AIM:To investigate the effect of interferon-a (IFN-α) on preventing or reversing hepatic fibrosis in rat experimental model induced by CCI4. METHODS: One hundred and ten Sprague-Dawley rats were divided into five gro...AIM:To investigate the effect of interferon-a (IFN-α) on preventing or reversing hepatic fibrosis in rat experimental model induced by CCI4. METHODS: One hundred and ten Sprague-Dawley rats were divided into five groups: group A (normal controls, n = 18), group B (fibrotic model controls, n = 22), group C (IFN-α prevention, n = 22) initially treated with intramuscular injection of IFN-a in saline daily at the doses of 1× 105 U for 6 wk, group D (IFN-a treatment, n = 24) treated with intra-muscular injection of IFN-a in saline daily at the doses of 1×105 U for 6 wk after the first 6 wk, group E (0.9% sodium chloride treatment control, n = 24) treated with intra-muscular injection of 0.01 mL/kg daily for 6 wk after the first 6 wk. At the end of the experiment, all rats of each group were killed. Samples of the liver obtained by biopsy were subjected to histological, immunohistochemical and electron microscopic studies for the expressions of transforming growth factor-pi (TGF- μ41) and α-smooth muscle actin (α-SMA). RESULTS: The expressions of TGF-pl, the number of activated hepatic stellate cells and a-SMA in hepatic tissue of group C were significantly less than those of group B (P<0.01). The degree of fibrosis score in group B was also significantly less than that of group C under light microscope (P<0.01). CONCLUSION: IFN-a can inhibit the production of TGF-pl, decrease HSC activation and stimulate its apoptosis.展开更多
Objective: To test the hypothesis that acute phase reactants, such as alpha 1-antitrypsin and alpha 1-acid glycoprotein, could protect mammalian cells from further damage. Methods: Human dermal fibroblasts (5×10 ...Objective: To test the hypothesis that acute phase reactants, such as alpha 1-antitrypsin and alpha 1-acid glycoprotein, could protect mammalian cells from further damage. Methods: Human dermal fibroblasts (5×10 4) were cultured with DMEM plus 10% FBS at 37℃ in a 5% CO 2 incubator. Different doses of LPS (lipopolysaccharide) and/or acute phase reactants were added. After 24 hours, the cultured supernatant was aspirated, the cells were washed, fixed and stained by methylene blue. The unbound stain was washed off. The stained cells were solubilized in 0.1 ml of 1% Triton X-100. The absorbance of each well was measured using an ELISA spectrophotometer. The concentration of LPS which decreased the absorbance to 70% of the control (LPS-free) cultures was defined as LD 30. Results: In order to achieve LD 30 in the presence of acute phase proteins, it was necessary to alter the LPS concentrations. The LD 30 of LPS treated with 0, 0.5, 2, 10 mg/ml antitrypsin and 0, 0.5, 2, 10 mg/ml glycoprotein was 5.4, 6.5, 7.6, 14.2 mg/ml and 5.2, 5.9, 6.9, 10.5 mg/ml, respectively. Statistically, with the treatment of more than 2 mg/ml antitrypsin or glycoprotein, LD 30 increased significantly. Conclusions: Our data show that fibroblasts are susceptible to the direct toxicity of LPS. Alpha 1-antitrypsin and alpha 1-acid glycoprotein can reduce the toxicity and/or increase the tolerance of mammalian cells to LPS.展开更多
文摘AIM:To investigate the effect of interferon-a (IFN-α) on preventing or reversing hepatic fibrosis in rat experimental model induced by CCI4. METHODS: One hundred and ten Sprague-Dawley rats were divided into five groups: group A (normal controls, n = 18), group B (fibrotic model controls, n = 22), group C (IFN-α prevention, n = 22) initially treated with intramuscular injection of IFN-a in saline daily at the doses of 1× 105 U for 6 wk, group D (IFN-a treatment, n = 24) treated with intra-muscular injection of IFN-a in saline daily at the doses of 1×105 U for 6 wk after the first 6 wk, group E (0.9% sodium chloride treatment control, n = 24) treated with intra-muscular injection of 0.01 mL/kg daily for 6 wk after the first 6 wk. At the end of the experiment, all rats of each group were killed. Samples of the liver obtained by biopsy were subjected to histological, immunohistochemical and electron microscopic studies for the expressions of transforming growth factor-pi (TGF- μ41) and α-smooth muscle actin (α-SMA). RESULTS: The expressions of TGF-pl, the number of activated hepatic stellate cells and a-SMA in hepatic tissue of group C were significantly less than those of group B (P<0.01). The degree of fibrosis score in group B was also significantly less than that of group C under light microscope (P<0.01). CONCLUSION: IFN-a can inhibit the production of TGF-pl, decrease HSC activation and stimulate its apoptosis.
基金NationalNatureScienceFundGrant (No .395 0 0 15 0 ) OutstandingTalentFundGrantof NationalNatureScienceFundCommittee (No .3972 5 0 2 9)
文摘Objective: To test the hypothesis that acute phase reactants, such as alpha 1-antitrypsin and alpha 1-acid glycoprotein, could protect mammalian cells from further damage. Methods: Human dermal fibroblasts (5×10 4) were cultured with DMEM plus 10% FBS at 37℃ in a 5% CO 2 incubator. Different doses of LPS (lipopolysaccharide) and/or acute phase reactants were added. After 24 hours, the cultured supernatant was aspirated, the cells were washed, fixed and stained by methylene blue. The unbound stain was washed off. The stained cells were solubilized in 0.1 ml of 1% Triton X-100. The absorbance of each well was measured using an ELISA spectrophotometer. The concentration of LPS which decreased the absorbance to 70% of the control (LPS-free) cultures was defined as LD 30. Results: In order to achieve LD 30 in the presence of acute phase proteins, it was necessary to alter the LPS concentrations. The LD 30 of LPS treated with 0, 0.5, 2, 10 mg/ml antitrypsin and 0, 0.5, 2, 10 mg/ml glycoprotein was 5.4, 6.5, 7.6, 14.2 mg/ml and 5.2, 5.9, 6.9, 10.5 mg/ml, respectively. Statistically, with the treatment of more than 2 mg/ml antitrypsin or glycoprotein, LD 30 increased significantly. Conclusions: Our data show that fibroblasts are susceptible to the direct toxicity of LPS. Alpha 1-antitrypsin and alpha 1-acid glycoprotein can reduce the toxicity and/or increase the tolerance of mammalian cells to LPS.
