Siyong Li, Peiyi He, Jiahe Liu, Shaochuan Zang, Jiahao Luo, Yi Luo, Shuguang Zhu, Linquan Zang
Excessive stress is a known contributor to cardiovascular diseases (CVD), and ferulic acid (FA), a natural phenolic compound, has demonstrated significant antioxidant and anti-inflammatory properties. This study investigates the protective effects of FA against stress-induced myocardial injury (SIMI) and elucidates the underlying mechanisms. An acute SIMI model was established in mice using low-temperature water immersion restraint. Cardiac function was assessed via cardiac index and histopathological analysis. Serum levels of corticosterone (CORT), lactate dehydrogenase (LDH), and brain natriuretic peptide (BNP) were quantified using enzyme-linked immunosorbent assay (ELISA), along with inflammatory markers TNF-�� and IL-1��. The oxidative stress parameters, including malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and reactive oxygen species (ROS), were analyzed using colorimetric methods and fluorescent probes. Immunohistochemistry (IHC) and Western Blot were used to analyze the expression of proteins related to TNF, MAPK, PPAR-��/PGC-1��, and Nrf2 signaling pathways. Results indicated that FA pretreatment improved cardiac index, myocardial structural integrity, and reduced inflammatory cell infiltration. Serum levels of LDH, BNP, CORT, TNF-��, and IL-1�� were significantly decreased in FA-treated SIMI mice. Elevated MDA and ROS levels, along with decreased GSH and SOD levels in the SIMI group, were reversed by FA pretreatment, likely through activation of the PPAR��/PGC-1�� and Nrf2 signaling pathways. Additionally, FA inhibited the TNF-��/TNFR1 and ERK/JNK MAPK pathways, contributing to its protective effects. In conclusion, FA mitigates SIMI by alleviating oxidative stress and inflammatory responses.
