Background: Microtubules play a role in maintaining cell shape and movement, organelle positioning and distribution. Our previous studies identified that MAP4 and Op18 involved in the
regulation of eccentric exercise-induced damage of microtubule in skeletal muscle cells. But mechanisms of variation in MAP4 and Op18 were not clear.To observe the effect of eccentric exercise on
microtubules and related proteins in skeletal muscle of rats. To explore the molecular mechanism of eccentric exercise on microtubules damage in skeletal muscle.
Methods: One hundred and twenty-six male SD rats were divided into five groups: control group(C), placebo group(D, intraperitoneal injection of 30% DMSO saline solution), blocking
group(S, intraperitoneal injection of SB203580, 15mg/kg), exercise group(E, running on a treadmill with 16° decline at 16m/min for 90min), blocking and exercise group(SE, intraperitoneal injection of
SB203580 at 30min before exercise, 15mg/kg). After the termination of experiments, each group was divided into 0h, 12h, 24h, 48h and 72h group.The soleus was detected in the corresponding time points.
The protein expressions of α-tubulin, MAP4, Op18, p-Op18, p38, p-p38 were measured by western blot. Co-Immunoprecipitation was used to detect the interaction of MAP4 and p38/MAPK.
Results: In blocking an exercise group, the protein expression of MAP4 decreased(P﹤0.05), Op18 expression increased, especially its phosphorylation increased（P﹤0.05）.There were
interactions between MAP4 and p38/MAPK by Co-Immunoprecipitation, especially strengthened after exercise.
Conclusions: The molecular mechanism of eccentric exercise on microtubules damage in skeletal muscle is that eccentric exercise activated p38 kinase, resulting in increasing MAP4 and
decreasing Op18, and both of them coordinately regulated causing the damage of microtubule.