Zingerone Alleviates Acetaminophen-Induced Liver Damage by Regulating Oxidative Stress, Inflammation, Apoptosis, Endoplasmic Reticulum Stress, and Autophagy.

The aim of this study is to investigate the protective effect of zingerone (ZNG), an antioxidant agent, against acetaminophen (APAP)-induced liver damage, which is used as an analgesic and antipyretic. For this purpose, twenty-eight male rats were divided into four groups: control, ZNG, APAP, and APAP + ZNG. ZNG was administered orally for 7 days, followed by a single dose of APAP on the 7th day. At the end of the study, biochemical, molecular, and immunohistochemical analyses were performed on the liver tissue. According to the data obtained, APAP was found to trigger oxidative stress, inflammation, autophagy, apoptosis, endoplasmic reticulum stress, autophagy, and heat shock proteins in liver tissue. On the other hand, it has been observed that after ZNG treatment, the activities of antioxidant enzymes SOD, GPx, and CAT increased, MDA levels, a significant indicator of lipid peroxidation, decreased, and GSH stores were replenished. Following ZNG treatment, apoptosis was attenuated, resulting in decreased mRNA transcript levels of Bax, caspase-3, and increase in Bcl-2 levels. ZNG treatment resulted in a decrease in endoplasmic reticulum stress, inflammation, autophagy mRNA transcript levels. In addition, a decrease in heat shock proteins was detected. In conclusion, it has been observed that ZNG may be a significant protective against APAP liver damage.