CAJ | 학술논문

目的：探讨晚期蛋白氧化产物（AOPP）对人近端肾小管上皮细胞转分化（EMT）的影响及作用机制。方法实验共3部分：④分别用不同浓度AOPP及BSA刺激细胞24 h后检测α-SMA、E-Cadherin蛋白表达；④AOPP刺激细胞不同时间后检测α-SMA、E-Cadherin表达；④分别予BSA、AOPP以及用DPI、C-SOD预处理后再加入AOPP刺激细胞，检测α-SMA、E-Cadherin表达和不同时间的MDA含量及SOD、CAT、GSH-px活力。结果AOPP以浓度和时间依赖方式诱导HK-2细胞α-SMA表达上调、E-Cadherin表达下调。AOPP引起细胞MDA含量上升，SOD、CAT和GSH-px活力下降。DPI、C-SOD预处理细胞可以部分抑制AOPP诱导的α-SMA表达上调和E-Cadherin表达下调；降低MDA含量，提高SOD、CAT和GSH-px活力。结论 AOPP通过氧化应激诱导肾小管上皮细胞EMT，抑制NADPH氧化酶活性及抗氧化治疗可以抑制肾小管上皮细胞EMT，延缓肾间质纤维化的进展。
목적：탐토만기단백양화산물（AOPP）대인근단신소관상피세포전분화（EMT）적영향급작용궤제。방법실험공3부분：④분별용불동농도AOPP급BSA자격세포24 h후검측α-SMA、E-Cadherin단백표체；④AOPP자격세포불동시간후검측α-SMA、E-Cadherin표체；④분별여BSA、AOPP이급용DPI、C-SOD예처리후재가입AOPP자격세포，검측α-SMA、E-Cadherin표체화불동시간적MDA함량급SOD、CAT、GSH-px활력。결과AOPP이농도화시간의뢰방식유도HK-2세포α-SMA표체상조、E-Cadherin표체하조。AOPP인기세포MDA함량상승，SOD、CAT화GSH-px활력하강。DPI、C-SOD예처리세포가이부분억제AOPP유도적α-SMA표체상조화E-Cadherin표체하조；강저MDA함량，제고SOD、CAT화GSH-px활력。결론 AOPP통과양화응격유도신소관상피세포EMT，억제NADPH양화매활성급항양화치료가이억제신소관상피세포EMT，연완신간질섬유화적진전。
Objective To investigate the effects of advanced oxidation protein products (AOPP) on epithelial-to-mesenchymal transition (EMT) in cultured human proximal tubular epithelial cells (HK-2) and explore the mechanism. Methods HK-2 cells treated with 50, 100, 200, and 400μg/ml AOPP or 50μg/m bovine serum albumin (BSA) for 24 h, or with 200μg/ml AOPP for 0.5, 1, 3, 6, 12, and 24 h were examined for the protein expression of α-SMA and E-cadherin. In cells pretreated with diphenyleneiodonium (DPI) or cytoplasmic superoxide dismutase (C-SOD), the effects of 50μg/ml BSA and 200μg/ml AOPP were assessed on the expressions of α-SMA and E-cadherin, malondialdehyde (MDA) level, superoxide dismutase (SOD) activity, catalase (CAT) activity, and glutathione peroxidase (GSH-px) activity. Results AOPP treatment up-regulatedα-SMA expression and down-regulated E-cadherin expression in a dose- and time-dependent fashion. AOPP exposure of the cells resulted in increased MDA level and lowered activities of SOD, CAT and GSH-PX. DPI and C-SOD partially attenuated the effects of AOPP onα-SMA, E-cadherin, MDA, SOD, CAT and GSH-px. Conclusion AOPP can induce EMT in cultured HK-2 cells via oxidative stress, and this effect can be attenuated by inhibiting the activation of NADPH oxidase and using antioxidants to delay the progression of renal interstitial fibrosis.