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Imatinib mesylate ameliorates the dystrophic phenotype in exercised mdx mice.

机译:甲磺酸伊马替尼改善了运动的mdx小鼠的营养不良表型。

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摘要

Myofiber degeneration, inflammation, and fibrosis are remarkable features of Duchenne muscular dystrophy. We hypothesized that the administration of imatinib mesylate, an inhibitor of tyrosine kinase and TGF-beta pro-fibrogenic activity, could improve the muscular conditions in mdx mice. Four-week old mdx mice were treated and exercised for 6 weeks. Gastrocnemius and diaphragm histopathology, strength, creatine kinase, and cytokine levels were evaluated. The treated group presented increased muscular strength and decreased CK levels, injured myofibers, and inflammatory infiltrates. Pro-inflammatory cytokines and TGF-beta were also reduced, while IL-10 was increased, suggesting an immunomodulatory effect of imatinib, which can ameliorate the dystrophic phenotype in mdx mice.
机译:肌纤维变性,炎症和纤维化是杜氏肌营养不良症的显着特征。我们假设甲磺酸伊马替尼(一种酪氨酸激酶和TGF-β促纤维化活性的抑制剂)的给药可以改善mdx小鼠的肌肉状况。治疗四周大的mdx小鼠,并锻炼6周。评估了腓肠肌和diaphragm肌的组织病理学,强度,肌酸激酶和细胞因子水平。治疗组表现出增加的肌肉力量和降低的CK水平,受伤的肌纤维和炎性浸润。促炎性细胞因子和TGF-β也降低,而IL-10升高,提示伊马替尼具有免疫调节作用,可改善mdx小鼠的营养不良表型。

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