CAJ | 학술논문

目的观察糖耐康对转化生长因子-β1(TGF-β1)诱导的人肾小管上皮细胞(HK-2)对细胞外基质成分表达的影响,探讨糖耐康治疗肾间质纤维化的作用机制。方法将HK-2细胞用含10%胎牛血清的DMEM/F12(1∶1)培养基培养,并分为6组：空白对照组、TGF-β1诱导组(TGF-β110 ng/mL)、空白血清对照组(TGF-β110 ng/mL＋10%空白血清)、干预1组(TGF-β110 ng/mL＋5%糖耐康药物血清)、干预2组(TGF-β110 ng/mL＋10%糖耐康药物血清)、干预3组(TGF-β110 ng/mL＋20%糖耐康药物血清)。药物干预24 h,荧光定量PCR检测Ⅰ型胶原(ColⅠ)、Ⅲ型胶原(ColⅢ)和纤连蛋白(FN)的mRNA表达。结果 HK-2细胞经TGF-β1诱导后,ColⅠ、ColⅢ和FN的mRNA表达显著上升,与空白对照组比较,差异有统计学意义(P＜0.05)。经糖耐康药物血清干预后,其表达逐步下降,与TGF-β1诱导组比较,差异有统计学意义(P＜0.05)。而空白血清无此作用。结论糖耐康在一定程度上能够抑制TGF-β1诱导的人肾小管上皮细胞ColⅠ、ColⅢ和FN的mRNA表达,减少细胞外基质成分的分泌,具有防治肾间质纤维化的作用。
목적관찰당내강대전화생장인자-β1(TGF-β1)유도적인신소관상피세포(HK-2)대세포외기질성분표체적영향,탐토당내강치료신간질섬유화적작용궤제。방법장HK-2세포용함10%태우혈청적DMEM/F12(1∶1)배양기배양,병분위6조：공백대조조、TGF-β1유도조(TGF-β110 ng/mL)、공백혈청대조조(TGF-β110 ng/mL＋10%공백혈청)、간예1조(TGF-β110 ng/mL＋5%당내강약물혈청)、간예2조(TGF-β110 ng/mL＋10%당내강약물혈청)、간예3조(TGF-β110 ng/mL＋20%당내강약물혈청)。약물간예24 h,형광정량PCR검측Ⅰ형효원(ColⅠ)、Ⅲ형효원(ColⅢ)화섬련단백(FN)적mRNA표체。결과 HK-2세포경TGF-β1유도후,ColⅠ、ColⅢ화FN적mRNA표체현저상승,여공백대조조비교,차이유통계학의의(P＜0.05)。경당내강약물혈청간예후,기표체축보하강,여TGF-β1유도조비교,차이유통계학의의(P＜0.05)。이공백혈청무차작용。결론당내강재일정정도상능구억제TGF-β1유도적인신소관상피세포ColⅠ、ColⅢ화FN적mRNA표체,감소세포외기질성분적분비,구유방치신간질섬유화적작용。
Objective To explore the effect of Tangnaikang (TNK) on extracellular matrix expression of human tubular epithelial cell HK-2 induced by TGF-β1 and explore its mechanism on the renal fibrosis. Methods The HK-2 cells were cultured by DMEM/F12 (1∶1) with 10%fetal bovine serum and divided into control group, TGF-β1 group (TGF-β110 ng/mL), rat serum control group (TGF-β110 ng/mL +10% rat serum), TNK-containing rat serum therapy groups (TGF-β110 ng/mL+5% Tangnaikang, or +10%Tangnaikang, or +20% TNK). After 24 h of administration, the expression of ColⅠ, Col Ⅲ and FN mRNA were tested by fluorescence quantitative PCR assay. Results The expression of ColⅠ, Col Ⅲ and FN mRNA of HK-2 cultured with TGF-β1 were much higher than the control, and significantly decreased in HK-2 cultured with TGF-β1 plus Tangnaikang compared with only TGF-β1 (P<0.05), but rat serum control had no effect. Conclusion TNK could inhibit the expression of ColⅠ, Col Ⅲ and FN mRNA of HK-2 cell induced by TGF-β1, and prevent the development of renal fibrosis to some extent.