2012•Journal of Hepatopancreatobiliary SurgeryRequires access

Effect of INF-γ on hepatic fibrosis in rats of TGF-β1/Smad3 protein expression

Yi Zhang

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Abstract

Objective To observe the INF-γ on hepatic fibrosis and changes of TGF-β 1,Smad3 protein expression,and explore the mechanism of INF-γ in treating hepatic fibrosis.Methods Male SD rats were divided into three groups,model group and experimental group were injected with thioacetamide(thioacetamide,TAA) 100 mg/kg,2 days by intraperitoneal injection to induce rat hepatic fibrosis,The control grounp was injected with equal amount of physiological saline,while the experimental group treated with INF-γ intramuscularly.Model group and control group injected with equal physiological saline.All rats were sacrificed at 8 weeks,stained with Masson to observate hepatic fibrosis,detected TGF-β 1,Smad3 protein levels with immunohistochemistry in hepatic tissue.Results The degree of experimental group hepatic fibrosis,the expression of TGF-β1,Smad3 was higher than that in the normal group(P 0.05),significantly lower than that in the model group(P 0.05).Conclusion IFN-γ may inhibit TGF-β1/Smad3 protein expression,and thus play a role in hepatic fibrosis.

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Objective To observe the INF-γ on hepatic fibrosis and changes of TGF-β 1,Smad3 protein expression,and explore the mechanism of INF-γ in treating hepatic fibrosis.Methods Male SD rats were divided into three groups,model group and experimental group were injected with thioacetamide(thioacetamide,TAA) 100 mg/kg,2 days by intraperitoneal injection to induce rat hepatic fibrosis,The control grounp was injected with equal amount of physiological saline,while the experimental group treated with INF-γ intramuscularly.Model group and control group injected with equal physiological saline.All rats were sacrificed at 8 weeks,stained with Masson to observate hepatic fibrosis,detected TGF-β 1,Smad3 protein levels with immunohistochemistry in hepatic tissue.Results The degree of experimental group hepatic fibrosis,the expression of TGF-β1,Smad3 was higher than that in the normal group(P 0.05),significantly lower than that in the model group(P 0.05).Conclusion IFN-γ may inhibit TGF-β1/Smad3 protein expression,and thus play a role in hepatic fibrosis.

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Available abstract

Objective To observe the INF-γ on hepatic fibrosis and changes of TGF-β 1,Smad3 protein expression,and explore the mechanism of INF-γ in treating hepatic fibrosis.Methods Male SD rats were divided into three groups,model group and experimental group were injected with thioacetamide(thioacetamide,TAA) 100 mg/kg,2 days by intraperitoneal injection to induce rat hepatic fibrosis,The control grounp was injected with equal amount of physiological saline,while the experimental group treated with INF-γ intramuscularly.Model group and control group injected with equal physiological saline.All rats were sacrificed at 8 weeks,stained with Masson to observate hepatic fibrosis,detected TGF-β 1,Smad3 protein levels with immunohistochemistry in hepatic tissue.Results The degree of experimental group hepatic fibrosis,the expression of TGF-β1,Smad3 was higher than that in the normal group(P 0.05),significantly lower than that in the model group(P 0.05).Conclusion IFN-γ may inhibit TGF-β1/Smad3 protein expression,and thus play a role in hepatic fibrosis.

Key concepts: Thioacetamide, Hepatic fibrosis, Intraperitoneal injection, Immunohistochemistry, Saline, Internal medicine, Fibrosis, Transforming growth factor

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