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Electroacupuncture (EA) at the Neiguan acupoint (PC6) has shown significant cardioprotective effects. Sympathetic nerves play an important role in maintaining cardiac function after myocardial infarction (MI). Previous studies have found that EA treatment may improve cardiac function by modulating sympathetic remodeling after MI. However, the mechanism in how EA affects sympathetic remodeling and improves cardiac function remains unclear. The aim of this study is to investigate the cardioprotective mechanism of EA after myocardial ischemic injury by improving sympathetic remodeling and promoting macrophage M2 polarization. We established a mouse model of MI by occluding coronary arteries in male C57/BL6 mice. EA treatment was performed at the PC6 with current intensity (1 mA) and frequency (2/15 Hz). Cardiac function was evaluated using echocardiography. Heart rate variability in mice was assessed via standard electrocardiography. Myocardial fibrosis was evaluated by Sirius red staining. Levels of inflammatory factors were assessed using RT-qPCR. Sympathetic nerve remodeling was assessed through ELISA, western blotting, immunohistochemistry, and immunofluorescence staining. Macrophage polarization was evaluated using flow cytometry. Our results indicated that cardiac systolic function improved significantly after EA treatment, with an increase in fractional shortening and ejection fraction. Myocardial fibrosis was significantly mitigated in the EA group. The sympathetic nerve marker tyrosine hydroxylase and the nerve sprouting marker growth-associated Protein 43 were significantly reduced in the EA group, indicating that sympathetic remodeling was significantly reduced. EA treatment also promoted macrophage M2 polarization, reduced levels of inflammatory factors TNF- α , IL-1 β , and IL-6, and decreased macrophage-associated nerve growth factor in myocardial tissue. To sum up, our results suggest that EA at PC6 attenuates sympathetic remodeling after MI to promote macrophage M2 polarization and improve cardiac function., Competing Interests: The authors declare that they have no competing interests., (Copyright © 2024 Rou Peng et al.)

Carfilzomib (CFZ), a proteasome inhibitor commonly used in the treatment of multiple myeloma (MM), exhibits limited clinical application due to its cardiotoxicity. In our study, electroacupuncture (EA) at Neiguan acupoint (PC6) effectively reversed CFZ-induced reduction in ejection fraction (EF) and fractional shortening (FS), demonstrating great potential effect for heart protection. Through comparative analysis of the transcriptome profile from heart samples of mice treated with DMSO control, CFZ injection, and EA stimulation, we identified a total of 770 differentially expressed genes (DEGs) in CFZ (vs. Control) group and 329 DEGs in EA (vs. CFZ) group. Specifically, CFZ (vs. Control) group exhibited 65 up-regulated DEGs and 705 down-regulated DEGs, while EA (vs. CFZ) group displayed 251 up-regulated DEGs and 78 down-regulated DEGs. Metascape analysis revealed that among these treatment groups, there were 137 co-expressed DEGs remarkably enriched in skeletal system development, cellular response to growth factor stimulus, negative regulation of Wnt signaling pathway, and muscle contraction. The expression patterns of miR-8114, Myl4, Col1a1, Tmem163, Myl7, Sln, and Fxyd3, which belong to the top 30 DEGs, were verified by quantitative real-time PCR (RT-qPCR). In summary, this study firstly discloses novel insights into the regulatory mechanisms underlying PC6-based EA therapy against CFZ-induced cardiotoxicity, potentially serving as a theoretical foundation for further clinical applications., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background: Accumulating evidence suggests that acupuncture may serve as a potent strategy to mitigate the deleterious effects of ischemic stroke on neural tissue. The present investigation delineated the neuroprotective potential of electroacupuncture (EA) administered pre-and post-stroke, with a focus on determining the commonalities and disparities between these two therapeutic approaches in ameliorating ischemic stroke-induced