Vitamin C Attenuates Hemorrhagic Shock-induced Dendritic Cell-specific Intercellular Adhesion Molecule 3-grabbing Nonintegrin Expression in Tubular Epithelial Cells and Renal Injury in Rats.
Vitamin C Attenuates Hemorrhagic Shock-induced Dendritic Cell-specific Intercellular Adhesion Molecule 3-grabbing Nonintegrin Expression in Tubular Epithelial Cells and Renal Injury in Rats.
复制标题
维生素 C 减轻失血性休克诱导的大鼠管状上皮细胞中树突状细胞特异性细胞间粘附分子 3 抓取非整合素表达和肾损伤
DOI：
10.4103/0366-6999.185868
复制
发表时间：
2016-07-20
影响因子：
6.1
通讯作者：
Mao EQ
中科院分区：
文献类型：
--
作者：
Ma L;Fei J;Chen Y;Zhao B;Yang ZT;Wang L;Sheng HQ;Chen EZ;Mao EQ
背景：肾小管上皮细胞中树突状细胞特异性细胞间粘附分子3-抓取非整合素（DC-SIGN）的表达被认为与多种肾脏疾病的发生高度相关，但失血性休克（HS）期间肾组织中是否发生这种情况尚不清楚。本研究旨在探讨这一现象以及维生素 C (VitC) 的抑制作用。方法：本研究建立Sprague-Dawley大鼠HS体内模型。观察肾脏中DC-SIGN的表达水平和位置。此外，组织学损伤的程度、肿瘤坏死因子-&agr的浓度也与组织学损伤的程度相关。评估肾组织中的白细胞介素-6和白细胞介素6，以及复苏后不同时间（2-24小时）血尿素氮和肌酐的血清浓度（每组6只大鼠），复苏前有或没有VitC治疗。结果：HS诱导大鼠肾小管上皮细胞表达DC-SIGN。促炎细胞因子浓度、组织学损伤评分和肾脏功能损伤均增加。复苏前给予VitC处理后，HS引起的所有这些现象均得到缓解。结论：本研究结果表明HS可诱导肾小管上皮细胞表达DC-SIGN，肾组织促炎细胞因子水平相应提高。结果还表明，VitC可以抑制HS诱导的肾小管上皮细胞中DC-SIGN的表达，减轻肾脏的炎症和功能损伤。
Background:The expression of dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin (DC-SIGN) in renal tubular epithelial cells has been thought to be highly correlated with the occurrence of several kidney diseases, but whether it takes place in renal tissues during hemorrhagic shock (HS) is unknown. The present study aimed to investigate this phenomenon and the inhibitory effect of Vitamin C (VitC). Methods:A Sprague–Dawley rat HS model was established in vivo in this study. The expression level and location of DC-SIGN were observed in kidneys. Also, the degree of histological damage, the concentrations of tumor necrosis factor-&agr; and interleukin-6 in the renal tissues, and the serum concentration of blood urea nitrogen and creatinine at different times (2–24 h) after HS (six rats in each group), with or without VitC treatment before resuscitation, were evaluated. Results:HS induced DC-SIGN expression in rat tubular epithelial cells. The proinflammatory cytokine concentration, histological damage scores, and functional injury of kidneys had increased. All these phenomena induced by HS were relieved when the rats were treated with VitC before resuscitation. Conclusions:The results of the present study illustrated that HS could induce tubular epithelial cells expressing DC-SIGN, and the levels of proinflammatory cytokines in the kidney tissues improved correspondingly. The results also indicated that VitC could suppress the DC-SIGN expression in the tubular epithelial cells induced by HS and alleviate the inflammation and functional injury in the kidney.