402. doi: 10.1007/s12265-023-10440-3. Epub 2023 Oct 13.
Total glucosides of paeony (TGP) have a potential protective effect on chronic heart failure (CHF) rats, but the mechanism remains unclear. PARP inhibition prevents the decrease in myocardial contractility. Therefore, we aim to investigate the effects and mechanisms of TGP on CHF and the role of PARP-1 in CHF. Left anterior descending ligation rats and adriamycin-treated H9C9 cells were used as CHF models, and captopril as a positive control for in vivo experiments. We found that TGP alleviated myocardial remodeling and improved cardiac morphology and function. TGP also reduced myocardial apoptosis and autophagy, decreased inflammatory factor release, and inhibited the PARP-1 and NF-κB proteins. Through cell transfection, we found that PAPR-1 knockdown inhibited NF-κB nuclear translocation. Additionally, TGP inhibited apoptosis, autophagy, and inflammation in CHF cells, while PARP-1 overexpression partially antagonized them. In conclusion, TGP has the potential to improve CHF and PARP-1 may be a potential target.
芍药总苷（TGP）对慢性心力衰竭（CHF）大鼠具有潜在的保护作用，但其机制尚不清楚。PARP抑制可防止心肌收缩力下降。因此，我们旨在研究TGP对CHF的影响及机制，以及PARP-1在CHF中的作用。采用左冠状动脉前降支结扎大鼠和阿霉素处理的H9C9细胞作为CHF模型，卡托普利作为体内实验的阳性对照。我们发现TGP减轻了心肌重构，改善了心脏形态和功能。TGP还减少了心肌细胞凋亡和自噬，降低了炎症因子释放，并抑制了PARP-1和NF-κB蛋白。通过细胞转染，我们发现PAPR-1基因敲低抑制了NF-κB核转位。此外，TGP抑制了CHF细胞的凋亡、自噬和炎症，而PARP-1过表达部分拮抗了这些作用。总之，TGP有改善CHF的潜力，PARP-1可能是一个潜在靶点。
