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本文采用乙酸及二硝基氯苯(DNCB)分别复制出二种豚鼠急性溃疡性结肠炎(UC)模型,其病理表现为肠粘膜溃疡、坏死,大量炎性细胞浸润并有出血及隐窝脓肿,类似于人类活动性UC.乙酸及DNCB导致UC的机理分别为化学直接损伤作用和迟发型超敏反应.测定豚鼠结肠粘膜过氧化物酶(POD)、5′—核苷酸酶(5′-NT)、碱性磷酸酶(ALP)、酸性磷酸酶(ACP)及乳酸脱氢酶(LDH)的活性,显示乙酸急性组POD中位数为28.65mIU/mg protein,DNCB急性组62.70mIU/mg protein,均高于正常对照组2.4mIU/mg protein,P<0.001.乙酸急性组5′—NT中位数为10.70mIU/mg protein,DNCB
In this paper, two kinds of guinea pig ulcerative colitis (UC) models were duplicated respectively by acetic acid and dinitrochlorobenzene (DNCB). The pathological manifestations were intestinal mucosal ulcer, necrosis, a large number of inflammatory cell infiltration and hemorrhage and crypt abscess , Similar to human activity of UC.Chloric acid and DNCB lead to the mechanism of UC were direct chemical damage and delayed hypersensitivity.Detection of guinea pig colonic mucosal peroxidase (POD), 5’-nucleotidase (5 ’ -NT), alkaline phosphatase (ALP), acid phosphatase (ACP) and lactate dehydrogenase (LDH) activity in acute acetic acid group showed that POD median was 28.65mIU / mg protein, DNCB acute group 62.70mIU / mg protein were higher than the normal control group 2.4mIU / mg protein, P <0.001. Acetate acute group 5’-NT median 10.70mIU / mg protein, DNCB