OBJECTIVE: To investigate the effect of electroacupuncture (EA) on neurological function in rats with cerebral ischemia-reperfusion injury (CIRI) by regulating adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/Unc-51-like kinase 1 (ULK1) signaling pathway. METHODS: Thirty-three male SD rats were randomly divided into a sham-operation group, a model group and an EA group, with 11 rats in each group. The right middle cerebral artery occlusion/reperfusion (MCAO/R) model was prepared by thread occlusion method in the model group and the EA group. In the sham-operation group, no thread was inserted after vascular separation. After the success of modeling, in the EA group, EA was applied to "Baihui" (GV 20) and "Zusanli" (ST 36) on the affected side, with disperse-dense wave, the frequency of 2 Hz/15 Hz, for 20 min, once a day. EA was delivered continuously for 3 days. On day 1 and day 3 of operation, the score of the modified neurological deficit scale (mNSS) was evaluated. After intervention completion, the cerebral infarction area was measured by the thiazolyl blue tetrazolium chloride (TTC) method. Nissl staining was used to observe the damage of cortical neurons on the ischemic side in each group. Using transmission electron microscopy, the ultrastructure of cortical neurons on the ischemic side was observed. With the immunofluorescence method adopted, the positive expression of the related protein 1 light chain 3 (LC3) and benzyl chloroform (Beclin-1) on the ischemic side was detected. The protein expression of p-AMPK, AMPK, p-mTOR, mTOR, pS757-ULK1, ULK1 and chelating ligand 1 (p62) in the ischemic cortex was detected using Western blot method. RESULTS: ① Compared with the sham-operation group, in the model group, the mNSS score increased (P<0.01), the percentage of infarction area was increased (P<0.01); the cortical neurons on the ischemic side were loosely distributed, with karyopyknosis and vacuolization, and the number of neurons was reduced (P<0.01); the cells were swollen and ruptured, mitochondrial shrunk, electron density higher, and there were a large number of autophagic debris. The positive expression of LC3 and Beclin-1 was elevated (P<0.01), and p-mTOR/mTOR, pS757-ULK1/ULK1 and the protein expression of p62 dropped (P<0.01) in the ischemic cortex. ② Compared with the model group, in the EA group, the mNSS score was reduced (P<0.05). The percentage of cerebral infarction area was descreased (P<0.01); and the neurons were regularly distributed, the number of neurons increased (P<0.01), the structure of mitochondria was clearer, the crest fracture alleviated, and the damage of neurons attenuated. The positive expression of LC3 and Beclin-1 was dropped (P<0.01), and p-AMPK/AMPK reduced (P<0.05), and p-mTOR/ mTOR, pS757-ULK1/ULK1 and the protein expression of p62 increased (P<0.01) in the ischemic cortex. CONCLUSION EA at "Baihui" (GV 20) and "Zusanli" (ST 36) inhibits autophay, attenuates neurological deficit and cerebral pathological damage in CIRI rats to protect the nerves, which may be obtained by regulating AMPK/mTOR/ULK1 signaling pathway.
Animals ; Electroacupuncture ; Male ; Rats ; TOR Serine-Threonine Kinases/genetics* ; Rats, Sprague-Dawley ; Autophagy-Related Protein-1 Homolog/genetics* ; Reperfusion Injury/metabolism* ; Signal Transduction ; AMP-Activated Protein Kinases/genetics* ; Brain Ischemia/metabolism* ; Humans ; Acupuncture Points

