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目的探讨抗炎细胞因子C1q/肿瘤坏死因子相关蛋白6(CTRP6)在庆大霉素所致急性肾损伤(AKI)中的作用。方法SD大鼠分为5组,对照组、模型组和3个实验组。模型组和实验组皮下注射庆大霉素400 mg/(kg·d),连续注射2 d,建立庆大霉素中毒性AKI动物模型;3个实验组大鼠在注射庆大霉素前2 d,分别给予(0.5、5、50)mg/kg的CTRP6腺病毒表达载体。苦味酸比色法检测肌酐(Cr)含量,紫外分光光度法检测血清尿素氮(BUN)含量,ELISA检测血清CTRP6的水平以及肾组织匀浆中白细胞介素1β(IL-1β)和肿瘤坏死因子α(TNF-α)的水平。Western blot法检测肾脏组织中CTRP6、NOD样受体家族含pyrin结构域蛋白3(NLRP3)和caspase-1的表达。结果与对照组相比,模型组大鼠AKI指标血清BUN和Cr水平较对照组显著增高,炎症因子IL-1β和TNF-α的分泌量以及NLRP3和caspase-1蛋白表达水平也显著增加。与模型组相比,实验组大鼠血清BUN和Cr水平降低,IL-1β和TNF-α的分泌减少,NLRP3和caspase-1的表达水平下降。随着注射CTRP6腺病毒表达载体注射剂量的增加,抑制效果逐渐增强。结论 CTRP6以剂量依赖的方式减弱庆大霉素所致的大鼠急性肾功能损伤。
Objective To investigate the role of anti-inflammatory cytokine Clq / tumor necrosis factor-related protein 6 (CTRP6) in gentamicin-induced acute kidney injury (AKI). Methods SD rats were divided into 5 groups, control group, model group and 3 experimental groups. Gentamicin toxic AKI animal model was established by injecting gentamicin 400 mg / (kg · d) subcutaneously in the model group and the experimental group for 2 days. The rats in the three experimental groups were injected gentamicin 2 d, were given (0.5,5,50) mg / kg of CTRP6 adenovirus expression vector. The content of creatinine (Cr) was measured by picric acid colorimetry, the level of serum urea nitrogen (BUN) was detected by ultraviolet spectrophotometry, the level of serum CTRP6 by ELISA and the levels of interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) levels. The expression of pykn domain protein 3 (NLRP3) and caspase-1 in CTRP6 and NOD-like receptor families in renal tissues were detected by Western blot. Results Compared with the control group, the level of serum BUN and Cr in the AKI index of the model group was significantly higher than that of the control group, and the secretion of IL-1β and TNF-α and the expression of NLRP3 and caspase-1 protein in the model group were significantly increased. Compared with the model group, serum BUN and Cr decreased, the secretion of IL-1β and TNF-α decreased and the expression of NLRP3 and caspase-1 decreased in the experimental group. With the injection of CTRP6 adenovirus expression vector injection dose increases, the inhibitory effect gradually increased. Conclusion CTRP6 attenuates gentamicin-induced acute renal injury in a dose-dependent manner.