Key Laboratory of Bioactive Materials, Ministry of Education and College of Life Science, Nankai University, Tianjin 300071, People's Republic of China.
Neurochem Res. 2011 Oct;36(10):1840-9. doi: 10.1007/s11064-011-0502-6. Epub 2011 May 21.
Many studies have demonstrated the cytoprotective effects of hydrogen sulfide (H(2)S) in vitro and/or in vivo ischemic injury. The aim of the current study was to investigate whether exogenous H(2)S attenuates the neuronal injury induced by brain ischemia. As an H(2)S donor, sodium hydrosulfide (NaHS) was administered intraperitoneally (5.6 mg/kg/day, i.p.). The effects of exogenous H(2)S on neurons of ischemic hippocampus were examined by using measurement of behavior, electrophysiology, morphology and immunohistochemical staining, respectively. Our results showed that exogenous H(2)S significantly improved spatial learning and memory deficits induced by brain ischemia (P < 0.01). Exogenous H(2)S enhanced synaptic plasticity in the hippocampus of brain-ischemic rats, inhibited the edema around pyramidal neurons and the nuclear shrink induced by ischemia, and promoted the expression of growth-associated protein-43 (GAP-43) in the CA1 region of hippocampus post ischemia. The results suggest a protective effect and therapeutic potential of H(2)S in the treatment of brain ischemia.
许多研究已经证明了硫化氢(H₂S)在体外和/或体内缺血损伤中的细胞保护作用。本研究的目的是探讨外源性 H₂S 是否能减轻脑缺血引起的神经元损伤。作为 H₂S 的供体,硫氢化钠(NaHS)通过腹腔内给药(5.6mg/kg/天,ip)。通过测量行为、电生理学、形态学和免疫组织化学染色,分别研究了外源性 H₂S 对缺血性海马神经元的影响。我们的结果表明,外源性 H₂S 显著改善了脑缺血引起的空间学习和记忆缺陷(P<0.01)。外源性 H₂S 增强了脑缺血大鼠海马的突触可塑性,抑制了缺血诱导的锥体神经元周围水肿和核收缩,并促进了缺血后海马 CA1 区生长相关蛋白-43(GAP-43)的表达。结果表明 H₂S 在治疗脑缺血方面具有保护作用和治疗潜力。