Inhibition of Oxidative Stress and Autophagy by Arbutin in Lipopolysaccharide‑Induced Myocardial Injury

Objective: The purpose of this study was to investigate the effect of Ar on LPS‑induced myocardial injury and its underlying mechanisms. Materials and Methods: The levels of tumor necrosis factor alpha, interleukin 6, cardiac troponin‑I, and procalcitonin were detected by ELISA. The levels of phosphorylated c‑Jun N‑terminal kinase (p‑JNK), phosphorylated extracellular regulated protein kinase (p‑ERK), and phosphorylated p38 (p‑p38) proteins were detected by flow cytometry using Cytometric Bead Array. Western blot was used to detect the expression of autophagy‑related and estrogen receptor (ER)‑associated proteins. Levels of the oxidative stress‑related markers were detected by the cuvette assay. Results: The levels of the inflammatory factors, LC3B, malondialdehyde, p‑JNK, and p‑p38 were increased in LPS‑treated rats, while the ERK, total superoxide dismutase, glutathione peroxidase, p62, and ER‑associated proteins were decreased. These effects could be effectively reversed by Ar, which could be blocked by ER antagonist ICI182780. Our previous study found Ar to possess an estrogen‑like activity. Conclusion: Ar inhibits the oxidative stress and autophagy and offers protection from the LPS‑induced myocardial injury via the ER pathway.