泰山照山白提取物对过氧化损伤的PC12细胞的保护作用

Rhododendrom micranthum Turcz. inhibits injury in H_2O_2 damaged nerve cell lines PC12

目的研究泰山照山白提取物(RME)对氧化损伤的神经细胞株(PC12)炎症反应的影响及与凋亡的关系,探讨药物抗炎以及抗凋亡效应的可能机制。方法体外培养PC12,RME三个浓度预处理,加入H2O2诱导氧化损伤,MTT比色法检测细胞存活率,ELISA测定培养液中白介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)含量、免疫荧光显微镜检测细胞凋亡率及凋亡的细胞形态变化。结果与正常对照组相比,经H2O2损伤后,细胞存活率降低(P<0.05、P<0.01)、而IL-1β和TNF-α的释放量增加(P<0.05、P<0.01)、凋亡细胞数目增多并呈现典型的凋亡形态学改变。而RME各剂量组预处理能提高细胞存活率(P<0.05、P<0.01)、降低细胞上清液IL-1β和TNF-α含量(P<0.05、P<0.01)、降低细胞凋亡率、改善细胞的凋亡形态。结论 RME可抑制H2O2诱导的神经细胞株氧化应激性炎性损伤和凋亡,提高细胞存活率,其作用机制可能是通过抑制凋亡转导途径而实现的。

Objective： To investigate the effect of extract of Rhododendrom micranthum Tumz. （RME）against inflammation reaction of oxidative damage in nerve cell lines PC12 induced by hydrogen peroxide （H202 ） and the possible mechanism. Aim Cultured in vitro, PC12 cells was pretreatment with three concentration of R.ME before injured induced by H2O2, MTr assay was used to detect cell viability, ELISA to detect content of IL - 16 and TNF - a in culture solution, immunofluorescence microscopy was used to determine the expression of caspase - 3. Results Compared with injured group, RME of three concentrations all separately increased the cell viability and reduced the contents of IL - 1β and TNF - a and the apoptotic pementage of PC12 cells. （P 〈0.05 and P 〈0.01 respectively） ,The typical apeptosis morphology was changed. Conclusion RME inhibit the H2O2 - induced apoptosis in nerve cell lines PC12. The mechanism may via Inhibition of apeptosis transduction pathways