中文摘要：

目的探讨钙调蛋白（Calmodulin,CaM）对急性骨骼肌炎症反应的影响。方法心毒素（Cardiotoxin,CTX）肌内注射,诱导C57BL/6小鼠胫骨前肌（tibialis anterior,TA）急性损伤。肌损伤小鼠腹腔注射钙调蛋白抑制剂R24571或激动剂CALP1。分别检测TA肌组织自身抗原和TLRs表达以及单核/巨噬细胞的肌内浸润程度。结果 CTX注射导致急性肌损伤,TA肌内出现大量的炎性渗出,并伴随肌纤维坏死。损伤肌组织内CaM、自身抗原（Mi-2,HRS和Ku70）以及TLR3表达上调。较之CTX损伤组,CALP1处理导致损伤TA肌内单核/巨噬细胞数量增多,肌内自身抗原和TLR3 mRNA和蛋白水平上调,R24571则减少肌内炎性浸润并下调上述炎性介质。结论 CaM信号参与介导急性骨骼肌炎症反应。

英文摘要：

The Calcium/Calmodulin（Ca^2＋/CaM） signaling has been reported to be essential for immune andinflammatory responses in peripheral tissues and organs. However, whether Ca M signaling interferes with muscleinflammation remains mostly unknown. In this study, we investigated the role of Ca M in acute skeletal muscleinflammation. B6 mice of 6-8-week old were induced acute myoinjury by Cardiotoxin（CTX） injection i.m., and thenintraperitoneally injected with Ca M inhibitor R24571 or CaM agonist CALP1, respectively. Muscle-autoantigens,TLRs, and mononuclear/macrophage cells infiltration were detected post-injury. We observed the increase levels ofCa M, muscle autoantigens（Mi-2, HRS and Ku70） and TLR3, as well as intensive intramuscular infiltration ofinflammatory cells after acute injury, while these indicators gradually reduced over time. We also found enhancedintramuscular infiltration of monocytes/macrophages, up-regulated m RNA and protein levels of muscle autoantigens（Mi-2, HRS and Ku70） and TLR3 in the damaged tibialis anterior muscle（TA） treated with CALP1, comparing tountreated one. In contrast, R24571 decreased the intramuscular infiltration, and down-regulated the m RNA andprotein levels of above inflammatory indicator. Thus, the present findings demonstrate Ca M-signal play a role inmediating acute muscle inflammatory responses.