Induction of heat-shock protein 72 expression by blood flow limit in a rat model of skeletal musclar myopachynsis

Abstract

Objective: To determine whether skeletal musclar myopachynsis was caused by ischemia, we investigated the mechanism of skeletal musclar myopachynsis by examining the gene and protein expressions in muscle tissue. Materials and methods : First of all, using SD rats, we established of a model soleus musclar myopachynsis by removing the gastrocnemius and plantaris in the same hind leg. The right hind leg of the rats was then used in this study. Male rats (8weeks old) were assigned to one of four experimental groups (n=6/group), 1) sedentary control (Con), 2) gastrocnemius and plantaris removed to establish soleus muscular myopachynsis (Op), 3) ischemia for 30minutes (RBF), or 4) Op+RBF. Ischemia was induced by limiting blood flow to the right hind leg with a rubber band four times with in two weeks. Twenty-four hours after the last ischemic episode, the animals were sacrificed, and the soleus muscles were removed and weighed, then the sectional area of myofibrillars and the relative levels of HSP72 were measured. Results: On comparison among Con and Op or RBF animals and among OP or RBF and OP+RBF animals, the relative HSP72 concentration in the soleus muscle was significantly higher. Although ischemia or removal of the gastrocnemius and plantaris resulted in musclar myopachynsis. In Op, RBF and Op+RBF animals, muscle weight and the sectional area of myofibrillars were both significantly elevated. Conclusions : These data demonstrate that the level of HSP72 expression was enhanced with skeletal musclar myopachynsis. It was shown that musclar myopachynsis was also caused by ischemia.