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Previous studies have suggested that miR-324-3p is related to the pathophysiology of cerebral ischemia, but the mechanism underlying this relationship is unclear. In this study, we found that miR-324-3p expression was decreased in patients with acute ischemic stroke and in in vitro and in vivo models of ischemic stroke. miR-324-3p agomir potentiated ischemic brain damage in rats subjected to middle cerebral artery occlusion, as indicated by increased infarct volumes and cell apoptosis rates and greater neurological deficits. In a PC12 cell oxygen-glucose deprivation/reoxygenation model, a miR-324-3p mimic decreased cell viability and expression of the anti-apoptotic protein BCL2 and increased expression of the pro-apoptotic protein BAX and rates of cell apoptosis, whereas treatment with a miR-324-3p inhibitor had the opposite effects. Silencing miR-324-3p increased adenosine A1 receptor (A1R) expression through regulation of GATA binding protein 2 (GATA2). These findings suggest that silencing miR-324-3p reduces ischemic brain damage via the GATA2/A1R axis., Competing Interests: None

Objective: To explore the efficacy difference between electroacupuncture (EA) at "Zusanli" (ST36) and "Baihui" (GV20) for inflammatory pain and cerebral ischemia-reperfusion injury (CIRI) in rats., Methods: In 1st part of this study, 90 male SD rats were randomly divided into sham-operation, model (induced by occlusion of the middle cerebral artery and reperfusion), GV20 EA, ST36 EA，and sham EA groups ( n =16 in each group). In the 2nd part of the study, 40 male SD rats were randomized into saline injection (control), inflammatory pain model (subcutaneous injection of complete Freund's adjuvant ［CFA］ into the right paw), ST36 EA, GV20 EA, and sham EA groups ( n =8 in each group). In these two parts, EA (2 Hz/15 Hz, 1 mA) was applied to ST36 or GV20. The mechanical withdrawal threshold (MWT) and thermal withdrawal latency （TWL） were detected 2.5 h after administration of CFA by using Von Frey and plantar tester, respectively. The neurological deficit scores (NDS) were assessed by using Longa's method and the infarct size of the brain assessed after staining with 2% triphenyltetrazolium chloride (TTC). The expression of c-fos protein in the dorsal horns (DHs) of the spinal cord was detected by immunohistochemistry., Results: (1) Twenty-four hours following CIRI, the NDS and infarct volume were significantly increased in the model group compared with the sham-operation group ( P <0.01), and obviously decreased in the GV20 EA and ST36 EA groups relevant to the CIRI model group ( P <0.05, P <0.01). There were no significant differences between the two EA groups in the NDS and infarct volume levels ( P >0.05). (2) After administration of CFA, both the MPT and TPT were notably decreased in the inflammatory pain model group in contrast to the saline-injection group ( P <0.01), but were considerably increased in both ST36 EA and GV20 EA groups ( P <0.05), rather than in the sham EA group ( P >0.05). The number of c-fos positive cells was significantly increased in the medial half of I-II and III-IV lamina of DHs in the L4-L6 segments of spinal cord in the inflammatory pain model group relevant to the saline-injection group ( P <0.01, P <0.05), and was remarkably decreased in the lamina I-II (not in the deeper lamina) in both ST36 EA and GV20 EA groups ( P <0.01), rather than in the sham EA group ( P >0.05). No significant differences were found in the number of c-fos positive cells between the ST36 EA and GV20 EA groups ( P >0.05)., Conclusion: Our data do not support the specificity of functions at least between GV20 EA and ST36 EA in both CIRI and inflammatory pain model rats. This is the first study reporting the effect of EA at GV20 for relieving CFA-induced inflammatory pain.

