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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 study the protective effect of ophiopogonin D (OPD) on intestinal epithelial cell injury and its mechanism. Methods The IEC-6 of rat intestinal epithelial cells was cultured in vitro. The effect of Radix Ophiopogonis D on the activity of IEC-6 in rat intestinal epithelial cells was detected by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay. The effects of lipopolysaccharide (LPS) ) Injury of rat intestinal epithelial cells IEC-6 model to detect the apoptosis effect of Ophiopogon japonicus D on epithelial cells and the role of tight junction barrier function. Results LPS significantly decreased the survival rate of IEC-6 cells. LPS significantly promoted the expression of nuclear transcription factor NF-κB, apoptosis-related protein caspase-9 and myosin light chain kinase kinase, MLCK) expression; LPS inhibits the expression of anti-apoptotic protein Bcl-2. Ophiopogon japonicus D could reverse the dysfunction caused by LPS, including promoting the expression of Bcl-2, inhibiting the expression of caspase-3 and MLCK and restoring the mucosal barrier function to a certain extent. Conclusion Ophiopogon japonicus saponin D can relieve the injury of intestinal epithelial cells induced by LPS, which is related to anti-inflammatory, inhibiting apoptosis and decreasing the expression of MLCK. Ophiopogon japonicus D may be a potential candidate for clinical treatment of inflammatory bowel disease.