目的:观察顺铂诱导急性肾损伤(acute kidney injury,AKI)模型中肾皮质Persephin(PSP)的变化。方法:雄性C57BL/6小鼠随机分为对照组及模型组,模型组应用顺铂单次腹腔注射(15mg/kg)制备AKI小鼠模型,对照组小鼠予以同等容积的0.9%的生理盐水单次腹腔注射,造模3天后观察各组小鼠肾功能变化、肾脏病理学改变、实时PCR法及Western印记法检测肾脏皮质PSP的表达。结果 :与对照组相比,模型组小鼠出现精神萎靡不振,反应迟钝,活动减少,造模后第3天尿素氮明显上升(P〈0.05),肾脏病理改变中模型组肾小管管型计数(0.63±0.62个/HPF)及坏死计数(3.71±1.14个/HPF)均高于正常对照组(P〈0.05)。PSP在模型组肾皮质的表达高于对照组(P〈0.05)。结论:AKI模型中肾脏皮质PSP表达升高,提示PSP可能参与了AKI的病程,但其相关作用机制尚需进一步研究。
Objective: To observe the change of Persephin(PSP) in renal cortex in cisplatin-induced acute kidney injury. Methods: The male C57BL/6 mice were divided into the control group and the model group. AKI was induced by subcutaneous injection of cisplatin(15mg/kg), the mice in the control group was injected by the same volume saline.Three days after cisplatin injection, the renal function and tubular structure were tested in each group.Expression of PSP was tested by real-time PCR and Western blot in renal cortex. Results: Compared with the control group, mice in the model group showed symptoms of malaise and reduced activity. Three days after cisplatin injection, the renal function, the number of tubular cast(0.63±0.62/HPF) and necrosis(3.71±1.14/HPF)were significantly increased in the model group(P0.05).The m RNA and protein expression of PSP in the renal cortex increased in the model group(P〈0.05). Conclusion: The increasing expression of PSP in the renal cortex suggests that PSP may participate in the process of AKI.