The present study explored the modulating apoptosis effect of hydrogen sulfide (H₂S) in subarachnoid hemorrhage (SAH) rats and its exact mechanism. A rat SAH model established by intravascular puncturing was used for the present study. After giving NaHS (donor of H₂S), an L-type calcium channel opener (Bay K8644), or a calcium channel agonist (nifedipine), the neurological function of the rats, associated pathological changes, and expression of apoptosis-related proteins (Bcl-2, Bax, and caspase-3) and microtubule-associated protein (MAP-2) were examined. The concentration of H₂S and expression of cystathionine beta synthase in the hippocampus changed upon early brain injury (EBI) after SAH. Compared with the SAH group, the neurological function of the rats and microstructure observed by electron microscopy were better in the SAH + NaHS group and SAH + Bay K8644 group. It was observed that apoptosis was more obvious in the SAH group than in the control group and was alleviated in the SAH + NaHS group. Furthermore, the alleviating effect of NaHS was partially weakened by nifedipine, indicating that the effect of anti-apoptosis in H₂S might be correlated with the calcium channel. The expression of Bax and caspase-3 was elevated, while the expression of Bcl-2 decreased in the SAH group but improved in the SAH + NaHS and SAH + Bay K8644 group. Compared with the SAH + NaHS group, the expression of pro-apoptotic proteins was higher in the SAH + NaHS + nifedipine group. Therefore, upon EBI following SAH, the H₂S system plays an important neurological protective effect by modulating the function of the L-type calcium channel and inhibiting apoptosis.

本研究探讨硫化氢（H ₂ S）对蛛网膜下腔出血（SAH）大鼠的凋亡作用及其确切机制。本研究采用血管内穿刺建立的大鼠SAH模型。给予 NaHS（H ₂ S 供体）、L 型钙通道开放剂（Bay K8644）或钙通道激动剂（硝苯地平）后，大鼠的神经功能、相关病理变化和凋亡相关蛋白的表达情况(Bcl-2、Bax 和 caspase-3) 和微管相关蛋白 (MAP-2) 进行了检查。_{H 2}的浓度SAH 后早期脑损伤 (EBI) 后海马中 S 和胱硫醚 β 合酶的表达发生变化。与SAH组相比，SAH+NaHS组和SAH+Bay K8644组大鼠的神经功能和电镜观察显微结构更好。观察到SAH组细胞凋亡比对照组更明显，SAH+NaHS组细胞凋亡减轻。此外，硝苯地平部分削弱了 NaHS 的缓解作用，表明 H _{2的抗细胞凋亡作用}S 可能与钙通道有关。SAH组Bax和caspase-3表达升高，而Bcl-2表达降低，而SAH+NaHS和SAH+Bay K8644组则有所改善。与SAH+NaHS组相比，SAH+NaHS+硝苯地平组促凋亡蛋白的表达更高。因此，SAH后EBI后，H ₂ S系统通过调节L型钙通道的功能，抑制细胞凋亡而发挥重要的神经保护作用。