brain injury. The ultimate objective is to inform optimal timing for acupuncture intervention in the clinical management and prevention of stroke., Methods: The extent of cerebral infarction was quantified with 2,3,5-triphenyltetrazolium chloride staining. The integrity of the blood-brain barrier was assessed by evaluating the extravasation of Evans blue (EB) dye, while neurological function was appraised using the Longa neurological scoring system. RNA sequencing was employed to examine the transcriptomic landscape of ischemic brain tissue, with subsequent bioinformatics annotation of the sequencing data facilitated by Metascape., Results: (1) A notable decrease in the ischemic infarct volume was observed in both the EA-preconditioned plus middle cerebral artery occlusion (MCAO), EA-preconditioned plus middle cerebral artery occlusion (EAM) and MCAO plus EA-treated (MEA) groups, compared to the MCAO group. Furthermore, the decreased leakage of EB and reduction in neurological function impairment scores were evident in the EAM and MEA groups compared with the MCAO group. (2) Relative to the Sham group, the MCAO group exhibited a total of 4798 differentially expressed genes (DEGs), with 67.84% demonstrating an expression fold change (FC) greater than 1.5, and 34.16% exceeding a FC of 2. The EAM and MEA groups displayed 4020 and 1956 DEGs, respectively, compared to the MCAO group. In both groups, more than 55% of DEGs showed an expression FC surpassing 1.5, whereas only approximately 10% exhibited a change greater than 2-fold. Remarkably, EA preconditioning and EA treatment resulted in the reversal of 18.72% and 28.91% of DEGs, respectively, in the MCAO group. (3) The DEGs upregulated in response to ischemic stroke were predominantly implicated in immune inflammatory processes and cellular apoptosis, whereas the downregulated DEGs were associated with neurogenesis and neuronal signal transduction. The MEA-induced upregulated DEGs were primarily involved in neural transmission and metabolic processes, whereas the downregulated DEGs were linked to excessive inflammatory responses to physical and chemical stimuli, as well as cell matrix adhesion chemotaxis. In the context of EAM, the upregulated DEGs were chiefly related to protein biosynthesis, and energy and metabolic processes, whereas the downregulated genes were connected to gene transcriptional activity, synaptic function, and neuronal architecture., Conclusions: Both preconditioning and post-event treatment with acupuncture demonstrated efficacy in mitigating pathological damage to brain tissue in a rat model of ischemic stroke, albeit with some divergences in their gene targets. The integration of EA preconditioning and treatment may potentially confer enhanced neuroprotection in the clinical management of stroke patients., Competing Interests: The authors declare no conflict of interest., (© 2023 The Author(s). Published by IMR Press.)

Background: Electro-acupuncture (EA) is an effective and safe treatment for ischemic stroke. It is not only capable of reducing cerebral damage but also alleviating intestinal inflammation. However, its mechanism has not been fully elucidated., Methods: All rats were randomly divided into three experimental groups: the SHAM group, the MCAO group, and the MEA (MCAO+EA) group. Ischemic-reperfusion (I/R) injury was induced by MCAO surgery. Rats in the MEA group were treated with EA stimulation in the "Baihui" acupoint (1 mA, 2/15 Hz, 20 min for each time). The Real-time (RT)-qPCR was used to evaluate the mRNA expression of inflammation factors in the ischemic brain and the small intestine after I/R injury. In addition, our research evaluated the effects of EA on regulatory T cells (Tregs) and γδ T cells in the small intestine and brain via Flow cytometry analysis. Finally, we applied CM-Dil and CFSE injection and explored the potential connections of T cells between the ischemic hemisphere and the small intestine., Results: Our results suggested that EA treatment could significantly reduce the inflammation response in the ischemic brain and small intestine 3 days after I/R injury in rats. To be specific, EA increased the percentage of Tregs in the brain and