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TLR4 信号转导可防止矛头蝮蛇蛇毒引起的过度肌肉损伤。

TLR4 signaling protects from excessive muscular damage induced by Bothrops jararacussu snake venom.

机构信息

Department of Immunobiology, Institute of Biology, Fluminense Federal University, Niteroi, Rio de Janeiro 24020-141, Brazil.

出版信息

Toxicon. 2012 Dec 15;60(8):1396-403. doi: 10.1016/j.toxicon.2012.10.003. Epub 2012 Oct 18.

Abstract

Immune cells and skeletal muscle express Toll-like receptors (TLRs) that participate as sensors of tissue injury triggering signals for activation of innate and adaptive immune responses. This study aimed to investigate the involvement of TLR4 in the process of skeletal muscle repair. Muscular injury was induced by injection of 0.6 mg/kg of Bothrops jararacussu snake venom in the gastrocnemius muscle of C3H/HeJ mice that express a non-functional TLR-4 receptor and C3H/HeN mice with functional receptor. TLR4-deficient mice had persistent muscular inflammation with few F4/80 macrophages at onset but increased MMP9 activity and collagen deposition during resolution of injury. Since such effect was not observed in the mouse strain with functional receptor it is concluded that TLR4 signaling exerts a protective role preventing from excessive muscular damage induced by B. jararacussu venom.

摘要

免疫细胞和骨骼肌表达 Toll 样受体 (TLR),作为组织损伤的传感器,触发固有和适应性免疫反应的激活信号。本研究旨在探讨 TLR4 在骨骼肌修复过程中的作用。通过向 C3H/HeJ 小鼠(表达无功能 TLR-4 受体)和 C3H/HeN 小鼠(表达功能受体)的腓肠肌注射 0.6mg/kg 的矛头蝮蛇蛇毒诱导肌肉损伤。TLR4 缺陷型小鼠在损伤开始时肌肉炎症持续存在,F4/80 巨噬细胞较少,但在损伤愈合过程中 MMP9 活性和胶原沉积增加。由于在具有功能受体的小鼠品系中未观察到这种作用,因此可以得出结论,TLR4 信号传导发挥保护作用,防止矛头蝮蛇蛇毒引起的过度肌肉损伤。

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