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目的探讨丹参酮ⅡA对大鼠IRI肾脏TLR4/NF-κB信号通路以及下游炎症因子的影响,分析其对肾脏保护的可能机制。方法建立大鼠肾脏缺血再灌注(IRI)模型,将60只SD大鼠随机均分为空白组、对照组、丹参酮ⅡA组、ST2825组及Bay11-7082组,行对应处理,24 h后取肾脏标本,行HE法观察组织病理学形态,以PT-PCR法、Western Blotting法检测TLR4、NF-κB mRNA及蛋白水平,行酶联免疫吸附试验检测组织肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)水平。结果与空白组相比,对照组肾组织病理学明显改变,且TLR4、NF-κB mRNA及蛋白水平,组织TNF-α、IL-1β、IL-6水平均明显上升;丹参酮ⅡA、ST2825及Bay11-7082均可有效保护肾组织,表现为细胞肿胀、坏死和脱落程度较轻,同时炎症反应更轻,表现为TLR4、NF-κB mRNA及蛋白水平,组织TNF-α、IL-1β、IL-6水平降低,与对照组相比,上述指标差异均有统计学意义(P<0.05)。结论丹参酮ⅡA对缺血再灌注肾脏组织有保护作用,其机制与抑制TLR4/NF-κB信号通路、减少下游炎症因子有关。
Objective To investigate the effect of tanshinone ⅡA on TLR4 / NF-κB signaling pathway and downstream inflammatory cytokines in IRI rats and its possible mechanism of renal protection. Methods The rat model of renal ischemia reperfusion (IRI) was established. 60 SD rats were randomly divided into blank group, control group, tanshinone Ⅱ A group, ST2825 group and Bay11-7082 group. The histopathological changes of HE staining were observed. The mRNA and protein expressions of TLR4 and NF-κB were detected by PT-PCR and Western Blotting. Tumor necrosis factor-α (TNF-α) , Interleukin-1β (IL-1β) and interleukin-6 (IL-6) levels. Results Compared with the blank group, the pathological changes of the kidney in the control group were significantly changed. The levels of TLR4, NF-κB mRNA and protein, TNF-α, IL-1β and IL-6 in the control group were significantly increased. Tanshinone ⅡA, ST2825 and Bay11 -7082 can effectively protect the kidney tissue, manifested as cell swelling, necrosis and shedding light degree, at the same time inflammation is lighter, showing TLR4, NF-κB mRNA and protein levels, tissue TNF-α, IL-1β, IL- 6 levels decreased compared with the control group, the above indicators were statistically significant differences (P <0.05). Conclusion Tanshinone ⅡA protects the kidney from ischemia-reperfusion injury. Its mechanism is related to the inhibition of TLR4 / NF-κB signaling pathway and the reduction of downstream inflammatory cytokines.