ABSTRACT
Objective:To observe the effect of Xiao Jianzhongtang on Adenylate-activated protein kinase/peroxidase proliferation-activated receptor coactivator 1-α （AMPK/PGC1-α） signaling pathway in skeletal muscle of exercise fatigue mice.Method:Forty Kunming mice were randomly divided into normal group， model group， Buzhong Yiqitang group and Xiao Jianzhongtang group， with 10 mice in each group. The model group， Buzhong Yiqitang group and Xiao Jianzhongtang group were trained on the treadmill to establish a fatigue model， and the normal group did not apply any intervention. At the same time as the treadmill training， the model group was given the same amount of normal saline. Xiao Jianzhongtang was administered with 5 g·kg-1 of medicine， and Buzhong Yiqitang was administered with 2.8 g·kg-1 of medicine for 6 days. After the experiment， the weight of each group of mice and the time of running out of exhaustion were measured，the colorimetric method was used to detect the serum urea （UREA）， lactate dehydrogenase （LDH）， muscle glycogen （MG）， and skeletal muscle of each group of mice Na+-K+-ATPase， Ca2+-Mg2+-ATPase content， pathological changes of skeletal muscle of each group were observed by hematoxylin-eosin （HE） staining， Western blot was used to detect the protein expression of AMPK and PGC1-α in skeletal muscle of each group .Result:Compared with normal group， the body weight of model group significantly decreased （P<0.01）， and the contents of Na+-K+-ATPase， Ca2+-Mg2+-ATPase， LDH， and MG significantly decreased （P<0.05，P<0.01）. The content of UREA increased significantly （P<0.01）， and the expression of AMPK and PGC1-α protein increased significantly （P<0.01）. Compared with model group， the mice in the Xiao Jianzhongtang group had significantly increased body weight （P<0.05）， significantly increased the time spent on treadmill exhaustion（P<0.01）， Na+-K+-ATPase， Ca2+-Mg2+-ATPase， LDH， and MG. The content increased significantly（P<0.05， P<0.01）， the content of UREA decreased significantly （P<0.01）， and the expression of AMPK and PGC1-α protein increased significantly （P<0.01）.Conclusion:Xiao Jianzhongtang has an anti-exercise fatigue effect， which may be related to enhancing skeletal muscle AMPK/PGC1-α pathway，enhancing mitochondrial oxidative phosphorylation，reducing accumulation of metabolites，slowing down glycogen consumption and decomposition，and enhancing skeletal muscle energy synthesis.
ABSTRACT
OBJECTIVE: To observe the effect of electroacupuncture (EA) of "Zusanli" (ST 36) on mitochondrial oxidative stress of skeletal muscle in rats with chronic fatigue syndrome (CFS) based on adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/ peroxlsome proliferator-activated receptor-γ coactivator-1 α (PGC-1 α) signaling, in order to reveal its mechanism underlying improvement of CFS. METHODS: Forty SD rats were randomly divided into normal control, CFS model, EA-Zusanli (ST 36) and EA-non-acupoint groups (n=10 rats in each group). The CFS model was established by forced exhausted load-bearing swimming (twice daily), chronic constraint (1 h) and sleep deprivation (20 h/day) for 14 days. Following modeling, EA (2 Hz/100 Hz, 2 V) was applied to bilateral Zusanli (ST 36) or non-acupoint (about 10-15 mm superior to the bilateral Iliac creast and about 20 mm lateral to the posterior median line) for 20 min, once a day for 10 days. The expression levels of ATP synthase, AMPK, phosphorylated (p)-AMPK, silent mating type information regulation 2 homolog-1 (SIRT 1) and PGC-1 α proteins, and ATP synthase, SIRT 1 and PGC-1 α mRNAs of the quadriceps femoris muscle were detected by Western blot and fluorescence quantitative PCR, respectively. The rats' grabbing force was detected by using a grabbing-force detector. RESULTS: Compared with the normal group, the grabbing force, and the expression levels of ATP synthase and PGC-1 α proteins and mRNAs were significantly decreased (P<0.05, P<0.01), while the expression of SIRT 1 protein was significantly up-regulated (P<0.05) in the CFS model group. Following EA intervention, the grabbing force and the expression levels of ATP synthase mRNA, SIRT 1 and PGC-1 α proteins and mRNAs, and p-AMPK/AMPK were significantly up-regulated in the EA-Zusanli (ST 36) group (P<0.05, P<0.01). CONCLUSION: EA of ST 36 can raise the grabbing force of CFS rats, which may be related to its effects in up-regulating the expression of ATP synthase mRNA, SIRT 1 and PGC-1 α proteins and mRNAs, and p-AMPK/AMPK to reduce mitochondrial oxidative stress reaction and in increasing ATP synthesis.