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目的:观察绞股蓝皂苷(GP)对晚期糖基化终末产物(AGEs)诱导的人肾小球系膜细胞(HMCs)增殖及分泌细胞外基质(ECM)的影响。方法:将对数生长期的HMCs分为空白组、模型组、药物组、阳性组。空白组不给予任何诱导和干预,模型组、药物组、阳性组均采用200mg/L的AGEs诱导HMCs,药物组同时给予低、中、高剂量(25、75、150mg/L)的GP干预,阳性组同时给予0.1mmol/L的氨基胍盐酸盐(AG)干预,培养72h。采用MTT法观察各组中HMCs的增殖活性;Western blotting法检测核因子-κB(NF-κB)的表达;Real-Time PCR法检测转化生长因子-β1(TGF-β1)和血小板衍化生长因子-BB(PDGF-BB)m RNA的表达。结果:模型组中,AGEs能够诱导HMCs增殖、促进NF-κB活化及上调TGF-β1、PDGF-BB m RNA的表达,与空白组相比差异有统计学意义(P<0.01);药物组中,GP可以抑制AGEs诱导的HMCs增殖、NF-κB活化及下调TGF-β1、PDGF-BB m RNA的表达,与模型组相比差异有统计学意义(P<0.01)。结论:GP对AGEs培养条件下的HMCs具有一定的保护作用,GP可能通过抑制NF-κB活化及下调TGF-β1、PDGF-BB m RNA的表达,进而减少ECM的分泌和聚集,达到延缓糖尿病肾病进展的作用。
Objective: To observe the effects of gypenosides (GPs) on proliferation and secretion of extracellular matrix (ECM) induced by advanced glycation end products (AGEs) in human mesangial cells (HMCs). Methods: The logarithmic growth phase HMCs were divided into blank group, model group, drug group, positive group. The rats in the blank group were given no induction and intervention. The HMCs were induced by 200 mg / L AGEs in the model group, the drug group and the positive group. The low-, middle- and high-dose (25,75,150 mg / L) Positive group also given 0.1mmol / L of aminoguanidine hydrochloride (AG) intervention, culture 72h. The proliferation of HMCs in each group was observed by MTT assay. The expression of NF-κB was detected by Western blotting. The expressions of TGF-β1, BB (PDGF-BB) m RNA expression. Results: In the model group, AGEs could induce the proliferation of HMCs, promote the activation of NF-κB and up-regulate the expression of TGF-β1 and PDGF-BB m RNA, compared with the blank group (P <0.01) , GP inhibited the proliferation of AGEs-induced HMCs, the activation of NF-κB and the expression of TGF-β1, PDGF-BB m RNA. Compared with the model group, the difference was statistically significant (P <0.01). CONCLUSION: GP can protect HMCs under AGEs culture condition. GP may reduce the secretion and accumulation of ECM by inhibiting the activation of NF-κB and down-regulating the expression of TGF-β1 and PDGF-BB m RNA, thereby prolonging the progression of diabetic nephropathy The role of progress.