Objective: To observe the effect of acupoint stimulation on the quality of recovery in patients with radical thyroidectomy under the concept of enhanced recovery after surgery (ERAS)., Methods: A total of 62 patients with radical thyroidectomy were randomized into an observation group and a control group, 31 cases in each one. In both of the two groups, general anesthesia with tracheal intubation was applied, the same anesthesia induction and maintenance medication were given. In the observation group, auricular point pressing with magnetic beads was adopted at bilateral shenmen (TF 4 ) and transcutaneous electrical acupoint stimulation (dilatational wave, 2 Hz/100 Hz in frequency, 6 to 12 mA) was performed at bilateral Hegu (LI 4) and Neiguan (PC 6) from 30 min before anesthesia induction to the end of the anesthesia. In the control group, medical adhesive plaster was pasted at bilateral shenmen (TF 4 ) and the electrodes were plastered at bilateral Hegu (LI 4) and Neiguan (PC 6) with no corresponding stimulation. In both of the two groups, visual analogue scale for anxiety (VAS-A) score was observed to evaluate the anxiety severity before anesthesia induction; the total intraoperative dosages of sufentanil, remifentanil and propofol were recorded; the numerical rating scale (NRS) score was used to assess the pain severity of instant time (T0) and 30 min (T1) of entering post-anesthesia recovery room (PACU), motor and static mode at 2 h (T2), 6 h (T3), 12 h (T4), 24 h (T5) after surgery; time of first anal exhaust, time of getting out of bed after surgery, total hospitalization time and the incidences of postoperative nausea and vomiting were observed; the quality of recovery was assessed by the 40-item quality of recovery score (QoR-40)., Results: The VAS-A score and the total intraoperative dosage of remifentanil in the observation group were reduced compared with the control group ( P <0.05). The NRS scores at T0-T4 in the observation group were lower than those in the control group ( P <0.01, P <0.05), while the difference between the two groups in NRS score at T5 was not significant ( P >0.05). The time of first anal exhaust and getting out of bed after surgery in the observation group were advanced than those in the control group ( P <0.05), there was no significant difference between the two groups in total hospitalization time and incidences of postoperative nausea and vomiting ( P >0.05). Compared with the control group, the QoR-40 score was increased in the observation group ( P <0.05)., Conclusion: Acupoint stimulation can improve the preoperative anxiety in patients with radical thyroidectomy, reduce the intraoperative anesthetic dosage and postoperative pain, advance the time of anal exhaust and getting out of bed, improve the quality of postoperative recovery and enhance the recovery process.

The activation of adenosine A1 receptors is important for protecting against ischemic brain injury and pretreatment with electroacupuncture has been shown to mitigate ischemic brain insult. The aim of this study was to test whether the adenosine A1 receptor mediates electroacupuncture pretreatment-induced neuroprotection against ischemic brain injury. We first performed 30 minutes of electroacupuncture pretreatment at the Baihui acupoint (GV20), delivered with a current of 1 mA, a frequency of 2/15 Hz, and a depth of 1 mm. High-performance liquid chromatography found that adenosine triphosphate and adenosine levels peaked in the cerebral cortex at 15 minutes and 120 minutes after electroacupuncture pretreatment, respectively. We further examined the effect of 15 or 120 minutes electroacupuncture treatment on ischemic brain injury in a rat middle cerebral artery-occlusion model. We found that at 24 hours reperfusion,120 minutes after electroacupuncture pretreatment, but not for 15 minutes, significantly reduced behavioral deficits and infarct volumes. Last, we demonstrated that the protective effect gained by 120 minutes after electroacupuncture treatment before ischemic injury was abolished by pretreatment with the A1-receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (1 mg/kg, intraperitoneally). Our results suggest that pretreatment with electroacupuncture at the Baihui acupoint elicits protection against transient cerebral ischemia via action at adenosine A1 receptors., Competing Interests: Conflicts of interest: None declared.

