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目的探讨虎杖苷对氧糖剥夺/再复氧(OGD/R)条件下肾小管上皮细胞的保护作用及其机制。方法给予HK-2人近端肾小管上皮细胞常氧或OGD/R培养、采用(10、20、40)μmol/L虎杖苷或磷脂酰肌醇3激酶(PI3K)通路抑制剂1μmol/L渥曼青霉素(Wortmannin)处理。MTT法评价HK-2细胞的存活能力,ELISA检测培养细胞上清液肿瘤坏死因子α(TNF-α)和白细胞介素1β(IL-1β)的水平,Western blot法检测总Akt、磷酸化的Akt和Shh的蛋白水平。结果虎杖苷能明显改善OGD/R条件下细胞的存活,并显著抑制OGD/R诱导的TNF-α和IL-1β的高分泌;抑制PI3K/Akt信号通路抵消了虎杖苷的抗炎和促存活作用,同时抑制虎杖苷对Shh蛋白表达的上调;外源给予Shh蛋白促进OGD/R细胞存活并显著降低细胞炎性反应。结论虎杖苷可能通过调控PI3K/Akt依赖的Shh信号对OGD/R下肾小管上皮细胞发挥保护作用。
Objective To investigate the protective effect of polydatin on renal tubular epithelial cells under oxygen glucose deprivation / reoxygenation (OGD / R) conditions and its mechanism. Methods HK-2 human proximal tubular epithelial cells were cultured in normoxia or OGD / R. The cells were treated with (10, 20, 40) μmol / L of polydatin or PI3K inhibitor 1 μmol / Wortmannin treatment. The viability of HK-2 cells was evaluated by MTT assay. The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in supernatant of cultured cells were detected by ELISA. Akt and Shh protein levels. Results Polydatin significantly improved cell viability under OGD / R condition and significantly inhibited OGD / R-induced high secretion of TNF-α and IL-1β. Inhibition of PI3K / Akt signaling pathway counteracted the anti-inflammatory and pro-survival effects of polydatin While inhibiting the up-regulation of Shh protein by polydatin. Exogenous administration of Shh protein promoted the survival of OGD / R cells and significantly reduced the inflammatory reaction. Conclusion Polydatin may protect renal tubular epithelial cells under OGD / R by regulating PI3K / Akt-dependent Shh signaling.