Background Our previous research confirmed that electroacupuncture (EA) stimulus elicits neuroprotective effects against cerebral ischemic injury through α7 nicotinic acetylcholine receptor (α7nAChR)-mediated inhibition of high-mobility group box 1 release mechanism. This study investigated whether the signal transducer of α7nAChR and inhibition of NLRP3 inflammasome are involved in the neuroprotective effects of EA stimulus. Methods In adult male Sprague-Dawley rats, the focal cerebral ischemic injury was induced by middle cerebral artery occlusion (MCAO) models for 1.5 h. The expression of NLRP3 inflammasome in the penumbral tissue following reperfusion was assessed by western blotting and immunoflourescent staining. The infarct size, neurological deficit score, TUNEL staining and the expression of proinflammatory factors or anti-inflammatory cytokines were evaluated at 72 h after reperfusion in the presence or absence of either α7nAChR antagonist (α-BGT) or agonist (PHA-543,613). Results The contents of inflammasome proteins were gradually increased after cerebral ischemia/reperfusion (I/R). EA stimulus attenuated NLRP3 inflammasome mediated inflammatory reaction and regulated the balance between proinflammatory factors and anti-inflammatory cytokines. The agonist of α7nAChR induced similar neuroprotective effects as EA stimulus. In contrast, α7nAChR antagonist reversed not only the neuroprotective effects, but also the inhibitory effects of NLRP3 inflammasome and the regulatory effects on the balance between proinflammatory factors and anti-inflammatory cytokines. Conclusions These results provided compelling evidence that α7nAChR played a pivotal role in regulating the activation and expression of NLRP3 inflammasome in neurons after cerebral I/R. These findings highlighted a novel anti-inflammatory mechanism of EA stimulus by α7nAChR modulating the inhibition of NLRP3 inflammasome, suggesting that α7nAChR-dependent cholinergic anti-inflammatory system and NLRP3 inflammasome in neurons might act as potential therapeutic targets in EA induced neuroprotection against cerebral ischemic injury.

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Background: Sepsis often accompanies gastrointestinal motility disorder that contributes to the development of sepsis in turn. Propofol and dexmedetomidine, as widely used sedatives in patients with sepsis, are likely to depress gastrointestinal peristalsis. We queried whether propofol or dexmedetomidine, at sedative doses, aggravated sepsisinduced ileus. Methods: Sedative/Anesthetic Scores and vital signs of lipopolysaccharide (LPS)-induced endotoxemic mice were measured during sedation with propofol or dexmedetomidine. Endotoxemic mice were divided into 10% fat emulsion, propofol, saline, and dexmedetomidine group. The gastric emptying, small intestinal transit, tests of colonic motility, gastrointestinal transit and whole gut transit were evaluated at 15 mins and 24 h after intraperitoneal injection of sedatives/vehicles respectively. Results: 40 mg•kg − 1 propofol and 80 μg•kg − 1 dexmedetomidine induced a similar depth of sedation with comparable vital signs except that dexmedetomidine strikingly decreased heart rate in endotoxemic mice. Dexmedetomidine markedly inhibited gastric emptying (P = 0.006), small intestinal transit (P = 0.006), colonic transit (P = 0.0006), gastrointestinal transit (P = 0.0001) and the whole gut transit (P = 0.034) compared with the vehicle, whereas propofol showed no depression on all parts of gastrointestinal motility 15 mins after administration. The inhibitive effects of dexmedetomidine in these tests vanished 24 h after the administration. Conclusions: Deep sedation with dexmedetomidine, but not propofol, significantly inhibited gastrointestinal peristalsis in endotoxemic mice while the inhibitory effect disappeared 24 h after sedation. These data suggested that both propofol and dexmedetomidine could be applied in septic patients while dexmedetomidine should be used cautiously in patients with cardiac disease or ileus.

Background Gastrointestinal functional recovery is an important factor affecting postoperative outcome. The aim of this study was to evaluate the effect of transcutaneous electrical acupoint stimulation (TEAS) on gastrointestinal function in women undergoing cesarean section. Methods 150 pregnant women undergoing cesarean section were randomly allocated into TEAS, nonacupoint stimulation (sham group), and no stimulation (control group). The primary outcome was indications of gastrointestinal functional recovery and the secondary outcomes included time to first mobilization, postoperative hospital stay, daily living activities at one week after surgery, postoperative side-effects, and serum levels of gastroenterological hormones. Results The time to first flatus in TEAS group was significantly shorter compared to control (P=0.004) and sham groups (P=0.003). The time to first oral liquid and solid intake was significantly shorter than that in control (P<0.001; P=0.021) and sham group (P=0.019; P=0.037). Besides, postoperative hospital stay was shorter in TEAS group than in control group (P=0.031) and sham group (P<0.001). TEAS also promoted daily living activities (P=0.001 versus control group and P=0.015 versus sham group). Postoperative complications were similar among all the groups except for the incidence of abdominal distention 24 h after surgery (P=0.013; P=0.040). The motilin level was increased by TEAS (P=0.014 versus control group and P=0.020 versus sham group). Conclusion TEAS accelerated gastrointestinal functional recovery after cesarean section, by reducing postoperative hospital length, and improved daily living activities after surgery. This effect was partially mediated by regulation of the gastroenterological hormones.

Neurotoxicity is induced by different toxic substances, including environmental chemicals, drugs, and pathogenic toxins, resulting in oxidative damage and neurodegeneration in mammals. The nervous system is extremely vulnerable to oxidative stress because of its high oxygen demand. Mitochondria are the main source of ATP production in the brain neuron, and oxidative stress-caused mitochondrial dysfunction is implicated in neurodegenerative diseases. H2S was initially identified as a toxic gas; however, more recently, it has been recognized as a neuromodulator as well as a neuroprotectant. Specifically, it modulates mitochondrial activity, and H2S oxidation in mitochondria produces various reactive sulfur species, thus modifying proteins through sulfhydration. This review focused on highlighting the neuron modulation role of H2S in regulating neurodegenerative diseases through anti-oxidative, anti-inflammatory, anti-apoptotic and S-sulfhydration, and emphasized the importance of H2S as a therapeutic molecule for neurological diseases.

Ligusticum chuanxiong (LC)-Gastrodia elata (GE) compatibility is widely used in the clinic for the treatment of migraine. It has been shown that the changes of neurotransmitters in the central nervous system are closely related to the pathogenesis of migraine; whether LC-GE compatibility might affect the neurotransmitters in migraine rats has not yet been studied. In this study, high performance liquid chromatography-fluorescence detector methods for quantification of serotonin (5-hydroxytryptamine, 5-HT) and excitatory amino acids (EAAs) in rat brain were developed. The 5-HT was measured directly, while EAAs were determined by using dansyl chloride as precolumn derivative reagent. The validation of the methods, including selectivity, linearity, sensitivity, precision, accuracy, recoveries, and stability were carried out and demonstrated to meet the requirements of quantitative analysis. Compared with the model group, the expression of 5-HT in migraine rat brain was enhanced from 30 minutes to 120 minutes and glutamate (L-Glu) was suppressed from 30 minutes to 60 minutes in an LC-GE (4:3) group compared with the model group (p < 0.05, p < 0.01, respectively). These findings showed that the analytical methods were simple, sensitive, selective, and low cost, and LC-GE 4:3 compatibility could have better efficacy for treating migraine through upregulating 5-HT levels and downregulating L-Glu levels.

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