Electroacupuncture (EA) pretreatment has been reported to induce tolerance against cerebral ischemia/reperfusion (I/R) injury; however, the mechanisms underlying the beneficial effects of EA remain to be elucidated. Increasing evidence has suggested that excess activation of autophagy is important in I/R injury. The present study aimed to investigate the hypothesis that EA pretreatment‑induced tolerance to cerebral I/R injury was mediated by inhibition of the autophagy pathway. Rats were treated with EA at the acupoint 'Baihui (GV20)' 30 min/day, for five consecutive days prior to the induction of focal cerebral ischemia for 120 min by middle cerebral artery occlusion. Levels of autophagy, cerebral apoptosis, infarct volumes, brain water content and motor deficit were evaluated 12 h following I/R. The autophagy inducer rapamycin was used to investigate the role of autophagy in mediating neuroprotective effects. The results showed that the number of autophagosomes and the expression of the marker proteins of autophagy, including microtubule‑associated protein 1A light chain 3 (LC3)‑II and Beclin 1 were significantly increased 12 h post‑I/R. EA pretreatment decreased the expression of autophagy markers and the number of autophagosomes in the ischemic cortex. In addition, EA pretreatment inhibited neuronal apoptosis, reduced infarct volume and water content, as well as improved neurological outcome of rats following I/R. Furthermore, the reduced expression of LC3‑II and Beclin 1 and the neuroprotective effects were reversed by the autophagy inducer rapamycin. In conclusion, the results of the present study demonstrated that EA pretreatment protected the brain against I/R injury via inhibition of the autophagy process.

Disruption of the blood-brain barrier (BBB) and subsequent brain edema are major contributors to the pathogenesis of ischemic stroke, however, current clinical therapeutic methods remains unsatisfactory. Electroacupuncture (EA) pretreatment has a protective effect against cerebral ischemia/reperfusion (I/R). However, the underlying mechanisms remain to be fully elucidated. In the present study, the effect of EA pretreatment on BBB disruption was investigated in a focal I/R rat model. Male Sprague-Dawley rats (280-320 g) were pretreated with EA at the acupoint 'Baihui' (GV20) 30 min/day, for five days consecutively prior to focal cerebral I/R, which was induced by middle cerebral artery occlusion (MCAO) for 2 h. The results demonstrated that the infarction volume, brain water content and neurological deficits increased in the MCAO model rats at 3 h and 24 h post-reperfusion, and were attenuated significantly by EA pretreatment. Furthermore, electron microscopy examination confirmed a reduction in brain edema reduction in the EA pretreated rats. Western blot analysis revealed that the tight junction proteins between endothelial cells, including claudin-5, occludin, were significantly degraded, while the protein expression of phosphorylated (p-)caveolin-1 and p-Akt increased following reperfusion, all of which were alleviated by EA pretreatment. However, no significant differences were observed in the expression of caveolin-1 or Akt. Overall, the results demonstrated that EA pretreatment significantly reduced BBB permeability and brain edema, which were correlated with alleviation of the degradation of tight junction proteins and inhibition of the expression of p-caveolin-1 in the endothelial cells.

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Sufentanil is a new kind of opioid analgesic and acts on μ opioid receptor. In this study, we aim to investigate the effects of sufentanil on gastric cancer cell line SGC-7901, after being exposed to different concentrations of sufentanil. Gastric cancer cells were exposed to sufentanil for a predetermined time at concentrations of 0, 0.5, 5, 50 and 500 nmol/l, respectively. Cell viability at different time points after exposure to sufentanil was tested by CCK-8 assay. FDA-PI staining was used to observe membrane integrity of gastric cancer SGC7901 cells. The apoptosis of gastric cancer cells was analyzed by Annexin V-FITC/PI Flow Cytometry and the changes of the cell cycle was determined by a detection kit. As a result, cell viability decreased in a dose- and time-dependent manner. Furthermore, with the concentration of sufentanil increased, the proportion of dead and apoptotic SGC-7901 cells increased, and more cells were arrested in G2/M phase. In a word, sufentanil can inhibit the cell viability and induce the apoptosis of gastric cancer SGC-7901 cells in vitro.