抑制或拮抗内源性bFGF活性对肠缺血-再灌注所致肠、肝、肾功能的影响

来源 :中国危重病急救医学 | 被引量 : 0次 | 上传用户:ZT0009
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目的 :观察抑制或拮抗内源性碱性成纤维细胞生长因子 (b FGF)对肠缺血再灌注所致肠、肝、肾功能的影响。方法 :96只大鼠分成 b FGF抗体预处理、丝氨酸苏氨酸蛋白激酶抑制剂 H7预处理以及生理盐水对照3组 ,肠系膜上动脉根部用微血管夹夹闭 45分钟之后放松血管夹形成再灌注。另 6只作为正常对照 (假手术组 )。分别于伤后即刻、2、6、2 4和 48小时将动物活杀 ,取血检测肝、肾功能以及二胺氧化酶 (DAO)变化 ;取肠、肝、肾组织进行形态学观察。结果 :与假手术组相比 ,3组动物血浆肝、肾以及肠道损伤指标均明显升高 ,其中伤后 2和 6小时 b FGF抗体组、H7组以及生理盐水对照组动物血浆丙氨酸转氨酶 (AL T)分别比对照组平均增加2 .5至 3.5倍 (P<0 .0 5或 P<0 .0 1) ;血浆 DAO变化及病理学结果均提示伤后 2和 6小时 3组动物肠屏障功能显著破坏。结论 :抑制或拮抗内源性 b FGF活性将进一步加重缺血再灌注所致肠、肝、肾损伤 ,其主要作用环节是影响了 b FGF与受体的结合以及随之发生的信号传导。 Objective: To observe the effect of inhibiting or antagonizing bFGF on intestine, liver and renal function induced by intestinal ischemia-reperfusion. Methods: Ninety-six rats were divided into three groups: b FGF antibody pretreatment, serine threonine protein kinase inhibitor H7 pretreatment and saline control group. The superior mesenteric artery was closed for 45 minutes with microvascular clamp and then the vascular clamp was reoperated. The other six were used as normal control (sham operation group). The animals were sacrificed at 2, 6, 2, 4 and 48 hours immediately after injury, respectively. The blood and liver were collected to detect the changes of liver and kidney function and diamine oxidase (DAO). The morphology of intestinal, liver and kidney was observed. Results: Compared with the sham-operation group, the indexes of liver, kidney and intestine injury were significantly increased in the three groups. The level of plasma alanine in bFGF antibody group, H7 group and saline control group at 2 and 6 hours after injury ALT increased by 2.5 to 3.5 folds (P <0.05 or P <0.01), respectively. The changes of plasma DAO and pathological results both indicated that the ALT levels were significantly lower in groups 3 and 6 Animal intestinal barrier function was significantly damaged. CONCLUSION: Inhibition or antagonism of endogenous b FGF activity will further aggravate the intestinal, liver and kidney injury induced by ischemia-reperfusion. The main effect of b FGF on receptor binding and the ensuing signal transduction.
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