The Protective Effect And Mechanism Of Curcumin Subtype B14to HK11Cell Injured By Angiotensint Ⅱ

Objective: To observe the protective role of Curcumin（Cur）subtypeB14in the renal cortical proximal tubule epithelial cells (Human Kidney11,HK11) injury induced by angiotensin II and to explore its mechanism.Methods: The cell viability was detected with cell counting and CCK-8assay to observe toxic effects of curcumin and its subtypes B13or B14onHK11cells. Then, Cleaved caspase-3expression at different time anddifferent concentration of angiotensin II was detected by ELISA method inorder to determine concentration and incubation time which angiotensin IItreated HK11cells for the establishment of diabetic nephropathy cell model.Finally,the protect role and mechanism of curcumin subtype B14in theHK11cell were researched with the cell model. The cells were divided intoten groups:CON group、 AngII group、 B13group、 Cur group、 B14group、 CON+PI3K inhibitor group、 AngII+PI3K inhibitor group、B13+PI3K inhibitor group、 Cur+PI3K inhibitor group、 B14+PI3Kinhibitor group. Cleaved caspase-3expressions were detected by ELISAmethod. The experiment was repeated three times.Results： The results of cell counting and CCK-8assay showed that curcumin and its subtypes B13or B14had no toxic effects on the HK11cells (P>0.05). The expression of Cleaved caspase-3was increased onHK11cells treated with250nM AngII for48h, compared with the CONgroup(p<0.05). The results of ELISA and Western-blot test showed that theexpression of Cleaved caspase-3was declined in Cur group and B14Group,compared with the Ang II group(p<0.05）, especially in B14group(P<0.01). When treating these cells with PI3K inhibitor, the expression ofCleaved caspase-3increased in Cur group and B14group, compared withthe Cur and B14group without PI3K inhibitor (P<0.05).Conclusion：Curcumin subtype B14can inhibit HK11injury induced byangiotensin II and this process may be associated with PI3K signalingpathway.