A model of carbon tetrachloride-induced hepatic fibrosis in mice
Jian Xu
Abstract
Jian Xu
Abstract
AIM To establish a model of carbon tetrachloride\|induced hepatic fibrosis in mice. METHODS Chronic adminstration of 20% carbon tetrachloride (CCl 4) was carried out in Kun\|Ming mice for 3 months, and then the changes of hepatic pathology and index of hepatic biochemistry observed as an interval of 30 days between experiments respectively. RESULTS The score of hepatic fibrosis and the content of hepatic hydroxyproline were gradually increased ( P 0 05~0 01). The content of molondiadehyde in liver monogenates and the activity of serumal aminotransferase were signifcantly higher than that of control groups in three observed stages ( P 0 01) either, but the rate of albumin in serum was signifcantly reduced only at the end stage of hepatic fibrosis in mice induced by CCl 4 ( P 0 05) CONCLUSION Chronic administration of CCl 4 to mice can induce histologically observable liver fibrosis with characteristic stages of hepatic fibrosis.
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AIM To establish a model of carbon tetrachloride\|induced hepatic fibrosis in mice. METHODS Chronic adminstration of 20% carbon tetrachloride (CCl 4) was carried out in Kun\|Ming mice for 3 months, and then the changes of hepatic pathology and index of hepatic biochemistry observed as an interval of 30 days between experiments respectively. RESULTS The score of hepatic fibrosis and the content of hepatic hydroxyproline were gradually increased ( P 0 05~0 01). The content of molondiadehyde in liver monogenates and the activity of serumal aminotransferase were signifcantly higher than that of control groups in three observed stages ( P 0 01) either, but the rate of albumin in serum was signifcantly reduced only at the end stage of hepatic fibrosis in mice induced by CCl 4 ( P 0 05) CONCLUSION Chronic administration of CCl 4 to mice can induce histologically observable liver fibrosis with characteristic stages of hepatic fibrosis.
Key concepts: Carbon tetrachloride, Hydroxyproline, Hepatic fibrosis, CCL4, Internal medicine, Albumin, Fibrosis, Pathology