the small intestine and decreased intestinal and cerebral γδ T cells. Concomitantly, after EA treatment, the percentage of cerebral CD3 + TCRγδ + CFSE + cells dropped from 12.06% to 6.52% compared with the MCAO group., Conclusions: These findings revealed that EA could regulate the Tregs and γδ T cells in the ischemic brain and the small intestine, which indicated its effect on inhibiting inflammation. And, EA could inhibit the mobilization of intestinal T cells, which may contribute to the protection of EA after ischemic stroke., Competing Interests: Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: Previous studies had suggested that electroacupuncture (EA) can promote white adipose tissue (WAT) browning to counter obesity. But the mechanism was still not very clear., Aim: In this study, we aim to study the effect of EA on promoting inguinal WAT (iWAT) browning and its possible mechanism., Method: Three-week-old rats were randomly divided into a normal diet (ND) group and a high-fat diet (HFD) group. After 10 weeks, the HFD rats were grouped into HFD + EA group and HFD control group. Rats in the EA group were electro-acupunctured for 4 weeks on Tianshu (ST25) acupoint under gas anesthesia with isoflurane, while the rats in HFD group were under gas anesthesia only. Body weight and cumulative food intake were monitored, and H&E staining was performed to assess adipocyte area. The effect of EA on WAT was assessed by qPCR, immunoblotting, immunoprecipitation and Co-immunoprecipitation. Mitochondria were isolated from IWAT to observe the expression of mitochondrial transcription factor A (TFAM)., Results: The body weight, WAT/body weight ratio and cumulative food consumption obviously decreased (P < 0.05) in the EA group. The expressions of brown adipose tissue (BAT) markers were increased in the iWAT of EA rats. Nevertheless, the mRNA expressions of WAT genes were suppressed by 4-week EA treatment. Moreover, EA increased the protein expressions of SIRT-1, PPAR γ , PGC-1 α , UCP1 and PRDM16 which trigger the molecular conversion of iWAT browning. The decrease of PPAR γ acetylation was also found in EA group, indicating EA could advance WAT-browning through SIRT-1 dependent PPAR γ deacetylation pathway. Besides, we found that EA could activate AMPK to further regulate PGC-1 α -TFAM-UCP1 pathway to induce mitochondrial biogenesis., Conclusion: In conclusion, EA can remodel WAT to BAT through inducing SIRT-1 dependent PPAR γ deacetylation, and regulating PGC-1 α -TFAM-UCP1 pathway to induce mitochondrial biogenesis. This may be one of the mechanisms by which EA affects weight loss., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Tang, Lu, Xu, Wang, Lu, Yu, Jing and Yuan.)

Electroacupuncture (EA) has been developed on the basis of traditional Chinese acupuncture. EA can suppress craving in opioid addicts and opioid-seeking responses in rodents. However, the molecular mechanism of EA on the rewarding properties of morphine and craving responses is not known. Here, we have applied a conditioned place preference paradigm in mice to measure morphine-induced rewarding effects along with EA treatment. Circular RNAs (circRNAs) can function as micro RNA (miRNA) sponges to effectively regulate gene expression levels. CircRNA profiling within the nucleus accumbens (NAc) was performed in EA-treated and sham-treated mice. Following RNAseq, data were analyzed by gene ontology (GO) and Kyoto Encyclopedia Genes and Genomes (KEGG) tools. We identified 112 significantly differentially expressed circRNAs, including 51 that were up-regulated and 61 that were down-regulated. Our bioinformatics analyses show that these differentially expressed circRNAs map into pathways that are mainly involved with renin secretion and the cGMP-PKG signaling. We further constructed a circRNA-miRNA network that predicts the potential roles of the differentially expressed circRNAs and the interaction of circRNAs with miRNAs. Our secondary sequencing and bioinformatics analysis in the NAc after EA treatment on morphine-induced CPP provides putative novel targets on molecular mechanisms involved in morphine reinforcement and possibly craving., (© 2019 Society for the Study of Addiction.)

