[Effects of transforming growth factor beta 3 on the histopathology and expression of collagen I in experimental hepatic fibrotic rats].
Ping Liu, Xiaoliang Gao, Jiao Yu, Weijun Qian, Keshu Xu
Abstract
Ping Liu, Xiaoliang Gao, Jiao Yu, Weijun Qian, Keshu Xu
Abstract
OBJECTIVE: To investgate the effects of TGFbeta3 on rat hepatic fibrosis. METHODS: The TGFbeta3 cDNA was cloned into rAAV2 vector. Rats were randomly divided into four groups: normal control group, model group, negative control group and TGFbeta3 group. Hepatic fibrosis was induced by hypodermic injection of 40% CCl(4). Recombinant AAV2-TGFbeta3 viral particles were injected via the vena caudalis one week before CCl(4) treatment. Rats were executed 8 weeks after CCl(4) treatment, global histological change was observed after HE staining, the distribution of the collagen fibers was observed after masson staining, histochemistry was done to observe the expression of collagen I; The positive area rate of the collagen fibers and the average optical rate of collagen I were quantified. RESULTS: HE staining indicated that collagen fibers were reduced in the TGFbeta3 group. Masson staining shown that the collagen fibers were distributed around the blood vessel, in the portal area and disse space. Compared to the model group (13.2%+/-2.2%) and negative control group (12.3%+/-1.5%), the collagen fibers in liver tissues of TGFbeta3 group (7.7%+/-1.5%) were significantly decreased (q = 9.456, P < 0.01; q = 8.217, P < 0.01). Histochemistry indicated that the collagen fibers of liver tissues of TGFbeta3 group (0.185+/-0.033) were significantly higher than those in the model group (0.252+/-0.042) and the negative control group (0.230+/-0.029), (q = 6.228, P < 0.01; q = 4.346, P < 0.01). CONCLUSION: TGFbeta3 alleviates the damage to hepatic cell and the level of fibrosis in CCl(4) treated rats and inhibits the expression of collagen I.
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OBJECTIVE: To investgate the effects of TGFbeta3 on rat hepatic fibrosis. METHODS: The TGFbeta3 cDNA was cloned into rAAV2 vector. Rats were randomly divided into four groups: normal control group, model group, negative control group and TGFbeta3 group. Hepatic fibrosis was induced by hypodermic injection of 40% CCl(4). Recombinant AAV2-TGFbeta3 viral particles were injected via the vena caudalis one week before CCl(4) treatment. Rats were executed 8 weeks after CCl(4) treatment, global histological change was observed after HE staining, the distribution of the collagen fibers was observed after masson staining, histochemistry was done to observe the expression of collagen I; The positive area rate of the collagen fibers and the average optical rate of collagen I were quantified. RESULTS: HE staining indicated that collagen fibers were reduced in the TGFbeta3 group. Masson staining shown that the collagen fibers were distributed around the blood vessel, in the portal area and disse space. Compared to the model group (13.2%+/-2.2%) and negative control group (12.3%+/-1.5%), the collagen fibers in liver tissues of TGFbeta3 group (7.7%+/-1.5%) were significantly decreased (q = 9.456, P < 0.01; q = 8.217, P < 0.01). Histochemistry indicated that the collagen fibers of liver tissues of TGFbeta3 group (0.185+/-0.033) were significantly higher than those in the model group (0.252+/-0.042) and the negative control group (0.230+/-0.029), (q = 6.228, P < 0.01; q = 4.346, P < 0.01). CONCLUSION: TGFbeta3 alleviates the damage to hepatic cell and the level of fibrosis in CCl(4) treated rats and inhibits the expression of collagen I.
Key concepts: Staining, Histopathology, Collagen fiber, Fibrosis, Transforming growth factor, H&E stain, Immunohistochemistry, Chemistry