Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering and Technology, Indian Institute of Technology, Banaras Hindu University, Varanasi, 221 005, U.P., India.
Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering and Technology, Indian Institute of Technology, Banaras Hindu University, Varanasi, 221 005, U.P., India.
Eur J Pharmacol. 2021 Oct 5;908:174361. doi: 10.1016/j.ejphar.2021.174361. Epub 2021 Jul 21.
Current pharmacotherapy for post-traumatic stress disorder (PTSD) is limited to few antidepressants. Mitochondrial dysfunction is observed in PTSD, along with altered potassium homeostasis. Nutritional supplementation of taurine can improve ionic homeostasis and thereby treat PTSD-like symptoms in rats.
The purpose is to study the pharmacological effect of taurine in stress re-stress-induced PTSD in rats.
As per protocol, animals were restrained for 2 h then exposed to footshock (FS) (2 mA/10 s) followed by halothane-induced anesthesia. Behavioral assessments such as elevated plus maze (EPM) and Y-maze tests were performed on days 2, 8, and 32 of experimental protocol after re-stress. In addition, daily oral administration of taurine (100, 200, and 300 mg/kg) and paroxetine (PAX) (10 mg/kg) was done from D-8 to D-32 followed by re-stress. The plasma concentration of taurine, corticosterone, and potassium was measured on Day-32 along with mitochondrial function in discrete brain regions.
Sub-chronic administration of taurine in high and medium doses significantly ameliorated PTSD-like symptoms such as hyperarousal, anxiety, and improved spatial recognition memory. Taurine in all doses restored the plasma concentration of corticosterone and potassium. SRS-induced alterations in mitochondrial bioenergetics, complex enzyme activities, and reduced mitochondrial membrane potential in different brain regions were ameliorated by taurine.
Nutritional supplementation of taurine improves potassium ionic homeostasis, mitochondrial function, and attenuated PTSD-like symptoms in SRS subjected rats.
目前,创伤后应激障碍(PTSD)的药物治疗仅限于少数几种抗抑郁药。在 PTSD 中观察到线粒体功能障碍,以及钾离子稳态改变。牛磺酸的营养补充可以改善离子稳态,从而治疗大鼠的 PTSD 样症状。
研究牛磺酸对大鼠应激再应激诱导 PTSD 的药理学作用。
根据方案,动物被束缚 2 小时,然后暴露于足部电击(FS)(2 mA/10 s),然后进行氟烷诱导麻醉。在实验方案的第 2、8 和 32 天,在再应激后进行高架十字迷宫(EPM)和 Y 迷宫测试等行为评估。此外,从第 8 天到第 32 天,每天口服牛磺酸(100、200 和 300 mg/kg)和帕罗西汀(PAX)(10 mg/kg),然后进行再应激。在第 32 天,还测量了血浆牛磺酸、皮质酮和钾的浓度,以及离散脑区的线粒体功能。
牛磺酸亚慢性高剂量和中剂量给药显著改善了 PTSD 样症状,如过度觉醒、焦虑,并改善了空间识别记忆。牛磺酸在所有剂量下均恢复了血浆皮质酮和钾的浓度。SRS 诱导的不同脑区线粒体生物能量学、复合酶活性改变和线粒体膜电位降低均被牛磺酸改善。
牛磺酸的营养补充可改善钾离子稳态、线粒体功能,并减轻 SRS 引起的大鼠 PTSD 样症状。