首页|期刊导航|眼科新进展|黄精多糖对高糖诱导的晶状体上皮细胞内质网应激及凋亡的影响

黄精多糖对高糖诱导的晶状体上皮细胞内质网应激及凋亡的影响OA

Effect of Polygonatum sibiricum polysaccharide on endoplasmic reticulum stress and apoptosis of lens epithelial cells induced by high glucose

中文摘要英文摘要

目的 探究黄精多糖(PSP)对高糖诱导的晶状体上皮细胞(LECs)内质网应激(ERS)及凋亡的影响.方法 将SRA01/04细胞分为Control组、HG组和HG+PSP组.通过CCK-8法检测细胞活力以筛选PSP最佳干预浓度.建立大鼠晶状体体外培养模型,观察PSP对晶状体混浊的影响.采用Western blot检测磷酸化蛋白激酶样内质网激酶(p-PERK)、蛋白激酶样内质网激酶(PERK)、转录因子C/EBP同源蛋白(CHOP)、葡萄糖调节蛋白78(GRP78)等ERS相关蛋白及B细胞淋巴瘤/白血病-2(Bcl-2)和Bcl-2相关X蛋白(Bax)等凋亡蛋白的表达.采用免疫荧光染色法检测GRP78的表达与分布,TUNEL法检测细胞凋亡.结果 CCK-8法检测结果显示,与Control组相比,HG组细胞活力降低(P<0.001);与HG组相比,不同浓度PSP干预后细胞活力有不同程度的回升,其中PSP浓度为25.00 μmol·L-1时细胞活力升高最显著(P<0.01).晶状体体外培养结果显示,HG组晶状体混浊面积占比较Control组明显升高(P<0.001),而HG+PSP组较HG组显著降低(P<0.01).Western blot检测结果显示,与 Control 组相比,HG组p-PERK/PERK、GRP78及CHOP蛋白表达均升高,Bcl-2/Bax比值降低(均为P<0.05);与HG组相比,HG+PSP组上述ERS相关蛋白表达均显著降低,Bcl-2/Bax比值显著升高(均为P<0.05).免疫荧光染色结果显示,与Control组相比,HG组GRP78荧光强度显著增加(P<0.01);与HG组相比,HG+PSP组荧光强度显著降低(P<0.01).TUNEL检测结果表明,HG组细胞凋亡水平较Control组升高,加入PSP后凋亡降低(均为P<0.05).结论 PSP能够通过抑制高糖诱导LECs的ERS和细胞凋亡,从而延缓晶状体混浊的发生.

Objective To investigate the effects of Polygonatum sibiricum polysaccharide(PSP)on endoplasmic re-ticulum stress(ERS)and apoptosis of lens epithelial cells(LECs)induced by high glucose(HG).Methods SRA01/04 cells were divided into the Control group,HG group,and HG+PSP group.Cell viability was measured by the Cell Counting Kit-8(CCK-8)assay to determine the optimal concentration of PSP.An in vitro rat lens culture model was established to observe the effect of PSP on lens opacity.The expression levels of ERS-related proteins,including phosphorylated protein kinase-like endoplasmic reticulum kinase(p-PERK),protein kinase-like endoplasmic reticulum kinase(PERK),transcrip-tion factor C/EBP homologous protein(CHOP),and glucose-regulated protein 78(GRP78),as well as apoptosis-related proteins,including B-cell lymphoma/leukemia-2(Bcl-2)and Bcl-2-associated X protein(Bax)were detected by Western blot.The expression and distribution of GRP78 were measured by immunofluorescence staining,and cell apoptosis was quantified by TUNEL assay.Results CCK-8 assay showed that compared with the Control group,cell viability in the HG group significantly decreased(P<0.001).Compared with the HG group,cell viability increased to varying degrees after in-tervention with different concentrations of PSP,with the most significant increase observed at a PSP concentration of 25.00μmol·L-1(P<0.01).In the in vitro lens culture,the percentage of lens opacity in the HG group was significantly higher than that in the Control group(P<0.001),while it decreased significantly in the HG+PSP group compared with the HG group(P<0.01).Western blot results revealed that compared with the Control group,the expression levels of p-PERK/PERK,GRP78,and CHOP proteins were up-regulated,while the Bcl-2/Bax ratio was down-regulated in the HG group(all P<0.05).Compared with the HG group,the expression levels of the aforementioned ERS-related proteins significantly de-creased,while the Bcl-2/Bax ratio significantly increased in the HG+PSP group(all P<0.05).Immunofluorescence stai-ning showed that the fluorescence intensity of GRP78 in the HG group was significantly higher than that in the Control group(P<0.01),while it was significantly reduced in the HG+PSP group compared with the HG group(P<0.01).TUNEL assay demonstrated that the apoptosis level in the HG group increased compared with the Control group,which was effectively at-tenuated by PSP treatment(all P<0.05).Conclusion PSP can delay the progression of lens opacity by inhibiting HG-in-duced ERS and apoptosis in LECs.

王融;李鹏飞;管怀进;陈威;季敏

226000 江苏省南通市,南通大学||226000 江苏省南通市,南通大学附属医院眼科研究所226000 江苏省南通市,南通大学||226000 江苏省南通市,南通大学附属医院眼科研究所226000 江苏省南通市,南通大学||226000 江苏省南通市,南通大学附属医院眼科研究所226000 江苏省南通市,南通大学||226000 江苏省南通市,南通大学附属医院眼科研究所226000 江苏省南通市,南通大学||226000 江苏省南通市,南通大学附属医院眼科研究所

医药卫生

糖尿病性白内障黄精多糖晶状体上皮细胞内质网应激凋亡

diabetic cataractPolygonatum sibiricum polysaccharidelens epithelial cellsendoplasmic reticulum stressapoptosis

《眼科新进展》 2026 (5)

341-346,6

国家自然科学基金项目(编号:82571192,82571190)

10.13389/j.cnki.rao.2026.0061

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