Myocardial ischemia/reperfusion (I/R) is an important complication of reperfusion therapy for myocardial infarction, and trimetazidine is used successfully for treatment of ischemic cardiomyopathy by regulating mitochondrial function. Moreover, electroacupuncture (EA) preconditioning was demonstrated to be cardioprotective in both in vivo rodent models and in patients undergoing heart valve replacement surgery. However, the mechanisms have not been well elucidated. Mitophagy, mediated by the mTORC1-ULK1-FUNDC1 (mTOR complex 1-unc-51-like autophagy-activating kinase 1-FUN14 domain-containing 1) pathway, can regulate mitochondrial mass and cell survival effectively to restrain the development of myocardial ischemia/reperfusion injury (MIRI). In this study, we hypothesized that EA preconditioning ameliorated MIRI via mitophagy. To test this, rapamycin, an mTOR inhibitor, was used. The results showed that EA preconditioning could reduce the infarct size and risk size, and decrease the ventricular arrhythmia score and serum creatine kinase-myocardial band isoenzyme (CK-MB), lactate dehydrogenase (LDH), and cardiac troponin T (cTnT) in MIRI rats. Moreover, it also attenuated MIRI-induced apoptosis and mitophagy accompanied by elevated mTORC1 level and decreased ULK1 and FUNDC1 levels. However, these effects of EA preconditioning were blocked by rapamycin, which aggravated MIRI, reduced adenosine triphosphate (ATP) production, and antagonized infarct size reduction. In conclusion, our results indicated that EA preconditioning protected the myocardium against I/R injury by inhibiting mitophagy mediated by the mTORC1-ULK1-FUNDC1 pathway., Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest., (Copyright © 2020 The Author(s). Published by Elsevier Masson SAS.. All rights reserved.)

Aims: Electro-acupuncture (EA) is frequently recommended as a complementary therapy for premature ovarian failure (POF) in the clinical. However, little information exists about its potential treatment mechanisms. The study was designed to observe the effect of EA to ovarian function and fertility in POF mice model, and investigated its potential mechanisms on PI3K/AKT/mTOR signaling pathway., Materials and Methods: Forty-five female C57/BL6 mice were divided into the Control, the Model and the EA group. The ovaries morphology of mice was observed by hematoxylin and eosin (HE) staining, and all follicles were counted under microscope. The protein expression of PI3K, phospho-PI3K, AKT, phospho-AKT, mTOR, phospho-mTOR, S6, phospho-S6, 4E-BP1 and phospho-4E-BP1 were detected by western blotting. The data was presented as the ratio of phosphorylation protein to total protein. Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol (E 2 ) and anti-Mullerian hormone (AMH) levels were measured by enzyme-linked immunosorbent assay (ELISA). The fertility was observed by giving treated mice 8 weeks for breeding., Key Findings: We found that primordial follicle counts were increased in EA group compared to Model group. The phosphorylation of PI3K, AKT, mTOR, 4E-BP1 and S6K in EA group significantly reduced compared to Model group. Serum FSH and LH levels in EA group were decreased compared to Model group, while, serum E 2 and AMH levels in EA group were increased compared with Model group. The litter size in EA group was improved compared to Model group., Significance: The effects of EA on the PI3K/AKT/mTOR signaling pathway may represent one of the mechanisms involved in attenuating the mice POF., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Objective: To compare the effects of electroacupuncture (EA) at different time during reperfusion on the expression of autophagy-related protein Bcl-2 and Beclin1 in myocardial tissue in rats with myocardial ischemia reperfusion injury (MIRI), and to explore the autophagy-related mechanism of EA on protecting MIRI., Methods: A total of 72 SD rats were randomly divided into a sham operation group, a model group, a RA group, a RB group, a RC group and a RD group, 12 rats in each group. Except the sham operation group, the rats in the remaining groups were treated with ligating the left anterior descending artery (LAD) for 30 minutes followed by reperfusion to establish the model of MIRI. The rats in the sham operation group were treated with crossing a line through the LAD. The rats in the model group did not receive treatment. The rats in the RA group, RB group, RC group and RD group