为探讨姜黄素对内毒素休克兔肾损伤模型磷脂酰肌醇-3-羟激酶（phosphatidylinositol-3-hydroxykinase，PI3K）/核转录因子E2相关因子2（nuclear transcription factor E2 related factor 2，Nrf2）信号通路的影响，采用耳缘静脉注射LPS（5 mg/kg）建立内毒素休克肾损伤模型。将造模兔随机分为模型组、姜黄素组（50 mg/kg）、渥曼青霉素组（0.6 mg/kg）和姜黄素+渥曼青霉素组各10只，另设对照组10只。苏木精-伊红（hematoxylin-eosin，HE）染色检测肾组织损伤情况；ELISA测定肾组织中超氧化物歧化酶（superoxide dismutase，SOD）和丙二醛（malondialdehyde，MDA）的水平；血生化和ELISA检测血肌酐（serum creatinine，Scr）、尿素氮（urea nitrogen，BUN）、TNF-α和IL-6水平，实时PCR和Western blotting检测磷酸化蛋白激酶B（phosphorylated protein kinase B，p-Akt）、Nrf2、血红素加氧酶1（hemeoxygenase 1，HO-1）、醌氧化还原酶1（quinone oxidoreductase 1，NQO-1）、Caspase-3的表达。结果显示，与对照组比较，模型组兔SOD活性显著下降（P＜0.05），肾组织评分、Scr、BUN、MDA、TNF-α和IL-6水平明显升高（P＜0.05），p-Akt、Nrf2、HO-1、NQO-1、Caspase-3的表达明显上调（P＜0.05）；与模型组比较，姜黄素组兔SOD活性显著升高（P＜0.05），肾组织评分、Scr、BUN、MDA、TNF-α和IL-6水平明显下降（P＜0.05），p-Akt、Nrf2、HO-1、NQO-1的表达明显上调（P ＜ 0.05），Caspase-3的表达明显下调（P＜0.05）；与渥曼青霉素组比较，姜黄素+渥曼青霉素组SOD活性显著升高（P＜0.05），肾组织评分、Scr、BUN、MDA、TNF-α和IL-6水平明显下降（P＜0.05），p-Akt、Nrf2、HO-1、NQO-1的表达明显上调（P＜0.05），Caspase-3的表达明显下调（P＜0.05），HE染色显示肾组织病理变化明显减少。提示姜黄素干预可能通过激活PI3K/Nrf2通路，清除机体过多的氧自由基和炎症反应，减轻肾组织损伤。

To analyze the effects of curcumin on phosphatidylinositol-3-hydroxykinase(PI3K)/nuclear transcription factor E2 related factor 2(Nrf2) signaling pathway in kidney injury model of endotoxin shock rabbit, the model of endotoxin shock kidney injury was established by LPS injection via ear margin vein.The model rabbits were randomly divided into the model group, the curcumin group (50 mg/kg), the wortmanin group (0.6 mg/kg) and the curcumin + wortmanin group, with 10 animals in each group.Another 10 animals were set as the control group. Renal tissue damage was detected by hematoxylin-eosin (HE) staining.The levels of superoxide dismutase(SOD) and malondialdehyde (MDA) in renal tissues were determined by ELISA. The levels of serum creatinine(Scr), urea nitrogen(BUN), TNF-α and IL-6 were detected by blood biochemistry and ELISA. RT-PCR and Western blotting were performed to detect expression of phosphorylated protein kinase B (p-Akt), Nrf2, hemeoxygenase 1 (HO-1), quinone oxidoreductase 1 (NQO-1) and Caspase-3. The results showed that,compared with the control group, SOD activity in the model group was significantly decreased (P<0.05), while renal tissue score and expression levels of Scr, BUN, MDA, TNF-α and IL-6 were significantly increased (P<0.05), as well as the expressions of p-Akt, Nrf2, HO-1, NQO-1 and Caspase-3(P<0.05). Compared with the model group, SOD activity in the curcumin group was significantly increased (P<0.05), while renal tissue score, levels of Scr, BUN, MDA, TNF-α and IL-6 were significantly decreased (P<0.05), expressions of p-Akt, Nrf2, HO-1 and NQO-1 were significantly up-regulated (P<0.05), while the expression of Caspase-3 was significantly down-regulated (P<0.05).Compared with the wortmanin group, SOD activity was significantly increased in the curcumin + wortmanin group (P<0.05), while renal tissue score, levels of Scr, BUN, MDA, TNF-α and IL-6 were significantly decreased (P<0.05), expression of p-Akt, Nrf2, HO-1 and NQO-1 was significantly up-regulated (P<0.05), and expression of Caspase-3 was significantly down-regulated (P<0.05). HE staining showed that pathological changes of renal tissues were significantly alleviated. In conclusion, curcumin intervention may protect kidney from tissue damage by activating PI3K/Nrf2 pathway, eliminating excessive oxygen free radicals and inflammatory responses in the body.