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.

Wooden breast (WB) is a widely prevalent myopathy in broiler chickens. However, the role of the gut microbiota in this myopathy remains largely unknown, in particular the regulatory effect of gut microbiota in the modulation of muscle metabolism. Totally, 300 1-day-old Arbor Acres broilers were raised until 49 days and euthanized, and the breast filets were classified as normal (NORM), mild (MILD), or severe wooden breast (SEV). Birds with WB comprised 27.02% of the individuals. Severe WB filets had a greater L* value, a* value, and dripping loss but a lower pH (P &lt; 0.05). WB filets had abundant myofiber fragmentation, with a lower average myofiber caliber and more fibers with a diameter of &lt;20 μm (P &lt; 0.05). The diversity of the intestinal microflora was decreased in birds with severe WB, with decreases in Chao 1, and observed species indices. At the phylum level, birds with severe WB had a lower Firmicutes/Bacteroidetes ratio (P = 0.098) and a decreased abundance of Verrucomicrobia (P &lt; 0.05). At the species level, gut microbiota were positively correlated with 131 digesta metabolites in pathways of glutamine and glutamate metabolism and arginine biosynthesis but were negatively correlated with 30 metabolites in the pathway of tyrosine metabolism. In plasma, WB induced five differentially expressed metabolites (DEMs), including anserine and choline, which were related to the severity of the WB lesion. The microbial-derived metabolites, including guanidoacetic acid, antiarol, and (2E)-decenoyl-ACP, which entered into plasma were related to meat quality traits and myofiber traits. In summary, WB filets differed in gut microbiota, digesta, and plasma metabolites. Gut microbiota respond to the wooden breast myopathy by driving dynamic changes in digesta metabolites that eventually enter the plasma.