were treated with EA at "Neiguan" (PC 6) for 20 min, starting at 0 h, 0.5 h, 1 h, 2 h after reperfusion. Evans Blue-TTC double-staining was employed to evaluate myocardial infarct size; the serum CK-MB was detected by ELISA and the expression of Bcl-2 and Beclin1 protein in myocardial tissue were detected by Western blot., Results: Compared with the model group, the percentage of myocardial infarct size in the RB group, RC group and RD group was decreased significantly (all P <0.05), and the reduction in the RB group was more significant than that in the RC group and RD group (both P <0.05). Compared with the sham operation group, the expression of CK-MB and Beclin1 in the model group was significantly increased, but the expression of Bcl-2 was significantly decreased (all P <0.01). Compared with the model group, the expression of CK-MB and Beclin1 was decreased significantly in RA group, RB group, RC group and RD group (all P <0.05), but the expression of Bcl-2 was significantly increased (all P <0.05). Compared with the RA group, the expression of CK-MB was decreased in the RB group and RC group (both P <0.05) but the expression of Bcl-2 was increased (both P <0.01); the expression was not significantly different from that in the RD group ( P >0.05); the increasing of Bcl-2 in the RB group was more significant than that in RC group ( P <0.05). The expression of Beclin 1 in the RB group was significantly lower than that in the RA group ( P <0.05), but there was no significant difference among other EA groups (all P >0.05)., Conclusion: EA at different time during reperfusion could reduce myocardial infarct size in rats with MIRI, and EA at 0.5 h after reperfusion has best efficacy; this protective effect may be achieved by increasing Bcl-2 expression and reducing Beclin1 expression to inhibit overautophagy during reperfusion.

Objective: To investigate the difference of protective effect of electroacupuncture (EA) at different times pretreating myocardial ischemia-reperfusion injury (MIRI) and the protein expressions of ULK1 and Beclin-1 in myocardial tissue, so as to explore the relation of the difference and autophagic mechanism., Methods: Sixty-three male SD rats were randomized into 7 groups, a sham group, a model group, an EA pretreating for 1 d (EA-1d) group, an EA pretreating for 2 d (EA-2d) group, an EA pretreating for 3 d (EA-3d) group, an EA pretreating for 4 d (EA-4d) group, an EA pretreating for 5 d (EA-5d) group, 9 rats in each group. All the rats in the pretreating groups were treated with EA 1-5 days before MIRI surgery. EA (2 Hz/100 Hz, 2 mA) was used at bilateral "Neiguan (PC 6)" for 20 min. All the rats except for those in the sham group was underwent left thoracotomy and ligation of the left anterior descending (LAD) coronary artery for 30 minutes followed by 4 hours of reperfusion to establish the MIRI model. The same operation was performed in the sham group except for the ligation of the LAD. Throughout the experiment, electrocardiogram was continuously monitored. The myocardial infarct sizes were assessed by Evans blue and triphenyltetrazolium chloride (TTC) staining. The serum concentrations of cardiac troponinⅠ(cTnⅠ) was detected by ELISA. The expressions of ULK1 and Beclin-1 in the heart tissues were analyze by Western blot., Results: Compared with the sham group, the concentrations of cTnⅠ and the protein expressions of ULK1 and Beclin-1 increased in the model group (all P <0.05). Compared with the model group, the infarct sizes decreased in the EA-1d, EA-2d, EA-3d, EA-4d and EA-5d groups (all P <0.05), with less risk sizes in the EA-3d, EA-4d and EA-5d groups (all P <0.05). The levels of cTnⅠin the EA-4d and EA-5d groups decreased ( both P <0.05); the expressions of ULK1 protein decreased in the EA-1d, EA-2d, EA-3d, EA-4d and EA-5d groups (all P <0.05); the expressions of Beclin-1 protein decreased in the EA-2d, EA-3d, EA-4d and EA-5d groups (all P <0.05). The infarct sizes in the EA-4d and EA-5d groups were lower than that in the EA-1d group (both P< 0.05). The cTnⅠconcentration in the EA-4d group was less than that in the EA-1d group ( P <0.05)., Conclusion: Pretreatment with EA for 1-5 days can improve the infarct size in MIRI, with better effect of the pretreatment for 4-5 days. The cardioprotective effect may be related to the inhibition of autophagy. But the difference of the protective effects is not related to the protein expressions of ULK1 and Beclin-1.

