Effect of heat stress on contractile properties of skeletal muscle from adjuvant-induced arthritis rat

类风湿性关节炎(RA)患者有明显的肌肉无力，这对结合疾病活动的残疾有重大影响。在本研究中，我们研究了佐剂性关节炎(AIA)大鼠骨骼肌收缩功能障碍的潜在机制，这是一种广泛应用于RA的动物模型。结果表明，AIA大鼠指长伸肌(EDL)存在内源性收缩功能障碍，这可以用肿瘤坏死因子诱导的过氧亚硝酸根过量产生的氧化应激来解释。此外，考虑到这些发现和热休克蛋白(HSP)72的抗氧化作用，我们研究了热应激对AIA EDL肌肉收缩特性和氧化还原状态的影响。我们的结果表明，热应激显著增加AIA EDL肌肉中HSP72的表达，但不能改善AIA EDL肌肉的收缩功能障碍和氧化还原修饰。

Patients with rheumatoid arthritis (RA) have significant muscle weakness, which has a major impact on disability in conjugation with disease activity. In the present study, we investigated the underlying mechanisms of contractile dysfunctions in skeletal muscle from adjuvant-induced arthritis (AIA) rats, which is a widely used animal model for RA. The results show intrinsic contractile dysfunction in extensor digitorum longus (EDL) muscles of AIA rats, which can be explained by the oxidative stress due to TNF-induced peroxynitrite overproduction. Moreover, take these findings and the antioxidative role of heat shock protein (Hsp) 72 into account, we investigated the effects of heat stress on the contractile properties and redox states of AIA EDL muscles. Our results show that heat stress markedly increases Hsp72 expression, but fails to ameliorate contractile dysfunctions and redox modifications in AIA EDL muscles.