Xiao Xianghua, Liu Juntian, Hu Jingwen, Zhu Xiuping, Yang Hua, Wang Chaoyun, Zhang Yuanhui
Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi 710061, People's Republic of China.
Eur J Pharmacol. 2008 Sep 4;591(1-3):21-7. doi: 10.1016/j.ejphar.2008.06.045. Epub 2008 Jun 15.
Calcium and lipid peroxidation play important roles in oxidative stress-induced cellular injury and apoptosis, which ultimately cause cell death. In this study we examined whether protopine had a neuroprotection against H(2)O(2)-induced injury in PC12 cells. Pretreatment of PC12 cells with protopine improved the cell viability, enhanced activities of superoxide dismutase, glutathione peroxidase and catalase, and decreased malondialdehyde level in the H(2)O(2) injured cells. Protopine also reversed the increased intracellular Ca(2+) concentration and the reduced mitochondrial membrane potential caused by H(2)O(2) in the cells. Furthermore, protopine was able to inhibit caspase-3 expression and cell apoptosis induced by H(2)O(2). In summary, this study demonstrates that protopine is able to relieve H(2)O(2)-induced oxidative stress and apoptosis in PC12 cells, at least in part, by Ca(2+) antagonism and antioxidant mechanisms.
钙和脂质过氧化在氧化应激诱导的细胞损伤和凋亡中起重要作用，最终导致细胞死亡。在本研究中，我们检测了普罗托品是否对H₂O₂诱导的PC12细胞损伤具有神经保护作用。用普罗托品预处理PC12细胞可提高细胞活力，增强超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶的活性，并降低H₂O₂损伤细胞中的丙二醛水平。普罗托品还可逆转H₂O₂引起的细胞内Ca²⁺浓度升高和线粒体膜电位降低。此外，普罗托品能够抑制H₂O₂诱导的caspase-3表达和细胞凋亡。总之，本研究表明，普罗托品至少部分地通过Ca²⁺拮抗和抗氧化机制减轻H₂O₂诱导的PC12细胞氧化应激和凋亡。