Objective: To explore the impact of electroacupuncture (EA) on the AMPKα-HDAC5-HIF-1α signaling in the heart of the rats with myocardial ischemia (MI) via detecting the expressions of AMP-activated protein kinase α (AMPKα), histone deacetylase 5 (HDAC5), hypoxia inducible factor (HIF-1α) and vascular endothelial growth factor (VEGF)., Methods: Thirty-six healthy male SD rats were randomized into a sham operation group (6 rats), a sham + EA group (6 rats), a model group (12 rats) and an EA group (12 rats). We ligated the left anterior descending artery (LAD) for MI model, and exposed the heart of rats after opening the chest without ligation for the rats in the sham operation gorup and the sham + EA group. On the 2nd day after LAD ligation, EA was applied at "Neiguan" (PC 6) with 2 Hz/15 Hz and 1.5-2 mA for 30 min in the EA group and sham+EA group, once a day for 4 days. The same fixation was used in the sham operation group and the model group, without EA. Myocardial infarction area was observed by TTC staining and serum cardiac troponin T (cTnT) was detected by radioimmunoassay. The expression of VEGF mRNA was detected by real time PCR. The protein expressions of AMPKα, HDAC5, HIF-1α and VEGF were detected by western blot., Results: Compared with the sham operation group, 4 days after LAD ligation, the myocardial infarction was obvious and the expression of serum cTnT increased in the model group ( P <0.01); and the proterin expression of HIF-1α in myocardial tissue ascended ( P <0.01); the expression of VEGF mRNA decreased ( P <0.05); the changes of the protein expressions of AMPKα、HDAC5、VEGF were not obvious (all P >0.05). After EA for 4 days, the myocardial infarction area and cTnT expression decreased in the EA group (both P <0.01); the VEGF mRNA and protein expressions and AMPKα, HDAC5, HIF-1α protein expressions increased ( P <0.05, P <0.01)., Conclusion: EA could regulate the AMPKα-HDAC5-HIF-1α signaling in myocardial tissue, which may activate VEGF expression for angiogenesis signaling, reduce myocardial infarction area so as to achieve cardioprotective effect.

Objective: To observe the effects of electroacupuncture (EA) on inflammatory reaction of acute myocardial ischemia (MI) in mice, and to explore its action mechanism., Methods: Forty adult male C57BL/6 mice were randomly divided into a control group, a sham operation group, a model group and an EA group, 10 mice in each one. The model was established in the model group and EA group by ligating the left anterior descending branch of coronary artery. The mice in the EA group were treated with EA at "Neiguan" (PC 6) with 2 mA of intensity and 2 Hz /100 Hz of frequency; EA was given 30 min per treatment, once a day for totally 5 days. The mice in the control group and model group were treated with immobilization and no EA was given. The mice in the sham operation group were not treated with ligating at the left anterior descending branch of coronary artery, but the remaining procedure was identical to the model group. The electrocardiogram was recorded and △ST was calculated to evaluate the model. TTC and HE staining methods were applied to evaluate the infarct size and pathologic change of myocardial tissue, respectively. Western blot method was applied to test the protein expression levels of tumor necrosis factor-α (TNF-α), nuclear factor-κB p65 (NF-κB p65), interleukin-1β (IL-1β) and interleukin-8 (IL-8)., Results: Compared with the sham operation group, the S-T segments in the model group and EA group were increased obviously after modeling (both P <0.01), indicating the MI model was established successfully. The TTC and HE staining results indicated, compared with the sham operation group, the model group had larger infarction size ( P <0.01), more myocardial fibers injury and inflammatory infiltration; compared with the model group, the infarction size of the EA group was significantly reduced ( P <0.01), and the myocardial fibers injury and inflammatory infiltration were improved. Compared with the control group, the protein expression levels in the sham operation group were similar (all P >0.05); compared with the sham operation group, the expression levels of TNF-α, NF-κB p65, IL-1β and IL-8 were significantly increased in the model group ( P <0.01, P <0.05); compared with the model group, the expression levels of TNF-α, NF-κB p65, IL-1β and IL-8 were significantly reduced in the EA group (all P <0.05)., Conclusion: EA might reduce the protein expression levels of TNF-α, NF-κB p65, IL-1β and IL-8 in cardiac muscle tissue to inhibit inflammatory reaction and achieve myocardial protective effect in mice with acute myocardial ischemia.