Objective To explore the effect of Xingnao acupuncture combined with swallowing rehabilitation training on dysphagia after stroke .Methods 66 patients with dysphagia after stroke were selected as the research subjects ,and they were randomly divided into the observation group and the control group ,33 cases in each group .The control group was given rehabilitation training on the basis of conventional treatment ,while the observation group was given Xingnao acupuncture method on the basis of the control group .The therapeutic effect ,swallowing function and adverse reactions were observed before and after treatment in the two groups .Results After treatment,the treatment effect in the observation group was significantly better than that in the control group ,there was statistically significant difference between the two groups (Z=-4.123,P<0.05).The total effective rates of the two groups were 93.94％, 75.76％,respectively,there was no statistically significant difference between the two groups (χ2 =1.906,P>0.05). After treatment,the Watian drinking water test scores,standardized swallowing assessment (SSA) score,dysphagia score in the control group were (1.39 ±0.47) points,(23.02 ±5.24) points,(1.25 ±0.55) points,respectively, which in the observation group were (0.74 ±0.39) points,(18.26 ±3.71) points,(0.74 ±0.28) points,and the differences were statistically significant compared with before treatment ( the control group:t =21.453,10.644, 26.212,all P<0.05;the observation group:t=27.779,14.15,37.469,all P<0.05),which in the observation group were better than those in the control group ,the differences were statistically significant ( t=6.114,4.259,4.747,all P<0.05).There was no statistically significant difference in the incidence of adverse events between the two groups (P>0.05).Conclusion Xingnao acupuncture combined with swallowing rehabilitation training in the treatment of dysphagia after stroke can effectively improve the swallowing function ,improve the quality of life of patients ,and it is safe,reliable and worthy of promotion in clinical practice .

OBJECTIVETo explore the central mechanism of postoperative fatigue syndrome by detecting the expression of NMDA receptor and tryptophan metabolism.

METHODSAfter being numbered according to the weight, ninety-six male SD rats were randomly divided into control group (bowel loop was flipped after laparotomy and received intraperitoneal injection of saline at a dose of 1 ml/kg), POFS model(70% of the length of small intestine was resected and received intraperitoneal injection of saline at a dose of 1 ml/kg), and NMDA antagonist groups(70% of the length of small intestine was resected and received intraperitoneal injection of MK801 at a dose of 1 ml/kg). Each group was divided into subgroups by postoperative 1, 3, 5 and 7 d, with 8 rats in each subgroup. The hippocampus was removed at each time point after open field test (OFT) to detect the mRNA expression levels of NMDA receptor 1 and kynurenine aminotransferase III((KATIII() by real-time PCR. Protein level of NMDA receptor 1 was detected by Western blot. High performance liquid chromatography (HPLC) was used to measure the concentrations of tryptophan (TRP), kynurenine (KYN) and kynurenic acid(KYNA). Ultra-structural changes of hippocampal neurons were observed by transmission electron microscopy(TEM).

RESULTSAs compared to control group, exercise score decreased(P<0.05), rest time and central panel residence time prolonged, periphery/central panel ratio increased (all P<0.05), mRNA and protein expressions of NMDA receptor 1 increased (P<0.05), mRNA expression of KAT III( decreased (P<0.05), KYN/TRP ratio and KYN/KYNA ratio decreased (all P<0.05) in POFS group on postoperative day 1 and 3. As compared to POFS group, central panel residence time and periphery/central panel ratio decreased on postoperative day 1, and mRNA and protein expressions of NMDA receptor 1 decreased on postoperative day 1 and 3 (all P<0.05) in antagonist group. TEM revealed that degenerated neuron was found in the hippocampus of POFS rats, while such damage was improved in antagonist group.

CONCLUSIONThe increased expression level of NMDA receptor may play an important role in POFS. NMDA receptor antagonist MK801 may improve the POFS.

