Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Neurochem Res. 2011 Dec;36(12):2216-26. doi: 10.1007/s11064-011-0545-8. Epub 2011 Jul 16.
Herein, we investigated the protective effect of Salvia sahendica against H(2)O(2)-induced cell death in rat pheochromocytoma (PC12) cells. Our data show that S. sahendica blocks apoptosis pathway by inhibition of cytochrome c release from mitochondria and leakage of calcium from endoplasmic reticulum. It also activates/inactivates two members of Bcl-2 family, Bax and Bcl-2. Bax inhibition and Bcl-2 activation suppress release of cytochrome c from mitochondria that prevents cleavage of caspase-3. Besides S. sahendica suppresses ER stress via attenuation of intracellular levels of calcium. Suppression of ER stress decreased calpain activation and subsequently cleavage of caspase-12. Altogether, these results indicate that S. sahendica protects PC12 cells treated with H(2)O(2) via suppression of upstream factors of apoptosis pathway. While oxidative stress is an early event in Alzheimer disease, it seems that S. sahendica prevents deleterious effects of reactive oxygen species by stabilizing mitochondrial membranes and inhibiting ER stress.
在这里，我们研究了藏丹参对 H(2)O(2)诱导的大鼠嗜铬细胞瘤 (PC12) 细胞死亡的保护作用。我们的数据表明，藏丹参通过抑制细胞色素 c 从线粒体释放和内质网钙泄漏来阻断细胞凋亡途径。它还激活/失活了 Bcl-2 家族的两个成员， Bax 和 Bcl-2。Bax 抑制和 Bcl-2 激活抑制了细胞色素 c 从线粒体的释放，防止了 caspase-3 的切割。此外，藏丹参通过降低细胞内钙水平来抑制内质网应激。内质网应激的抑制降低了钙蛋白酶的激活，随后 caspase-12 的切割。总之，这些结果表明，藏丹参通过抑制凋亡途径的上游因子来保护 H(2)O(2)处理的 PC12 细胞。虽然氧化应激是阿尔茨海默病的早期事件，但藏丹参似乎通过稳定线粒体膜和抑制内质网应激来防止活性氧的有害影响。
