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作 者:王亮[1] 周子娟[1] 詹红微[1] 雒东 陈大朋[1] 王靖宇[1]
机构地区:[1]大连医科大学实验动物中心,辽宁大连116044
出 处:《沈阳药科大学学报》2017年第6期509-512,518,共5页Journal of Shenyang Pharmaceutical University
基 金:国家自然科学基金资助项目(81600440)
摘 要:目的研究麦冬皂苷D(ophiopogonin D,OPD)对小肠上皮细胞损伤的保护作用及其作用机制。方法体外培养大鼠小肠上皮细胞IEC-6,用噻唑兰(methylthiazolyldiphenyl-tetrazolium bromide,MTT)法检测麦冬皂苷D对大鼠小肠上皮细胞IEC-6活性的影响;建立细菌脂多糖(lipopolysaccharides,LPS)损伤大鼠小肠上皮细胞IEC-6模型,检测麦冬皂苷D对上皮细胞的凋亡作用以及紧密连接屏障功能作用的影响。结果 LPS可显著降低IEC-6细胞的存活率;LPS显著促进炎症指标核转录因子NF-κB、凋亡相关蛋白caspase-9以及可导致紧密连接功能紊乱的肌球蛋白轻链激酶(myosin light chain kinase,MLCK)的表达;LPS抑制抗凋亡蛋白Bcl-2的表达。麦冬皂苷D可逆转LPS造成的功能紊乱,包括促进Bcl-2的表达,抑制caspase-3及MLCK的表达,一定程度上恢复黏膜屏障功能。结论麦冬皂苷D可缓解LPS造成的肠上皮细胞损伤,该作用与抗炎、抑制细胞凋亡及降低MLCK表达相关;麦冬皂苷D可能成为炎症性肠病临床治疗的一个潜在的候选药物。Objective To investigate the protective effect and mechanisms of ophiopogonin D on intestinal epithelial cell injury. Methods The rat intestinal epithelial IEC-6 cells were cultured and the MTT assay was used to determine the effects of the ophiopogonin D on IEC-6 cell activity. The IEC-6 cell injury model was established through incubation of cells with bacterial lipopolysaccharides ( LPS ). The effects of ophiopogonin D on apoptosis and tight junction barrier function were respectively studied. Results LPS significantly reduced IEC-6 cell viability; LPS significantly induced the high expression of NF-xB which is one of inflammatory markers, apoptosis-related protein caspase-9 and myosin light chain kinase (MLCK)which can lead to tight junction barrier dysfunciton; LPS also inhibited the expression of anti-apoptotic protein Bcl-2 expression, ophiopogonin D significangly reversed the effects induced by LPS, including upregulation of Bcl- 2, inhibition of caspase-3 and MLCK, finally lead to restoration of barrier function. Conclusions ophiopogonin D alleviates the epithelial cell injury induced by LPS through the anti-inflammatory, inhibition of cell apoptosis and downregulation of MLCK. ophiopogonin D might be a potential candidate drug for the clinical treatment of inflammatory bowel disease.
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