Hunan Engineering Research Center of Livestock and Poultry Health Care, College of Veterinary Medicine, Hunan Agricultural University, Changsha, 410128, China.
Environ Sci Pollut Res Int. 2022 Jul;29(34):52098-52110. doi: 10.1007/s11356-022-19498-z. Epub 2022 Mar 7.
T-2 toxin is a mycotoxin that has harmful effects on the immune system and cognitive function. Betulinic acid (BA) is a plant-derived pentacyclic lupane-type triterpenoid which possesses a wide spectrum of bioactivities. The study was aimed to explore whether BA has a protective effect on cognitive impairment and oxidative stress caused by T-2 toxin. BA was suspended in 1% soluble starch by continuous intragastric administration for 14 days, then the brain damage in mice was induced by a single intraperitoneal injection of T-2 toxin (4 mg/kg). It was found that BA alleviated the reduction of discrimination index in T-2 toxin-treated mice, and enhanced dopamine (DA), 5-hydroxytryptamine (5-HT), and acetylcholine (ACH) levels of brain neurotransmitter. Meanwhile, BA pretreatment ameliorated oxidative stress through increase of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione (GSH) levels, and inhibition of the generation of reactive oxygen species (ROS) and malondialdehyde (MDA) in the brain of mice exposed to T-2 toxin. Moreover, BA reduced brain hemorrhage and ecchymosis, improved the mitochondrial morphology, enriched the number of organelles, and inhibited cell apoptosis in brain challenged with T-2 toxin. Furthermore, BA inhibited mRNA expression of pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) as well as enhanced mRNA expression of anti-inflammatory cytokine such as IL-10 in the brain of T-2 toxin-triggered mice. Therefore, BA could improve the cognitive function, enhance the antioxidant capacity, and inhibit the secretion of proinflammatory cytokines in brain, thereby playing a preventive and protective role against brain damage caused by T-2 toxin.
T-2 毒素是一种对免疫系统和认知功能有害的真菌毒素。白桦脂酸（BA）是一种植物来源的五环三萜类化合物，具有广泛的生物活性。本研究旨在探讨 BA 是否对 T-2 毒素引起的认知功能障碍和氧化应激具有保护作用。BA 通过连续胃内给药悬浮在 1%可溶性淀粉中，持续 14 天，然后用 T-2 毒素（4mg/kg）单次腹腔注射诱导小鼠脑损伤。结果发现，BA 减轻了 T-2 毒素处理小鼠辨别指数的降低，并增强了脑神经递质多巴胺（DA）、5-羟色胺（5-HT）和乙酰胆碱（ACH）的水平。同时，BA 通过增加超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）和谷胱甘肽（GSH）水平，抑制 T-2 毒素暴露小鼠大脑中活性氧（ROS）和丙二醛（MDA）的产生，从而改善氧化应激。此外，BA 减少了脑出血和淤血，改善了线粒体形态，增加了细胞器数量，并抑制了 T-2 毒素作用下大脑中的细胞凋亡。此外，BA 抑制了促炎细胞因子如白细胞介素-1β（IL-1β）、IL-6 和肿瘤坏死因子-α（TNF-α）的 mRNA 表达，同时增强了抗炎细胞因子如 IL-10 的 mRNA 表达。因此，BA 可以改善认知功能，增强抗氧化能力，抑制促炎细胞因子的分泌，从而对 T-2 毒素引起的脑损伤发挥预防和保护作用。
