Arginine Enhances Ovarian Antioxidant Capability via Nrf2/Keap1 Pathway during the Luteal Phase in Ewes.

This study evaluated the effect of arginine (Arg) on ovarian antioxidant capability during the luteal phase in ewes. A total of 108 multiparous Hu sheep at two years of age were randomly allocated to three groups: a control group (CG), a restriction group (RG), and an Arg group (AG), with six replicates per group and six ewes per replicate. Our results showed that the end body weight was significantly decreased in the RG group (p < 0.05), while the Arg addition reversed this reduction. The estrous cycle days were significantly increased in the RG group (p < 0.05), while Arg addition reversed this time extension. Compared with the control group, restricting feeding could significantly enhance the number of small follicles (SF), total follicles (TF), large corpora lutea, and the SF/TF (p < 0.05), while Arg addition reduced the number of SF and TF. However, the large follicles/TF were significantly decreased (p < 0.05), while Arg addition reversed this reduction. In addition, nutrition restriction significantly increased the malondialdehyde (MDA) level (p < 0.05), while significantly decreased the glutathione/glutathione disulfide and the activities of superoxidative dismutase, catalase, and glutathione peroxidase in the ovaries (p < 0.05). However, Arg addition reversed this enhancement of the MDA level and the reductions in these antioxidant enzymes activities. In addition, positive relationships occurred between antioxidant enzyme activities and the enzyme mRNA expressions. Meanwhile, the nuclear factor erythroid 2-related factor 2 (Nrf2) mRNA expression was positively connected with antioxidant mRNA expressions and negatively related to the Kelch-like ECH-associated protein 1 (Keap1) mRNA expression. The Nrf2 protein expression was negatively related to the Keap1 protein expression. In conclusion, nutrition restriction reduced the ovarian antioxidant capability in ewes, while this was significantly improved by Arg supplementation, which was associated with the Nrf2/Keap1 pathway.