Effect of warming needle moxibustion on mitochondrial autophagy in rats with chronic fatigue syndrome based on AMPK/ULK1 signaling pathway

ObjectiveTo observe the effect of warming needle moxibustion （WNM） on the expression of AMP-activated protein kinase （AMPK）/Unc-51 like autophagy activating kinase 1 （ULK1） signaling pathway in chronic fatigue syndrome （CFS） rats， so as to explore its mechanism underlying improvement of CFS.MethodsMale SD rats were randomly divided into control， model， WNM and coenzyme groups， with 10 rats in each group. The CFS model was established by multi-factor compound stress stimulation method （exhaustive swimming + chronic restraint + alternate-day fasting）. The rats of the WNM group received warming needle moxibustion stimulation at bilateral “Zusanli” （ST36）， “Guanyuan” （CV4） and “Zhongwan” （CV12）for 15 min， once daily for 14 days. The rats of the coenzyme group were administered coenzyme Q10 （1 mg/kg） by gavage once daily for 14 days. Body weight and swimming time of the rats were recorded before and after modeling and after intervention. Behavioral changes were assessed using the open-field test. Histological changes in skeletal muscle were observed via HE staining. The structure of mitochondria and autophagosomes in skeletal muscle were observed using transmission electron microscopy. The protein expression levels of AMPK， phosphorylated （p）-AMPK， ULK1， p-ULK1， microtubule-associated protein 1 light chain 3 （LC3）-Ⅰ and LC3-Ⅱ in skeletal muscle were detected by Western blot， and the ratios of p-AMPK/AMPK， p-ULK1/ULK1 and LC3-Ⅱ/LC3-Ⅰ were calculated. The mRNA expression levels of AMPK， ULK1 and LC3 in skeletal muscle were detected by real-time PCR.ResultsCompared with the control group， the body weight， swimming time， and the duration of standing and the number of grid crossing were significantly reduced （PPPPConclusionWarming needle moxibustion can alleviate chronic fatigue syndrome by activating the AMPK/ULK1 pathway， upregulating the expression of AMPK/ULK1/LC3， and promoting mitochondrial autophagy， thereby enhancing mitochondrial morphology.