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目的观察干扰素γ(IFN γ)对肝星状细胞(HSC)-T6细胞Ⅰ型胶原(ColⅠ)、Ⅲ型胶原(colⅢ)、基质金属蛋白酶组织抑制因子1(TIMP1)基因表达的影响。方法浓度0.1、1、10、102、103、104、2.5×105、5×105U/ml IFN γ作用于HSC-T6细胞48 h,采用四甲基偶氮唑盐比色法观察其对HSC-T6细胞生长指数的影响;以1、102、104U/ml IFN γ作用于HSC-T6细胞48 h,采用逆转录聚合酶链反应方法测定其对HSC-T6细胞Col Ⅰ、ColⅢ、TIMP1基因表达的影响。结果空白对照组ColⅠ、ColⅢ、TIMP1基因表达水平分别为2.86±0.21、2.00±0.23、3.90±0.81;1U/m1、102U/ml、104U/ml IFNγ作用于HSC-T6细胞,ColⅠ基因表达水平依次为1.00±0.11、0.42±0.12、0.33±0.12,与空白对照组比较, 差异有统计学意义;ColⅢ基因表达水平依次为1.09±0.1 5、0.52±0.14、0.43±0.18,与空白对照组比较, 差异有统计学意义;TIMP1基因表达水平依次为3.81±0.37、3.50±0.51、3.41±0.31,与空白对照组比较,差异无统计学意义。结论IFNγ明显抑制HSC-T6细胞colⅠ、ColⅢ基因表达水平,而对TIMP1基因表达水平无明显影响,从而可抑制Ⅰ、Ⅲ型胶原的合成,这可能是其抗纤维化的作用机制之一。
Objective To investigate the effect of interferon γ (IFNγ) on the gene expression of type Ⅰ collagen, type Ⅲ collagen Ⅲ and matrix metalloproteinase 1 (TIMP1) in hepatic stellate cells (HSC) -T6 cells. Methods The HSC-T6 cells were treated with 0.1, 10,102,103,104,2.5 × 105,5 × 105U / ml IFNγ for 48 h. The inhibitory effect on HSC- T6 cell growth index; HSC-T6 cells treated with 1,102,104U / ml IFNγ for 48 h, the expression of Col Ⅰ, Col Ⅲ, TIMP1 gene in HSC-T6 cells was determined by reverse transcription polymerase chain reaction influences. Results The gene expression of ColⅠ, Col Ⅲ and TIMP1 in blank control group were 2.86 ± 0.21, 2.00 ± 0.23 and 3.90 ± 0.81, respectively. The expression of ColⅠ gene in HSC-T6 cells was affected by 1U / ml, 102U / ml and 104U / ml IFNγ 1.00 ± 0.11, 0.42 ± 0.12 and 0.33 ± 0.12, respectively. The difference was statistically significant compared with the control group. The expression level of Col Ⅲ gene was 1.09 ± 0.1 5,0.52 ± 0.14 and 0.43 ± 0.18, respectively. Compared with the blank control group, The difference was statistically significant; TIMP1 gene expression levels were 3.81 ± 0.37,3.50 ± 0.51,3.41 ± 0.31, compared with the blank control group, the difference was not statistically significant. Conclusion IFNγ significantly inhibits the expression of col Ⅰ and Col Ⅲ gene in HSC-T6 cells, but has no effect on the expression of TIMP1 gene, which can inhibit the synthesis of type Ⅰ and Ⅲ collagen. This may be one of its anti-fibrosis mechanisms.