CAJ | 학술논문

目的观察归芪多糖对过氧化氢(H2O2)诱导的 WI-38 早衰细胞端粒酶活性的影响,并探讨其作用机制.方法 H2O2诱导建立早衰WI-38细胞模型,MTT法检测不同浓度H2O2对WI-38细胞活力的影响,筛选出用于诱导细胞早衰的H2O2浓度.实验细胞分为正常组、模型组和归芪多糖组,化学染色法和ELISA检测归芪多糖对衰老细胞β-半乳糖苷酶和端粒酶活性的影响.结果 200μmol/L H2O2可诱导18代WI-38细胞出现早衰.归芪多糖干预后早衰细胞β-半乳糖苷酶和端粒酶活性均未呈现出衰老样变化,与模型组比较差异有统计学意义(P<0.01),与正常组比较差异无统计学意义(P>0.05).结论归芪多糖可明显增强衰老细胞的端粒酶活性并显著抑制衰老相关β-半乳糖苷酶活性.
목적 관찰귀기다당대과양화경(H2O2)유도적 WI-38 조쇠세포단립매활성적영향,병탐토기작용궤제.방법 H2O2유도건립조쇠WI-38세포모형,MTT법검측불동농도H2O2대WI-38세포활력적영향,사선출용우유도세포조쇠적H2O2농도.실험세포분위정상조、모형조화귀기다당조,화학염색법화ELISA검측귀기다당대쇠로세포β-반유당감매화단립매활성적영향.결과 200μmol/L H2O2가유도18대WI-38세포출현조쇠.귀기다당간예후조쇠세포β-반유당감매화단립매활성균미정현출쇠로양변화,여모형조비교차이유통계학의의(P<0.01),여정상조비교차이무통계학의의(P>0.05).결론 귀기다당가명현증강쇠로세포적단립매활성병현저억제쇠로상관β-반유당감매활성.
Objective To investigate the effects of Guiqi polysaccharide (GQP) on the telomerase activity in premature senescence of WI-38 cells;To discuss its mechanism of action.Methods MTT assay was used to observe the effects of different concentrations of H2O2 on the proliferation of WI-38 cells and screened the best concentration of H2O2 to induce premature senescence cellular model in WI-38 cells. ELISA and chemical staining method were used to evaluate the protection of GQP in telomerase activity and senescence-associated β-galactosidase activity in premature cellular senescence.Results 200μmol/L H2O2 treatment could induce premature senescence in WI-38 cells. There were no significant differences in senescence-associated β-galactosidase and telomerase activity between GQP group and normal control group (P>0.05), but had significant difference with model group (P<0.01).Conclusion GQP can increase the telomerase activity and inhibit the senescence-associated β-galactosidase activity in premature senescence of WI-38 cells.