Dodd Stephen, Hain Brian, Judge Andrew
Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, 32611, USA.
Biogerontology. 2009 Oct;10(5):605-11. doi: 10.1007/s10522-008-9203-1. Epub 2008 Dec 13.
This study determined the effects of heat shock protein 70 (Hsp70) overexpression on disuse muscle atrophy in senescent rats. Solei of young and senescent rats were co-injected with Hsp70 plus a nuclear factor kappa B (NF-kappaBeta) reporter plasmid. After 4 days, the hind limbs of half the young and senescent rats were immobilized for 6 days with the remainder serving as weight bearing controls. Hsp70 protein levels and cross-sectional area decreased in both groups (20%) after immobilization. Atrophy was prevented in those fibers overexpressing Hsp70. NF-kappaBeta activity increased in the soleus of both young (three-fold) and senescent (five-fold) animals after immobilization and was prevented by Hsp70 overexpression. Inhibitor of kappaBeta decreased in young (30%) and senescent (~10%) animals with immobilization and returned to normal with Hsp70. Heat shock protein 70 overexpression prevents disuse atrophy in senescent rats, possibly through suppression of the NF-kappaB pathway.
本研究确定了热休克蛋白70（Hsp70）过表达对衰老大鼠废用性肌肉萎缩的影响。将年轻和衰老大鼠的比目鱼肌共同注射Hsp70及核因子κB（NF-κB）报告质粒。4天后，将一半年轻和衰老大鼠的后肢固定6天，其余作为负重对照。固定后两组的Hsp70蛋白水平和横截面积均下降（约20%）。过表达Hsp70的纤维未出现萎缩。固定后，年轻（三倍）和衰老（五倍）动物比目鱼肌中的NF-κB活性均增加，而Hsp70过表达可阻止其增加。κB抑制剂在固定的年轻（约30%）和衰老（约10%）动物中减少，而Hsp70可使其恢复正常。热休克蛋白70过表达可预防衰老大鼠的废用性萎缩，可能是通过抑制NF-κB途径实现的。
