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硫化氢对蛛网膜下腔出血大鼠额顶叶脑区神经损伤的保护作用
Protective effect of hydrogen sulfide on brain damage in rats with subarachnoid hemorrhage
目的 探讨外源性硫化氢对蛛网膜下腔出血(SAH)大鼠早期脑损伤的保护作用及可能机制。 方法30只清洁级SD大鼠随机分成3组：对照组、SAH模型组、硫化氢作用组，每组各10只。后两组大鼠应用大脑中动脉穿刺法制作SAH模型，硫化氢组于模型制作成功后立即腹腔注射100mg/kg硫氢化钠。各组大鼠24h后进行神经功能评分，取额顶叶脑组织,用免疫荧光和Western blotting等方法检测额顶叶脑区神经细胞GFAP、S-100b、B淋巴细胞瘤-2基因（Bcl-2）、Caspase-3、c-Fos、基质金属蛋白酶-9(MMP-9)蛋白表达的变化。 结果 硫化氢组与SAH组相比神经功能评分有明显改善（P<0.01）。硫化氢组神经评分得3分以上的只有2只动物，而SAH组有8只。免疫荧光结果显示，SAH组GFAP、S-100b蛋白表达较对照组明显增高 (P＜0.05)；硫化氢作用后两者表达较SAH组明显下降 (P＜0.05)。SAH组Bcl-2、Caspase-3均有表达，硫化氢作用后Bcl-2表达明显增加，而Caspase-3则明显下降 (P＜0.05)。Western blotting结果进一步显示，SAH组c-Fos、MMP-9表达较对照组均明显增高(P＜0.05)；硫化氢作用后两者表达则明显下降 (P＜0.05)。结论 硫化氢对SAH后脑损伤有明显保护作用，其机制可能与改善胶质细胞的功能及与凋亡机制有关。
Objective To explore the effect of hydrogen sulfide (H2S) to the brain injury in rats with subarachnoid hemorrhage (SAH). Method Thirty experimental rats were randomly divided into Control group (n=10), SAH model group (n=10) and NaHS (100 mg/Kg)group (n=10),The experimental rats of the H2S group were injected NaHS 100 mg /Kg body weight in intraperitoneal and after surviving for 24 hours to do the neurological assessment and take the whole brain. The expression changes of GFAP, S-100b, Bcl-2, C-fos, caspase -3, MMP-9 were detected with fluorescent immunocytochemistry and Western blot method. Results Neurological assessment showed that severe neurological symptoms was significantly relieved in hydrogen sulfide group. GFAP and S-100b have a high expression in SAH rats group and were significantly decreased in H2S pretreatment group. The expression of Bcl-2 and caspase -3 in SAH group were high than in the control group but the expression of Bcl-2 was increased in H2S pretreatment group than SAH group, and caspase -3 was decreased in H2S pretreatment group. Western blot analysis showed that the expression of c-fos and MMP-9 were increased in SAH group and was significantly decreased in H2S pretreatment group. Conclusion The hydrogen sulfide have an significant protective effect on brain injury after SAH and its mechanism may be improved the function of glial cells and apoptotic pathways.
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