TITLE:
Chinese Herbal Formula Zhuangtongyin Decoction Protects against Myocardial Ischemia by Inhibiting the NF-κB/NLRP3 Inflammasome Pathway
AUTHORS:
Meiye Song, Hanqing Tang, Keming Li, Jiahui Li, Jing Zhou, Songyi Mo, Lingling Huang, Caiyan Yang, Wenchong Wang
KEYWORDS:
Zhuangtongyin, Myocardial Ischemia, Inflammation, NF-κB, NLRP3
JOURNAL NAME:
Journal of Biosciences and Medicines,
Vol.12 No.12,
December
24,
2024
ABSTRACT: Background: The medical community has been trying to reduce the high mortality rate of cardiovascular diseases and find effective treatments; however, the results have not been satisfactory. Zhuangtongyin (ZTY), a Chinese herbal formula, has received significant attention owing to its efficacy in the treatment of myocardial ischemia. However, there are few reports on the mechanisms of its action, which hinder its widespread dissemination. Recent studies have shown that the effects of ZTY are associated with the NF-κB/NLRP3 inflammasome pathway. In this study, we investigated the underlying mechanisms of ZTY in myocardial ischemia through the NF-κB/NLRP3 inflammasome pathway. Methods: A myocardial ischemia model was established by ligating rats’ left anterior descending coronary artery. The rats were randomly divided into five groups: control group, model group, sham operation group, ZTY group (13.6 g/kg), and NF-κB group (0.12 g/kg). All groups, except the control group, received oral administration for 28 days. The NF-κB group received peritoneal injection of PDTC for 28 days. ECG, assessment of myocardial ischemia injury, histological examination, and analysis of biochemical indices of myocardial tissue were performed to evaluate myocardial injury and drug protection. Inflammation levels were assessed by Masson staining and Elisa, and expression of transforming growth factor (TGF-β1), α-smooth muscle actin (α-SMA), and connexin 43 (Cx43) was detected by immunohistochemistry. Results: Compared to the control group, the model group showed obvious abnormalities in myocardial tissue and increased levels of inflammatory cytokines. ZTY therapy inhibited the increases in lactate dehydrogenase (LDH), creatinine kinase (CK), creatinine kinase isoenzyme (CK-MB), tumour necrosis factor α (TNF-α), and interleukin-6 (IL-6). The immunohistochemical results showed that ZTY treatment inhibited TGF-β1 expression, suggesting that the anti-inflammatory effect of ZTY was achieved by inhibiting NF-κB signalling. Conclusion: ZTY can effectively alleviate myocardial injury, and its protective effect against myocardial injury is related to inhibition of the NF-κB/NLRP3 inflammasome pathway.