Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, P.R. China.
Department of Thyroid and Breast Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei, P.R. China.
Aging (Albany NY). 2021 Feb 26;13(5):7180-7189. doi: 10.18632/aging.202575.
Several reports suggest that hydrogen sulfide (HS) exerts multiple biological and physiological effects on the pathogenesis of traumatic brain injury (TBI). However, the exact molecular mechanism involved in this effect is not yet fully known. In this study, we found that HS alleviated TBI-induced motor and spatial memory deficits, brain pathology, and brain edema. Moreover, sodium hydrosulfide (NaHS), an HS donor, treatment markedly increased the expression of Bcl-2, while inhibited the expression of Bax and Cleaved caspase-3 in TBI-challenged rats. Tunnel staining also demonstrated these results. Treatment with NaHS significantly reduced the glutamate and glutaminase 2 (GLS-2) protein levels, and glutamate-mediated oxidative stress in TBI-challenged rats. Furthermore, we demonstrated that HS treatment inhibited glutamate-mediated oxidative stress through the p53/GLS-2 pathway. Therefore, our results suggested that HS protects brain injury induced by TBI through modulation of the glutamate-mediated oxidative stress in the p53/GLS-2 pathway-dependent manner.
一些报告表明，硫化氢（HS）对创伤性脑损伤（TBI）的发病机制具有多种生物学和生理学作用。然而，这一效应的确切分子机制尚不完全清楚。在这项研究中，我们发现 HS 减轻了 TBI 引起的运动和空间记忆缺陷、脑病理学和脑水肿。此外，HS 的供体硫氢化钠（NaHS）治疗显著增加了 TBI 大鼠中 Bcl-2 的表达，同时抑制了 Bax 和Cleaved caspase-3 的表达。隧道染色也证明了这些结果。NaHS 治疗显著降低了 TBI 大鼠中谷氨酸和谷氨酰胺酶 2（GLS-2）蛋白水平以及谷氨酸介导的氧化应激。此外，我们证明 HS 通过 p53/GLS-2 途径抑制谷氨酸介导的氧化应激。因此，我们的研究结果表明，HS 通过调节 p53/GLS-2 途径依赖性的谷氨酸介导的氧化应激来保护 TBI 引起的脑损伤。
