Yang Ya-Chen, Wu Wen-Tzu, Mong Mei-Chin, Wang Zhi-Hong
Department of Food Nutrition and Health Biotechnology, Asia University, Taichung 413, Taiwan.
Department of Food Nutrition and Health Biotechnology, Asia University, Taichung 413, Taiwan - Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 404, Taiwan.
Biomedicine (Taipei). 2019 Jun;9(2):12. doi: 10.1051/bmdcn/2019090212. Epub 2019 May 24.
Protective effects of Gynura bicolor aqueous extract (GAE) at three concentrations upon nerve growth factor (NGF) differentiated-PC12 cells against HO induced injury were examined.
NGF differentiated-PC12 cells were treated with GAE at 0.25%, 0.5% or 1%. 100 μM HO was used to treat cells with GAE pre-treatments. After incubating at 37 °C for 12 hr, experimental analyses were processed.
HO exposure decreased cell viability, increased plasma membrane damage, suppressed Bcl-2 mRNA expression and enhanced Bax mRNA expression. GAE pre-treatments reversed these changes. HO exposure reduced mitochondrial membrane potential, lowered Na-K-ATPase activity, and increased DNA fragmentation and Ca release. GAE pre-treatments attenuated these alterations. HO stimulated the production of reactive oxygen species (ROS), interleukin (IL)-1beta, IL-6 and tumor necrosis factor-alpha, lowered glutathione content, and reduced glutathione peroxidase (GPX) and catalase activities. GAE pretreatments maintained GPX and catalase activities; and concentration-dependently diminished the generation of ROS and inflammatory cytokines. HO enhanced mRNA expression of nuclear factor kappa (NF-κ) B and p38. GAE pre-treatments decreased mRNA expression of NF-κB and p38.
These findings suggested that GAE might be a potent neuronal protective agent.
研究了三种浓度的红凤菜水提取物（GAE）对神经生长因子（NGF）分化的PC12细胞抗HO诱导损伤的保护作用。
用0.25%、0.5%或1%的GAE处理NGF分化的PC12细胞。用100μM HO处理经GAE预处理的细胞。在37℃孵育12小时后，进行实验分析。
HO暴露降低了细胞活力，增加了质膜损伤，抑制了Bcl-2 mRNA表达并增强了Bax mRNA表达。GAE预处理逆转了这些变化。HO暴露降低了线粒体膜电位，降低了钠钾ATP酶活性，并增加了DNA片段化和钙释放。GAE预处理减弱了这些改变。HO刺激了活性氧（ROS）、白细胞介素（IL）-1β、IL-6和肿瘤坏死因子-α的产生，降低了谷胱甘肽含量，并降低了谷胱甘肽过氧化物酶（GPX）和过氧化氢酶活性。GAE预处理维持了GPX和过氧化氢酶活性；并浓度依赖性地减少了ROS和炎性细胞因子的产生。HO增强了核因子κB（NF-κB）和p38的mRNA表达。GAE预处理降低了NF-κB和p38的mRNA表达。
这些发现表明GAE可能是一种有效的神经元保护剂。
