蛋白激酶Cβ抑制剂对肾缺血-再灌注损伤模型及其巨噬细胞亚型表达的影响  

Effect of protein kinase C β inhibitor on renal ischemia-reperfusion injury and expression level of macrophage subtypes in rat models

作　　者：樊雪梅 容松 Fan Xuemei;Rong Song(Department of Urology,Affiliated Hospital of Zunyi Medical University,Zunyi 563000,China)

机构地区：[1]遵义医科大学附属医院泌尿内科

出　　处：《器官移植》2019年第4期423-428,共6页Organ Transplantation

基　　金：国家自然科学基金(81260056)

摘　　要：目的探讨蛋白激酶C(PKC)β抑制剂对大鼠肾缺血-再灌注损伤(RIRI)模型的影响并检测巨噬细胞亚型的表达情况。方法健康SD雄性大鼠18只,按照随机数字表法分为假手术组(Sham组)、RIRI组、PKCβ抑制剂+RIRI组(Inhibitor+RIRI组),每组6只。术后24h取血清、左肾组织标本,用全自动生化仪检测血清肌酐(Scr)、血尿素氮(BUN)含量,苏木素-伊红(HE)染色观察肾组织内炎症细胞浸润和病理损伤情况,用免疫组织化学法和WesternBlot法检测各组大鼠肾组织CD68、诱生型一氧化氮合酶(iNOS)及CD206蛋白表达情况。结果RIRI组大鼠血清Scr、BUN含量明显高于Sham组(均为P<0.05),Inhibitor+RIRI组大鼠血清Scr、BUN含量明显低于RIRI组(均为P<0.05)。Sham组肾脏无明显损伤,RIRI组肾脏炎症细胞浸润及肾小管结构损伤明显,Inhibitor+RIRI组肾脏炎症细胞浸润及肾小管结构损伤轻于RIRI组。RIRI组大鼠肾组织中CD68、iNOS及CD206的蛋白表达量均明显高于Sham组(均为P<0.05);Inhibitor+RIRI组CD68、iNOS的蛋白表达量均明显低于RIRI组(均为P<0.05);Inhibitor+RIRI组CD206的蛋白表达量明显高于RIRI组(P<0.05)。结论PKCβ抑制剂可在一定程度上减轻大鼠RIRI,这可能与PKCβ抑制剂改善缺血肾组织中炎症细胞浸润、促进巨噬细胞向M2表达有关。Objective To investigate the effect of protein kinase C (PKC)β inhibitor on the renal ischemiareperfusion injury (RIRI) in rat models and detect the expression level of macrophage subtypes. Methods Eighteen healthy SD male rats were randomly divided into the Sham operation group (Sham group, n=6), RIRI group (n=6), PKCβ inhibitor +RIRI group (Inhibitor+RIRI group, n=6). Serum and left renal tissue samples were collected at postoperative 24 h. The contents of serum creatinine (Scr) and blood urea nitrogen (BUN) were detected by automatic biochemical analyzer. The infiltration of inflammatory cells and pathological injury in the renal tissues were observed by hematoxylin-eosin (HE) staining. The expression levels of CD68, inducible nitric oxide synthase (iNOS) and CD206 proteins in the renal tissues of rats in each group were assessed by immunohistochemistry and Western blot.Results The contents of serum Scr and BUN in the RIRI group were significantly higher than those in the Sham group (both P<0.05). The contents of serum Scr and BUN in the Inhibitor+RIRI group were considerably lower than those in the RIRI group (both P<0.05). No obvious renal injury was noted in the Sham group, whereas renal inflammatory cell infiltration and renal tubular structural damage were observed in the RIRI group. The renal inflammatory cell infiltration and renal tubular structural damage in the Inhibitor+RIRI group was slighter than that in the RIRI group. The protein expression levels of CD68, iNOS and CD206 in the renal tissue of rats in the RIRI group were significantly higher than those in the Sham group (all P<0.05). The protein expression levels of CD68 and iNOS in the Inhibitor+RIRI group were remarkably lower than those in the RIRI group (all P<0.05). The expression level of CD206 protein in the Inhibitor+RIRI group was significantly higher than that in the RIRI group (P<0.05). Conclusions PKC β inhibitor can alleviate the RIRI in rat models to certain extent, which may be correlated with the role of PKC β inhibitor in mi

关 键 词：PKCβ抑制剂 肾缺血-再灌注损伤 巨噬细胞 炎症细胞 经典活化的巨噬细胞(M1) 替代活化的巨噬细胞(M2) 诱生型一氧化氮合酶 

分 类 号：R617[医药卫生—外科学]