College of Animal Science and Veterinary Medicine, Shandong Agricultural University, 61 Daizong Street, Tai'an City, Shandong Province 271018, China; Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Agricultural University, 61 Daizong Street, Tai'an City, Shandong Province 271018, China; Shandong Provincial Engineering Technology Research Center of Animal Disease Control and Prevention, Shandong Agricultural University, 61 Daizong Street, Tai'an City, Shandong Province 271018, China.
College of Veterinary Medicine, Shanxi Agricultural University, 1 Mingxian South Road, Jinzhong CIty, Shanxi Province 030801, China.
J Inorg Biochem. 2022 Apr;229:111716. doi: 10.1016/j.jinorgbio.2022.111716. Epub 2022 Jan 5.
Mercuric chloride (HgCl), a heavy metal compound, causes neurotoxicity of animals and humans. Selenium (Se) antagonizes heavy metal-induced organ damage with the properties of anti-oxidation and anti-inflammation. Nevertheless, the molecular mechanism underlying the protective effects of sodium selenite (NaSeO) against HgCl-induced neurotoxicity remains obscure. Therefore, the present study aimed to explore the protective mechanism of NaSeO on HgCl-induced brain damage in chickens. Morphological observations showed that NaSeO alleviated HgCl-induced brain tissues damage. The results also showed that NaSeO decreased the protein expression of S100 calcium binding protein B (S100B), and increased the levels of nerve growth factors (NGF), doublecortin domain containing 2 (DCDC2), as well as neurotransmitter to reverse HgCl-induced brain dysfunction. Further, NaSeO attenuated HgCl-induced oxidative stress by decreasing the level of malondialdehyde (MDA) and increasing the activities of total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC). Mechanistically, NaSeO activated the brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase receptor type B (TrKB)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway and suppressed the nuclear factor kappa B (NF-κB) signaling pathway to inhibit apoptosis and inflammation caused by HgCl exposure. In summary, NaSeO ameliorated HgCl-induced brain injury via inhibiting apoptosis and inflammation through activating BDNF/TrKB/PI3K/AKT and suppressing NF-κB pathways.
氯化汞（HgCl）是一种重金属化合物，可导致动物和人类的神经毒性。硒（Se）具有抗氧化和抗炎作用，可拮抗重金属引起的器官损伤。然而，亚硒酸钠（NaSeO）对 HgCl 诱导的神经毒性的保护作用的分子机制尚不清楚。因此，本研究旨在探讨 NaSeO 对鸡 HgCl 诱导的脑损伤的保护机制。形态学观察表明，NaSeO 减轻了 HgCl 诱导的脑组织损伤。结果还表明，NaSeO 降低了 S100 钙结合蛋白 B（S100B）的蛋白表达，并增加了神经生长因子（NGF）、双皮质素结构域包含 2 （DCDC2）和神经递质的水平，以逆转 HgCl 诱导的脑功能障碍。此外，NaSeO 通过降低丙二醛（MDA）水平和增加总超氧化物歧化酶（T-SOD）、谷胱甘肽过氧化物酶（GSH-Px）和总抗氧化能力（T-AOC）的活性来减轻 HgCl 诱导的氧化应激。在机制上，NaSeO 激活了脑源性神经营养因子（BDNF）/原肌球蛋白相关激酶受体 B（TrKB）/磷酸肌醇 3-激酶（PI3K）/蛋白激酶 B（AKT）信号通路，并抑制了核因子 kappa B（NF-κB）信号通路，以抑制 HgCl 暴露引起的细胞凋亡和炎症。总之，NaSeO 通过激活 BDNF/TrKB/PI3K/AKT 并抑制 NF-κB 通路抑制凋亡和炎症来改善 HgCl 诱导的脑损伤。
