The Journal of pharmacy and pharmacology · 2025
Taoren Honghua Jian improves ferroptosis-mediated myocardial damage following myocardial infarction via Nrf2-dependent enhancement of GPX4/FSP1.
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Zhang Guo-Yong, Zhang Feng, Xie Ling-Peng, Han Xin, Wang Zhi-Xin, Wang Wen-Long, Peng Yan, Xu Hong-Lin, Xu Tong, Pang Ming-Jie, Liu Bin, Wang Dong, Zhou Ying-Chun, Wu Yu-Ting
Аннотация
OBJECTIVES: Myocardial infarction (MI) remains a leading cause of global mortality, and the inhibition of ferroptosis has cardioprotective potential. Taoren Honghua Jian (TRHHJ) has been used clinically to improve cardiovascular disorders. However, whether TRHHJ inhibits cardiomyocyte ferroptosis and ameliorates myocardial damage after MI requires further investigation. This study aimed to assess the ferroptosis-inhibiting effects of TRHHJ on post-MI myocardial injury and its underlying mechanisms.
METHODS: In vivo MI models were established via left anterior descending coronary artery ligation, and the cardioprotective effects of TRHHJ were assessed by echocardiography and histopathology combined with ferroptosis biomarker detection and Nrf2 signaling protein analysis. In vitro, erastin induced ferroptosis in H9C2 cells, and the anti-ferroptotic effects of TRHHJ was evaluated using the MTT assay, ferroptosis markers, and Nrf2 signaling analysis. Mechanistically, Nrf2 inhibitor and knockout mice were used for validation.
RESULTS: TRHHJ suppressed cardiomyocyte ferroptosis, reduced myocardial damage, and improved cardiac function in post-MI mice by activating the Nrf2 signaling pathway in vivo. TRHHJ enhanced cell viability and inhibited erastin-induced ferroptosis in H9C2 cells by increasing Nrf2 level and activating downstream signaling in vitro. Inhibition or knockout of Nrf2 partially abolished these protective effects.
CONCLUSIONS: TRHHJ inhibits cardiomyocyte ferroptosis and improves myocardial damage after MI through activation of Nrf2 signaling.
METHODS: In vivo MI models were established via left anterior descending coronary artery ligation, and the cardioprotective effects of TRHHJ were assessed by echocardiography and histopathology combined with ferroptosis biomarker detection and Nrf2 signaling protein analysis. In vitro, erastin induced ferroptosis in H9C2 cells, and the anti-ferroptotic effects of TRHHJ was evaluated using the MTT assay, ferroptosis markers, and Nrf2 signaling analysis. Mechanistically, Nrf2 inhibitor and knockout mice were used for validation.
RESULTS: TRHHJ suppressed cardiomyocyte ferroptosis, reduced myocardial damage, and improved cardiac function in post-MI mice by activating the Nrf2 signaling pathway in vivo. TRHHJ enhanced cell viability and inhibited erastin-induced ferroptosis in H9C2 cells by increasing Nrf2 level and activating downstream signaling in vitro. Inhibition or knockout of Nrf2 partially abolished these protective effects.
CONCLUSIONS: TRHHJ inhibits cardiomyocyte ferroptosis and improves myocardial damage after MI through activation of Nrf2 signaling.