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toplasmic edema with basic disappearance of the rough endoplasmic reticulum and glycogen particles in neurons of the frontal cortex and hippocampal CA1 region after modeling, which was relatively milder in the moxibustion group. CONCLUSION Moxibustion of acupoints of the Governor Vessel may reduce the content of APP in the frontal cortex and hippocampus by regulating the expression of RAGE and LRP-1 proteins and mRNA in VD rats.OBJECTIVE To investigate the effect of electroacupuncture (EA) on silent information regulator 1 (SIRT1), forkhead transcription factor O1 (FoxO1), and proopiomelanocortin (POMC) in the hypothalamus of rats with high-fat diet-induced obesity (DIO), as well as the mechanism of EA in regulating central appetite peptides to help lose weight. METHODS Male Wistar rats were randomly divided into normal group, model group, EA group, EA＋inhibitor group, inhibitor group, and sham-operation group, with 10 rats in each group. High-fat diet was used to establish a rat model of DIO. The rats in the EA group and EA＋inhibitor group were given EA at "Fenglong" (ST40), "Zhongwan "(CV12)，"Guanyuan "(CV4), and"Zusanli" (ST36) with continuous wave at a frequency of 2 Hz and an intensity of 1 mA, for 10 minutes each time. The rats in the EA＋inhibitor group and inhibitor group were given tube placement in the third ventricle and injection of the specific SIRT1 antagonist EX-527. The rats in the sham-operation group were given tubeficant increases in body weight, food intake, the serum levels of TC, TG, FFA, and the protein expression of AC-FoxO1 (P less then 0.01), as well as significant reductions in the protein expression of SIRT1, FoxO1 and POMC (P less then 0.01). CONCLUSION In rats with DIO, EA can effectively up-regulate the expression of SIRT1 in the hypothalamus, exert a deacetylation effect on FoxO1, and promote the expression of the downstream appetite-inhibiting peptide POMC, which may be one of the mechanisms of EA to help lose weight by regulating central appetite peptides in the obesity model.OBJECTIVE To observe the effect of electroacupuncture (EA) stimulation on the expression of c-Jun terminal kinase(JNK)signaling pathway-related proteins in the hippocampus of vascular dementia (VD) rats, so as to explore its mechanisms underlying improvement of VD. METHODS Male Sprague-Dawley rats were randomly divided into sham operation, model and EA groups (n＝10 rats per group). The VD model was prepared by repeated occlusion of the bilateral common carotid arteries for 10 min and reperfusion for 10 min (3 times in total). The rats in the EA group received EA (2 Hz, 2 mA) at "Dazhui"(GV14)，"Baihui"(GV20), and bilateral "Housanli"(ST36) ，"Geshu"(BL17) for 10 min, once daily for 14 days. The learning-memory abi-lity was detected by Morris water maze tests, the distribution of hippocampal neurons detected by Nissl staining, and the apoptosis of hippocampal neurons detected by using TdT-mediated dUTP nick-end labeling (TUNEL) method. The expressions of JNK, phosphorylated JNK (p-JNK), cysteine-containing asparaspase-8 and Caspase-3 were significantly down-regulated (P less then 0.01). Semaglutide purchase CONCLUSION EA intervention can improve the learning-memory ability of VD rats, which may be associated with its effects in reducing hippocampal apoptosis by suppressing JNK signaling pathway.OBJECTIVE To observe the effects of electroacupuncture (EA) at "Zusanli" (ST36) on the ultrastructure and mitochondrial dynamics of skeletal muscle tissue in spleen qi deficiency rats, so as to explore the partial action mechanism of EA at ST36 for spleen deficiency syndrome. METHODS Twenty-four male SD rats were randomly divided into 4 groups normal group, model group, ST36 group and non-acupoint group (n＝6 in each group). The model of spleen qi deficiency syndrome was established by improper diet and exhaustive swimming. EA (2 Hz/15 Hz, 0.5 mA) was applied to bilateral ST36 in the ST36 group and non-acupoint in the non-acupoint group for 20 min, once daily for 7 days. The colorimetric method was used to detect the ATP content in skeletal muscle tissue. The ultrastructure changes of skeletal muscle tissue were observed by transmission electron microscopy. The expression levels of optic atrophy 1 (Opa1) and dynamin-related protein 1 (Drp1) mRNA and proteins in the skeletal muscle tissue were determined by flu After the treatment, the expression levels of Opa1 and Drp1 mRNAs and proteins were up-regulated in the ST36 group (P less then 0.05), and the expression of Drp1 protein was up-regulated in the non-acupoint group (P less then 0.05)．. CONCLUSION EA at ST36 can correct the imbalance of mitochondrial fission and fusion in skeletal muscle of rats with spleen qi deficiency, thereby improving the damage of mitochondrial structure and function, and leading to an increase of energy metabolism.OBJECTIVE To investigate the effect of manual acupuncture (MA) and electroacupuncture (EA) on histopathological changes, and levels of oxidative-stress related cytokines and key proteins of the endoplasmic reticulum stress (ERS) pathway in ulcerative colitis (UC) rats, so as to reveal their mechanisms underlying improvement of UC. METHODS Twenty-eight male SD rats were randomly divided into control, model, EA and MA groups (n＝ 7 rats per group). The UC model was established by enema of mixture solution of 5% 2, 4, 6-trinitrobenzene sulfonic acid (TNBS, 100 mg/kg). Rats of the control group received intra-rectal perfusion of normal saline. After modeling, the left "Quchi"(LI11) and "Zusanli"(ST36) were stimulated with EA (2-4 mA，8 Hz/25 Hz) or MA for 20 min, once every other day for consecutive 2 weeks. The rats in the control and model group were just anesthetized and fixed. At the end of experiments, the colon tissue was collected for observing histopathological changes with H．E. staining. The contents of ox levels of SOD, CAT, GSH and T-AOC were all significantly decreased (P less then 0.01), and the content of MDA, and expression levels of p-IκBα， p-p65 and GRP78, p-PERK and p-eIF2α proteins were all significantly increased in the model group relevant to the control group (P less then 0.01). After the treatment, modeling-induced down-regulation of SOD, CAT and GSH in both EA and MA groups, and T-AOC in the EA group, and up-regulation of levels of MDA, p-IκBα， p-p65, GRP78, p-PERK and p-eIF2α in both groups were reversed (P less then 0.01, P less then 0.05). CONCLUSION Both EA and MA treatment can obviously alleviate colonic inflammation in UC rats via inhibiting oxidative stress and ERS.