Department of Pharmacology, KIET School of Pharmacy, Krishna Institute of Engineering and Technology, Ghaziabad, Uttar Pradesh, India.
Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Guwahati, Assam, India.
Neurochem Res. 2020 Apr;45(4):731-740. doi: 10.1007/s11064-019-02945-8. Epub 2020 Jan 2.
Taurine, an essential neutraceutical, has been reported to exhibit antioxidant and anti-inflammatory properties. Substantial evidence indicates that prolonged stress is one of the leading causes of psychological and physiological anomalies. Restraint stress (RS) rat model is the most widely used experimental model for the induction of chronic psycho-emotional stress. In the present study, Swiss albino male mice were restrained for 6 h/day for 28 consecutive days. Animals were divided into four groups: control, RS, RS + taurine, and taurine control group. Taurine, a potent antioxidant, was administered (200 mg/kg) orally along with RS for 28 days. The taurine intervention significantly restored the RS-induced neurobehavioral alterations evident by the elevated plus-maze, Morris water maze test, forced swim test, tail suspension test, and a sucrose preference test. Moreover, taurine significantly prevented hippocampal oxidative stress (lipid peroxidation, reduced glutathione, and nitrite) and other neurochemical (acetylcholinesterase, and IL-1β) anomalies. Using western blotting analyses, we demonstrate that taurine treatment significantly ameliorated the alterations in Brain-derived neurotrophic factor, caspase-3, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) level in the hippocampus. Thus, Taurine effectively inhibited RS-induced oxidative stress, neuroinflammation, and apoptosis via a mechanism involving the inhibition of the NF-κB signaling pathway. In summary, our study is the first to demonstrate that NF-κB and caspase-3 inhibition, as well as BDNF augmentation, was involved in neuroprotective potential of taurine against RS-induced behavioural anomalies.
牛磺酸是一种必需的营养保健品,已被报道具有抗氧化和抗炎特性。大量证据表明,长期压力是导致心理和生理异常的主要原因之一。束缚应激(RS)大鼠模型是诱导慢性心理情绪应激的最广泛使用的实验模型。在本研究中,将瑞士白化雄性小鼠束缚 6 小时/天,连续 28 天。动物分为四组:对照组、RS 组、RS+牛磺酸组和牛磺酸对照组。牛磺酸是一种有效的抗氧化剂,以 200mg/kg 的剂量经口给予 RS 28 天。牛磺酸干预显著恢复了 RS 诱导的神经行为改变,表现在高架十字迷宫、莫里斯水迷宫测试、强迫游泳测试、悬尾测试和蔗糖偏好测试中。此外,牛磺酸显著防止了海马氧化应激(脂质过氧化、还原型谷胱甘肽和亚硝酸盐)和其他神经化学物质(乙酰胆碱酯酶和 IL-1β)异常。通过 Western blot 分析,我们证明牛磺酸治疗显著改善了海马中脑源性神经营养因子、半胱天冬酶-3 和核因子κB 轻链增强子的激活 B 细胞(NF-κB)水平的改变。因此,牛磺酸通过抑制 NF-κB 信号通路,有效抑制 RS 诱导的氧化应激、神经炎症和细胞凋亡。总之,我们的研究首次表明,NF-κB 和半胱天冬酶-3 的抑制以及 BDNF 的增加,参与了牛磺酸对 RS 诱导的行为异常的神经保护潜力。