This study aimed to investigate the protective effects and molecular mechanism of magnolol supplementation on rotenone-induced oxidative stress in broilers. Two hundred and eighty-eight old male AA broilers were randomly divided into four groups: the CON group: basic diet with sunflower oil injection; the ROT group: basic diet with 24 mg/kg BW rotenone; the MAG + ROT group: basic diet with 300 mg/kg magnolol and rotenone injection; and the MAG group: basic diet with 300 mg/kg magnolol and sunflower oil injection. At 21−27 days of age, the broilers in each group were intraperitoneally injected with rotenone (24 mg/kg BW) or the same volume of sunflower oil. The results showed that magnolol reversed the decrease in ADG post-injection and FBW via rotenone induction. Compared to the ROT group, MAG + ROT group enhanced the average daily gain post injection (p < 0.05). Magnolol supplement could improve the activity and mRNA expression of rotenone-suppressed antioxidant enzymes such as GSH and GSH-PX (p < 0.05). Similarly, the MDA content as an oxidative damage marker was significantly reduced after magnolol addition (p < 0.05). The hepatocyte apoptosis and the mRNA expression of apoptosis-related signaling pathway in the ROT group increased, but magnolol supplementation inhibited rotenone-induced apoptosis through the Nrf2 signaling pathway. Through RNA transcriptome analysis, there were 277 differential genes expressions (DEGs) among the CON group with ROT group, and 748 DEGs were found between the ROT group and the MAG + ROT group. KEGG pathway enrichment found that magnolol relieved rotenone-induced energy metabolism disorder and oxidative damage through signaling pathways such as MAPK and mTOR. In conclusion, magnolol attenuates rotenone-induced hepatic injury and oxidative stress of broilers, presumably by restoring hepatic antioxidant function via the MAPK/mTOR/Nrf2 signaling pathway.
Keywords: MAPK/mTOR/Nrf2 pathway; broilers; liver damage; magnolol; rotenone.