Animals ; Fatigue ; Hippocampus ; Humans ; Injections, Intraperitoneal ; Male ; Postoperative Period ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate ; Signal Transduction ; Transaminases

Objective To explore the central mechanism of postoperative fatigue syndrome by detecting the expression of NMDA receptor and tryptophan metabolism. Methods After being numbered according to the weight, ninety-six male SD rats were randomly divided into control group (bowel loop was flipped after laparotomy and received intraperitoneal injection of saline at a dose of 1 ml/kg ), POFS model (70% of the length of small intestine was resected and received intraperitoneal injection of saline at a dose of 1 ml/kg), and NMDA antagonist groups (70% of the length of small intestine was resected and received intraperitoneal injection of MK801 at a dose of 1 ml/kg ). Each group was divided into subgroups by postoperative 1, 3, 5 and 7 d, with 8 rats in each subgroup. The hippocampus was removed at each time point after open field test (OFT) to detect the mRNA expression levels of NMDA receptor 1 and kynurenine aminotransferase Ⅲ (KATⅢ) by real-time PCR. Protein level of NMDA receptor 1 was detected by Western blot. High performance liquid chromatography (HPLC) was used to measure the concentrations of tryptophan (TRP), kynurenine (KYN) and kynurenic acid(KYNA). Ultra-structural changes of hippocampal neurons were observed by transmission electron microscopy (TEM). Results As compared to control group, exercise score decreased (P<0.05), rest time and central panel residence time prolonged, periphery/central panel ratio increased (all P<0.05), mRNA and protein expressions of NMDA receptor 1 increased (P<0.05), mRNA expression of KAT Ⅲ decreased (P<0.05), KYN/TRP ratio and KYN/KYNA ratio decreased (all P<0.05) in POFS group on postoperative day 1 and 3. As compared to POFS group, central panel residence time and periphery/central panel ratio decreased on postoperative day 1 , and mRNA and protein expressions of NMDA receptor 1 decreased on postoperative day 1 and 3 (all P<0.05) in antagonist group. TEM revealed that degenerated neuron was found in the hippocampus of POFS rats , while such damage was improved in antagonist group. Conclusion The increased expression level of NMDA receptor may play an important role in POFS. NMDA receptor antagonist MK801 may improve the POFS.

Objective To explore the central mechanism of postoperative fatigue syndrome by detecting the expression of NMDA receptor and tryptophan metabolism. Methods After being numbered according to the weight, ninety-six male SD rats were randomly divided into control group (bowel loop was flipped after laparotomy and received intraperitoneal injection of saline at a dose of 1 ml/kg ), POFS model (70% of the length of small intestine was resected and received intraperitoneal injection of saline at a dose of 1 ml/kg), and NMDA antagonist groups (70% of the length of small intestine was resected and received intraperitoneal injection of MK801 at a dose of 1 ml/kg ). Each group was divided into subgroups by postoperative 1, 3, 5 and 7 d, with 8 rats in each subgroup. The hippocampus was removed at each time point after open field test (OFT) to detect the mRNA expression levels of NMDA receptor 1 and kynurenine aminotransferase Ⅲ (KATⅢ) by real-time PCR. Protein level of NMDA receptor 1 was detected by Western blot. High performance liquid chromatography (HPLC) was used to measure the concentrations of tryptophan (TRP), kynurenine (KYN) and kynurenic acid(KYNA). Ultra-structural changes of hippocampal neurons were observed by transmission electron microscopy (TEM). Results As compared to control group, exercise score decreased (P<0.05), rest time and central panel residence time prolonged, periphery/central panel ratio increased (all P<0.05), mRNA and protein expressions of NMDA receptor 1 increased (P<0.05), mRNA expression of KAT Ⅲ decreased (P<0.05), KYN/TRP ratio and KYN/KYNA ratio decreased (all P<0.05) in POFS group on postoperative day 1 and 3. As compared to POFS group, central panel residence time and periphery/central panel ratio decreased on postoperative day 1 , and mRNA and protein expressions of NMDA receptor 1 decreased on postoperative day 1 and 3 (all P<0.05) in antagonist group. TEM revealed that degenerated neuron was found in the hippocampus of POFS rats , while such damage was improved in antagonist group. Conclusion The increased expression level of NMDA receptor may play an important role in POFS. NMDA receptor antagonist MK801 may improve the POFS.