College of Animal Science and Technology, Hainan University, Haikou, Hainan 570228, China.
Hainan Academy of Agricultural Sciences, Haikou, Hainan 570228, China.
Oxid Med Cell Longev. 2021 Nov 16;2021:6776956. doi: 10.1155/2021/6776956. eCollection 2021.
Vitamin D, as an indispensable and fat-soluble micronutrient, plays an important role in the health of humans and animals. At present, studies are focusing on the calcium absorption and immunoregulation function of vitamin D; this study was aimed at exploring the antioxidative stress ability of vitamin D on diquat-induced intestinal dysfunction of ICR mice and the underlying mechanism. The results showed that oral gavage of vitamin D daily significantly improved the body weight gain and immune organ index and significantly reverted the abnormal changes of ALT, AST, SOD, GSH-Px, T-AOC, and MDA in the serum and jejunum induced by diquat. The addition of vitamin D also significantly reduced the concentration of DAO, D-LA, and certain proinflammatory cytokines in serum. Moreover, vitamin D improved the pathological morphology of the duodenum, jejunum, colon, liver, and kidney tissues, and it also largely attenuated the degree of inflammatory infiltration of macrophages and cell apoptotic index of jejunal epithelial tissue induced by diquat. The results demonstrated that vitamin D significantly recovered the intestinal barrier injury by enhancing the expression of mucins and tight junction proteins in the jejunum. In addition, the results indicated that vitamin D could significantly reduce the phosphorylation level of NF-B (p65) and enhance the expression of Nrf2 and HO-1 in the jejunum compared with the diquat-induced group. This study suggested that oral administration of vitamin D can protect mice against oxidative damage by inhibiting the phosphorylation level of NF-B (p65) and activating Nrf2-related signaling pathways.
维生素 D 作为一种不可或缺的脂溶性微量营养素，在人类和动物的健康中起着重要作用。目前，研究集中在维生素 D 的钙吸收和免疫调节功能上；本研究旨在探讨维生素 D 对百草枯诱导的 ICR 小鼠肠道功能障碍的抗氧化应激能力及其作用机制。结果表明，每日口服维生素 D 可显著改善体重增加和免疫器官指数，并显著逆转百草枯诱导的血清和空肠中 ALT、AST、SOD、GSH-Px、T-AOC 和 MDA 的异常变化。添加维生素 D 还显著降低了血清中 DAO、D-LA 和某些促炎细胞因子的浓度。此外，维生素 D 改善了十二指肠、空肠、结肠、肝和肾组织的病理形态，还大大减轻了百草枯诱导的空肠上皮组织中巨噬细胞炎症浸润和细胞凋亡指数的程度。结果表明，维生素 D 通过增强空肠中黏蛋白和紧密连接蛋白的表达，显著恢复了肠道屏障损伤。此外，与百草枯诱导组相比，维生素 D 可显著降低 NF-B（p65）的磷酸化水平，并增强 Nrf2 和 HO-1 在空肠中的表达。本研究表明，口服维生素 D 可以通过抑制 NF-B（p65）的磷酸化水平和激活 Nrf2 相关信号通路来保护小鼠免受氧化损伤。
