右美托咪定预处理对小鼠肾缺血再灌注后肝肾组织炎性因子和氧化应激的影响
发布时间：2018-11-05 20:51
【摘要】：目的探讨右美托咪定预处理对小鼠缺血再灌注损伤后肝肾功能的影响。方法选取8周龄C57BL/6雄性小鼠24只,随机分为3组(n=8):正常对照组(Sham组)、缺血再灌注组(IR组)和右美托咪定处理组(IR+Dex组)。IR+Dex组小鼠于造模前25 min腹腔注射右美托咪定(50μg/kg),Sham组和IR组于造模前25min腹腔注射同等量的生理盐水,小鼠肾缺血再灌注模型建立成功后于再灌注24 h处死取材。分别取小鼠血清检测血肌酐(Scr)、尿素氮(BUN)、丙氨酸氨基转移酶(ALT)和天门氨酸氨基转移酶(AST)等肾功能及肝功能指标,取肾脏和肝脏组织匀浆液检测超氧化物歧化酶(SOD)、丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、单核细胞趋化因子-1(MCP-1)和白细胞介素-10(IL-10)等指标。结果与Sham组比较,IR组小鼠血清中Scr、BUN、ALT和AST等指标含量明显升高(P0.05);IR组小鼠肾脏、肝脏组织匀浆液中SOD明显降低(P0.05),MDA、TNF-α、IL-6、MCP-1和IL-10明显升高(P0.05);与IR组比较,IR+Dex组小鼠血清中Scr、BUN、ALT和AST等指标含量明显降低(P0.05);IR+Dex组小鼠肾脏、肝脏组织匀浆液中SOD和IL-10明显升高(P0.05),MDA、TNF-α、IL-6和MCP-1明显降低(P0.05)。结论右美托咪定能明显减轻小鼠肾缺血再灌注致肾、肝损伤的程度,其机制可能与提高小鼠缺血再灌注后肾、肝的抗氧化能力,抑制氧自由基堆积有关。
[Abstract]:Objective to investigate the effect of dexmetomidine preconditioning on liver and kidney function after ischemia reperfusion injury in mice. Methods Twenty-four 8-week-old C57BL/6 mice were randomly divided into 3 groups: normal control group (Sham group). The mice in the ischemic reperfusion group (IR group) and dexmetomidine group (IR Dex group) were intraperitoneally injected with dexmetomidine (50 渭 g/kg), Sham group and IR group) by intraperitoneal injection of dexmetomidine (50 渭 g/kg), Sham group and IR group) at 25 min before the establishment of the model, and the same amount of normal saline was injected intraperitoneally to the). IR Dex group before modeling. The kidney ischemia reperfusion model of mice was successfully established and killed 24 h after reperfusion. Serum levels of serum creatinine, (Scr), urea nitrogen, (BUN), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured for renal function and liver function. Superoxide dismutase (SOD), malondialdehyde (MDA),) tumor necrosis factor- 伪 (TNF- 伪) and interleukin-6 (IL-6) were detected in kidney and liver tissue homogenate. Monocyte chemokine-1 (MCP-1) and interleukin-10 (IL-10). Results compared with Sham group, the contents of Scr,BUN,ALT and AST in serum of IR group were significantly higher than those of Sham group (P0.05). In IR group, SOD in kidney and liver homogenate significantly decreased (P0.05), MDA,TNF- 伪, IL-6,MCP-1 and IL-10 increased significantly (P0.05). Compared with IR group, the contents of Scr,BUN,ALT and AST in serum of, IR Dex group were significantly lower than those of, IR Dex group (P0.05). In IR Dex group, SOD and IL-10 in kidney and liver tissue homogenate increased significantly (P0.05), MDA,TNF- 伪, IL-6 and MCP-1 decreased significantly (P0.05). Conclusion dexmetomidine can significantly reduce the degree of renal and liver injury induced by renal ischemia reperfusion in mice. The mechanism may be related to the increase of the antioxidant capacity of kidney and liver and the inhibition of oxygen free radical accumulation after ischemia reperfusion in mice.
【作者单位】： 河南大学淮河医院麻醉科;锦州医科大学研究生院;
【基金】：河南省医学科技攻关计划项目(编号:201404029) 开封市科技发展计划项目(编号:1603065)
【分类号】：R614
本文编号：2313420
[Abstract]:Objective to investigate the effect of dexmetomidine preconditioning on liver and kidney function after ischemia reperfusion injury in mice. Methods Twenty-four 8-week-old C57BL/6 mice were randomly divided into 3 groups: normal control group (Sham group). The mice in the ischemic reperfusion group (IR group) and dexmetomidine group (IR Dex group) were intraperitoneally injected with dexmetomidine (50 渭 g/kg), Sham group and IR group) by intraperitoneal injection of dexmetomidine (50 渭 g/kg), Sham group and IR group) at 25 min before the establishment of the model, and the same amount of normal saline was injected intraperitoneally to the). IR Dex group before modeling. The kidney ischemia reperfusion model of mice was successfully established and killed 24 h after reperfusion. Serum levels of serum creatinine, (Scr), urea nitrogen, (BUN), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured for renal function and liver function. Superoxide dismutase (SOD), malondialdehyde (MDA),) tumor necrosis factor- 伪 (TNF- 伪) and interleukin-6 (IL-6) were detected in kidney and liver tissue homogenate. Monocyte chemokine-1 (MCP-1) and interleukin-10 (IL-10). Results compared with Sham group, the contents of Scr,BUN,ALT and AST in serum of IR group were significantly higher than those of Sham group (P0.05). In IR group, SOD in kidney and liver homogenate significantly decreased (P0.05), MDA,TNF- 伪, IL-6,MCP-1 and IL-10 increased significantly (P0.05). Compared with IR group, the contents of Scr,BUN,ALT and AST in serum of, IR Dex group were significantly lower than those of, IR Dex group (P0.05). In IR Dex group, SOD and IL-10 in kidney and liver tissue homogenate increased significantly (P0.05), MDA,TNF- 伪, IL-6 and MCP-1 decreased significantly (P0.05). Conclusion dexmetomidine can significantly reduce the degree of renal and liver injury induced by renal ischemia reperfusion in mice. The mechanism may be related to the increase of the antioxidant capacity of kidney and liver and the inhibition of oxygen free radical accumulation after ischemia reperfusion in mice.
【作者单位】： 河南大学淮河医院麻醉科;锦州医科大学研究生院;
【基金】：河南省医学科技攻关计划项目(编号:201404029) 开封市科技发展计划项目(编号:1603065)
【分类号】：R614
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