Curcumin improves the egg quality, antioxidant activity, and intestinal microbiota of quails during the late laying period.

This study aimed to investigate the effects of dietary curcumin supplementation on laying performance, egg quality, egg metabolites, lipid metabolism, antioxidant activity, and intestinal microbial composition of quails in the late laying period. A total of 960 late-laying quails (240-day-old) were randomly divided into 4 groups of 6 replicates each (n = 40/replicate). The experimental diets of the 4 groups consisted of basal diets supplemented with 0, 50, 100, and 200 mg/kg curcumin, respectively. The feeding experiment lasted for 8 wk. The results showed that 200 mg/kg curcumin supplementation decreased mortality and increased eggshell thickness and strength compared with the 0 mg/kg curcumin supplementation during wk 5 to 8. In addition, dietary supplementation of curcumin promoted lipid metabolism, enhanced antioxidant activity, and modified intestinal microbiota structure. In conclusion, dietary supplemented with 200 mg/kg curcumin significantly improved the egg quality of quails in the late laying period, primarily by improving lipid metabolism and selectively regulating the intestinal microbial community.

Grape seed extract proanthocyanidin antagonizes aristolochic acid I-induced liver injury in rats by activating PI3K-AKT pathway.

Aristolochic acid is internationally recognized as a carcinogen. It has been shown that the main toxic mechanism of aristolochic acid on the liver and kidney is the induction of ROS-induced oxidative stress damage. To investigate whether proanthocyanidins (GSPE), a natural antioxidant product from grape seed extract, could antagonize AA-I-induced liver injury. Thirty-two SD rats were selected and divided into aristolochic acid exposure group (AA-I), normal control group, GSPE group and GSPE intervention group. The protective effects of GSPE on AA-I liver injury were evaluated by examining the body weight, liver index, liver function and liver pathological sections of rats. The results of body weight, liver index, liver function and liver pathological sections of rats showed that GSPE had antagonistic effects on AA-I-induced liver injury. antioxidant enzyme activity in the GSPE intervention group was significantly higher than that in the aristolochic acid group, apoptotic cells were significantly lower than that in the aristolochic acid group, protein and mRNA expression of PI3K-AKT and BCL-2 were significantly higher than that in the aristolochic acid group, BAX, The protein and mRNA expression of BAX, CASPAES-3, CASPAES-9 were significantly lower than those of the aristolochic acid group. GSPE can antagonize aristolochic acid-induced hepatotoxicity, and its mechanism of action is to antagonize aristolochic acid I-induced liver injury by inhibiting PI3K-AKT pathway-mediated hepatocyte apoptosis.