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首页> 外文期刊>Life sciences >Gadolinium chloride reverses dimethylnitrosamine (DMN)-induced rat liver fibrosis with increased matrix metalloproteinases (MMPs) of Kupffer cells.
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Gadolinium chloride reverses dimethylnitrosamine (DMN)-induced rat liver fibrosis with increased matrix metalloproteinases (MMPs) of Kupffer cells.

机译：氯化通过增加Kupffer细胞的基质金属蛋白酶（MMP）逆转二甲基亚硝胺（DMN）诱导的大鼠肝纤维化。

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The aim of this study was to investigate whether matrix metalloproteinases (MMP-13, 9) of Kupffer cells induced by gadolinium chloride (GdCl(3)) treatment can reverse dimethylnitrosamine (DMN)-induced liver fibrosis (in vivo) and the effect of GdCl(3) on MAP kinase activity (in vitro). Male Wistar rats 6 weeks of age received DMN (10 mg/kg) three successive days a week for 4 weeks. Then two groups of rats (n = 6 each) were treated twice weekly with either GdCl(3) (7 mg/kg) or saline solution intravenously for the next 4 weeks. Animals were sacrificed to estimate the degree of liver fibrosis. Isolated Kuppfer cells were treated with GdCl(3) and the expressions of MMPs, MAP kinase activity (ERK, SAPK/JNK, P38) as well as apoptosis were also examined. Rats that received DMN for 4 weeks followed by GdCl(3) injection for 4 weeks showed an reduced liver hydroxyproline content compared to rats treated with DEN followed by saline (277 +/- 22 VS 348 +/- 34 microg/g, n = 6 each, P < 0.01). There were significantly increased MMP-13 mRNA levels in GdCl(3)-treated rats. However, no significant change was observed in procollagen type I mRNA levels. Isolated Kuppfer cells treated with GdCl(3) showed increased MAP kinase activity, especially P38 pathway as well as MMP-13, 9 mRNA and type I collagen-degrading activity leading to apoptosis. SB203580, inhibitor of P38 pathway diminished these activation and prevented apoptosis. These results suggest that Kuppfer cells can reverse liver fibrosis via the expression of MMPs mainly through P38 pathway.
机译：这项研究的目的是调查氯化g（GdCl（3））处理诱导的Kupffer细胞的基质金属蛋白酶（MMP-13，9）是否可以逆转二甲基亚硝胺（DMN）诱导的肝纤维化（体内）和GdCl（3）对MAP激酶活性（体外）。 6周龄的雄性Wistar大鼠每周连续3天接受DMN（10 mg / kg），持续4周。然后，在接下来的4周中，每周两次用GdCl（3）（7 mg / kg）或盐溶液治疗两组大鼠（每组n = 6）。处死动物以估计肝纤维化程度。用GdCl（3）处理分离的Kuppfer细胞，并检查MMPs的表达，MAP激酶活性（ERK，SAPK / JNK，P38）以及细胞凋亡。与先用DEN再加生理盐水（277 +/- 22 VS 348 +/- +/- 34 microg / g，n = 2）的大鼠相比，接受DMN 4周，GdCl（3）注射4周的大鼠肝脏羟脯氨酸含量降低。每个6个，P <0.01）。在GdCl（3）治疗的大鼠中MMP-13 mRNA水平显着增加。但是，未观察到前胶原I型mRNA水平的显着变化。用GdCl（3）处理的分离的Kuppfer细胞显示出增加的MAP激酶活性，尤其是P38途径以及MMP-13、9 mRNA和I型胶原降解活性，导致细胞凋亡。 SB203580，P38途径的抑制剂可减少这些活化并防止细胞凋亡。这些结果表明，Kuppfer细胞可以通过主要通过P38途径表达MMPs来逆转肝纤维化。

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