Yao Ke, Zhang Li, Ye Pan-Pan, Tang Xia-Jing, Zhang Yi-Dong
Eye Center, Affiliated Second Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Am J Chin Med. 2009;37(4):785-96. doi: 10.1142/S0192415X09007247.
Oxidative stress plays a significant role in the progression of cataract. We aimed to investigate the protective effect of magnolol, a compound extracted from the Chinese herb Magnolia officinalis, against oxidative stress in human lens epithelial (HLE) cells as well as the possible molecular mechanism involved. In this study, magnolol was observed to protect against H2O2-induced cytotoxicity in HLE B-3 cells. Magnolol inhibited the generation of reactive oxygen species (ROS), loss of mitochondrial membrane potential (Delta psi m) and release of cytochrome c from mitochondria caused by H2O2 into cytosol in HLE B-3 cells. Magnolol also inhibited H2O2-induced expressions of caspase-9 and caspase-3 and reduction of Bcl-2/Bax ratio. Moreover, magnolol attenuated the deactivation of ERK/MAPK (extracellular signal-regulated kinase/mitogen activated protein kinase) and the enhanced activation of p38, JNK (c-Jun N-terminal kinase) induced by H2O2. Magnolol could be useful in protecting against oxidative stress in HLE cells, suggesting a potential protective effect against cataractogenesis effect against cataractogenesis.
氧化应激在白内障的发展过程中起着重要作用。我们旨在研究从中药厚朴中提取的化合物厚朴酚对人晶状体上皮（HLE）细胞氧化应激的保护作用及其可能涉及的分子机制。在本研究中，观察到厚朴酚可保护HLE B - 3细胞免受H2O2诱导的细胞毒性。厚朴酚抑制了H2O2诱导的HLE B - 3细胞中活性氧（ROS）的产生、线粒体膜电位（Δψm）的丧失以及细胞色素c从线粒体释放到细胞质中。厚朴酚还抑制了H2O2诱导的caspase - 9和caspase - 3的表达以及Bcl - 2/Bax比值的降低。此外，厚朴酚减弱了H2O2诱导的ERK/MAPK（细胞外信号调节激酶/丝裂原活化蛋白激酶）失活以及p38、JNK（c - Jun氨基末端激酶）的激活增强。厚朴酚可能有助于保护HLE细胞免受氧化应激，提示其对白内障发生具有潜在的保护作用。