Objective: To study the effect of transcutaneous acupoint electrical stimulation (TAES) on stress who received propofol target controlled infusion (TCI) general anesthesia in brain surgery., Methods: Totally 40 neurosurgical patients of I-II grade (ASA grading) in our hospital were randomly divided into the TAES group (T group) and the control group (C group), 20 in each group. All patients received intravenous anesthesia by propofol TCI. The TAES intervention was adopted in those of C group. Electrodes were only applied to corresponding acupoints without electric stimulation. The arterial blood was withdrawn before TAES (T0), before anesthesia (T1), before cutting (T2), at 60 min after encephalic incision (T3), immediately after incisions suture (T4), at about 10 min after removing tracheal catheters (T5) to detect beta-endorphin (beta-EP), cortisol (COR), adrenalin (E), blood sugar (Glu). The heart rate (HR) and mean arterial pressure (MAP) were recorded. The total time of surgery, anesthesia, total infusion amount, blood lost amount, and urine amount were recorded., Results: In both groups, HR, MAP, COR, and E at T2 were lower than at T0 significantly (P < 0.05). beta-EP in group C at T2 was lower than at T0 significantly (P < 0.05). HR, MAP, COR in group C at T3 were higher than at T0 significantly (P < 0.05). HR, MAP, E, and Glu in group C at T4 and T5 were higher than at T0 significantly (P < 0.05). beta-EP in group T at T1 and T3 were higher than at T0 significantly (P < 0.05). HR, COR, E, Glu, and beta-EP in group T at T4 and T5 were higher than at T0 significantly (P < 0.05). Between groups, comparing with the time point T0, the amplitude of variation of MAP, COR, and E at T2 in group C were significantly less (P < 0.05); the amplitude of variation of HR, MAP, and COR at T3 in group C were less significantly, when compared with the time point T0 (P < 0.05); the amplitude of variation of HR, MAP, COR, E, and Glu at T4 and T5 in group C were less significantly, when compared with the time point T0 (P < 0.05). When comparing the two groups, the amplitude of variation of beta-EP at time points of T1, T3, T4, and T5 in group T were larger than at T0 in group C (P < 0.05)., Conclusion: TAES could reduce stress and stabilize the internal environment when used in brain surgery with propofol TCI general anesthesia.

Objective: To observe the effect of transcutaneous acupoint electrical stimulation (TAES) combined with target controlled infusion of Propofol on the doses of Propofol and adjuvant drugs, and on the resuscitation time of general anesthesia for craniotomy patients., Methods: Forty patients (aged 27 - 65 years), scheduled for craniotomy and signed the informed consent, were randomly and equally divided into TAES group and control group. Patients of the two groups received intravenous anesthesia mainly with target controlled infusion of Propofol. TAES (2 Hz/100 Hz, 1-12 mA) was applied to bilateral Yuyao (EX-HN 4) and Taiyang (EX-HN5) for 20 min first before surgery, and then to bilateral Hegu (LI 4), Quanliao (SI 18) and Fengchi (GB 20) during operation and till the end of the operation. The dosages of Propofol and adjuvant drugs, the duration of surgery and anesthesia, and the time of resuscitation and extubation were recorded., Results: Compared with the control group, the dosages of Propofol and Nicardipine for craniotomy patients in the TAES group were significantly lower (P < 0.05), and the resuscitation time was obviously earlier and the tracheal catheter indwelling time markedly shorter in the TAES group (P < 0.05)., Conclusion: TAES combined with target controlled infusion of Propofol can reduce the dosage of Propofol and Nicardipine, and shorten the resuscitation time and tracheal catheter indwelling time in craniotomy patients.

Objective: To investigate whether local A1R of Baihui acupoint mediate cerebral ischemia tolerance induced by electro-acupuncture (EA)., Methods: Sixty SD rats were randomly divided into five groups, i.e., the sham-operation (S) group, the model group (M), the electroacupuncture (E) group, the CCPA group and the DMSO group. The focal cerebral ischemia/reperfusion model was established by middle cerebral artery occlusion (MCAO) in rats. Rats in the E group were received EA pretreatment baihui acupoint at 2 h before established MCAO. The rats in DMSO group and the CCPA group were injected with DMSO (20 µl) and CCPA (0.1 mmol/L) 20 µl into Baihui, respectively, at 2 h before established MCAO. After 24 h reperfusion, the rats' behavior, cerebral infarct volume, the cerebral Bcl-2 protein expression were assessed., Results: Compared with M group, the rats' behavior was improved, the cerebral infarct volume was decreased and the Bcl-2 protein expression was up-regulated (P < 0.05) in the E group. Compared with M and DMSO group, the rats' behavior was improved, the cerebral infarct volume was decreased and the Bcl-2 protein expression was up-regulated (P < 0.05) in the CCPA group. There were no statistical differences between CCPA and E group., Conclusions: EA induced cerebral ischemia tolerance. Local A1R of Baihui acupoint possible mediate cerebral ischemia tolerance induced by Electroacupuncture.

Objective: To observe the electroacupuncture (EA) pretreatment at Baihui (GV20) on the concentration of adenosine deaminase (ADA) and adenosine, and to evaluate its effects on the neurologic function score and the infarction volume after middle cerebral artery occlusion (MCAO) ischemia/reperfusion (I/R), thus exploring its mechanisms for relieving the ischemia/reperfusion injury., Methods: Totally 54 male SD rats were randomly divided into 3 groups, the sham-EA group, the EA group, and the control group, 18 in each group. Rats in the control group were not intervened after anesthesia. Rats in the EA group were needled at Baihui (GV20) for 30 min. Rats in the sham-EA group received the same procedure as those performed in the EA group without electricity connected. The changes of adenosine and ADA contents were detected at 30, 60, and 120 min after EA respectively. The I/R model was established. Totally 48 male SD rats were randomly divided into 6 groups, i.e., the model group (Group A), the EA group (Group B), the EA +8-Cyclopentyl-1,3-dipropylxanthine (DPCPX) group (Group C), the EA + DMSO group (Group D), the Deoxycoformycin (Deo) group (Group E), and the normal saline group (Group F). Rats in Group B, C, and D received EA for 30 min before modeling. Rats in Group C and D were peritoneally injected with DPCPX (1 mg/kg) and DMSO (1 mL/kg) at 30 min before EA. The neurologic function score was evaluated and the infarct volumes were detected after 24-h reperfusion., Results: Compared with the sham-EA group, there was no statistical difference in the contents of the adenosine or ADA in the control group at each time point (P > 0.05). Compared with the control group at the same time point, the content of ADA significantly decreased at 60 min in the EA group [(315.0 +/- 22.9 U/L), P < 0.05], and restored to the normal level at 120 min after EA. The content of adenosine increased in the EA group at 120 min [(20.4 +/- 2.2) ng/microL, P < 0.05]. Compared with the model group, the neurologic function score decreased (P < 0.05) and the infarct volumes were obviously reduced (P < 0.01) in Group B, D and E. There was no statistical difference in the neurologic function score or the infarct volumes in other groups, when compared with the model group (P > 0.05), Conclusion: EA at Baihui (GV20) showed protective effects on the cerebral I/R rats, which might be achieved through lowering the ADA concentration and elevating the adenosine content, and further activating adenosine A1 receptor.

Objective: To investigate the effects of nimodipine on symptomatic cerebral vasospasm in rabbits., Methods: Twenty four japanese white rabbits which ligation of bilateral common carotid arteries and no neurological deficits were randomized to sham-operation, subarachnoid hemorrhage (SAH) and nimodipine which injected of nimodipine 0.1 mg/kg, continuous vein administration 5 day. The behavior scores, neurological scores were observed everyday and cerebral angiography changes were measured twice by 3D-CTA, and basilar artery was removed for pathological examination after last CTA examination., Results: In SAH group, The basilar artery were significantly vasoconstrictive on 5 days, neurological scores were increased, and the basilar artery was found apoptosis-like changes under light microscopic and electron microscope. Nimodipine group could not dilated the basilar artery arteriospasm after SAH, but it could attenuate neurological deficit, and obviously alleviate the pathological changes of basilar artery., Conclusion: Nimodipine could not vasodilation of basilar artery in SCVS, but obviously could alleviate neurological changes and pathological changes of basilar artery in rabbits with symptomatic cerebral vasospasm.

Objective: To evaluate the effects of urinary kallidinogenase on subarachnoid hemorrhage (SAH) in rabbits., Methods: Rabbits symptomatic cerebral vasospasm model was built though Endo method, among the 40 rabbits, 8 died or had severe nervous system syndrome, the other 32 were randomly divided into 4 groups:group A, control group, injection of normal saline to the cisterna magna;group B, subarachnoid hemorrhage;group C, injection of human urinary tissue kallikreins;group D, treated with Nimodipine. The behavior scores, neurological scores and cerebral angiography changes were observed., Results: Food intake obviously decreased and neurological deficit were seen in group B, while which were attenuated in group C and group D, and group A was normal. Comparing the diameter of basilar artery was (1.9 +/- 0.3) mm before SAH, the diameter of group B 4 d later was (1.5 +/- 0.3) mm, 7 d later (1.4 +/- 0.3) mm, the difference was significant (P < 0.05). Comparing with group C on the day 4th and 7th, the diameters of basilar artery were significantly different (P < 0.001). Comparing with group D on the day 4th, 7th and 14th, there was no obvious improvement., Conclusion: Urinary kallidinogenase and Nimodipine can obviously alleviate symptomatic cerebral vasospasm in rabbits remarkably, but the former's effect of attenuating vasospasm is better than that of Nimodipine.