Objective: To explore the impact of electroacupuncture (EA) on the protein expression of adenosine receptors in the heart of the rats with myocardial ischemia (MI)., Methods: Thirty healthy male SD rats were divided randomly into a control group ( n =6), a model group ( n =12) and an EA group ( n =12). We ligated the left anterior descending artery (LAD) for MI model in the model group and EA group, and exposed the heart after opening the chest without ligation in the control group. EA, 2 Hz /15 Hz and 1.5-2 mA, was applied at bilateral"Neiguan"(PC 6) in the EA group for 20 min, once a day for continuous 5 days. No intervention except grabbing and fixation was used in the control group and model group. We applied 2% TTC staining to observe the infarct size of myocardium, colorimetry to analyze serum lactic dehydrogenase (LDH), creatine kinase (CK), creatine kinase isoenzyme (CK-MB), radio-immunity assessment to detect cardiac troponin T (cTnT), Western blot to evaluate the adenosine A1 receptor (A1AR), A2aAR, A2bAR and A3AR., Results: After treatment, myocardial infarction of (27.56±3.24)% was obvious in the model group; the myocardial infarction in the EA group was (21.04±3.61)%, with statistical significance ( P <0.05). The expressions of serum LDH, CK, CK-MB and cTnT levels in the model group increased compared with those in the control group (all P <0.01), and the expressions of LDH, CK, CK-MB and cTnT levels in the EA group decreased compared with those in the model group ( P <0.05， P <0.01). The A1AR expression in the model group was not different from that in the control group ( P >0.05), and A2aAR、A2bAR、A3AR expressions decreased ( P <0.05, P <0.01). A2aAR and A2bAR expressions in the EA group increased compared with those in the model group (both P <0.01), and there was no statistical significance between A1AR and A3AR expressions (both P >0.05). ., Conclusion: EA may achieve cardioprotective effect by regulating the expressions of A2aAR and A2bAR in myocardial tissue, which induce the corresponding signal cascade for reducing myocardial infarction area.

Regarding the effects of electro-acupuncture for severe hypertension, we assessed its acute cardiovascular consequences with 4 subjects of the chronic atrioventricular block dogs having severe hypertension and chronic heart failure. The electro-acupuncture consisting of 2 mA at 2 Hz frequency was carried out for 30 min at Renying (ST-9) and Taichong (LR-3) every other day. Seven sessions were performed within 2 weeks. In the 1st and 7th sessions, the animals were anesthetized with pentobarbital to analyze the effects of the electro-acupuncture on cardiovascular variables. No significant change was detected in any of the basal control values of the cardiohemodynamic or electrophysiological variables between the 1st and 7th sessions. During the 1st session, electo-acupuncture produced a peak increase in mean blood pressure by 8.7% at 35 min (p < 0.05), whereas during the 7th session the peak increase was 6.5% at 35 min (p = 0.06). There was no significant change in the cardiac output, total peripheral resistance, a product of the heart rate and systolic blood pressure (= double product) reflecting myocardial oxygen consumption, QRS width or QT interval during the electrical stimulation in the 1st or 7th session. The results suggest that electroacupuncture may not exert lethal adverse effect except the vasopressor response, but that it can decrease the treatment-induced sympathetic response including vasopressor reaction and tachycardia. Since electro-acupuncture may have some potential to induce hypertensive crisis at the beginning, clinicians have to pay attention on its use for patients with hypertension.

Acupuncture promotes the recovery of neurological function by the overall improvement of ischemic brain injury. It is not only regarded as a rehabilitative treatment but also a pretreatment method for stroke. However, its mechanism has not been fully elucidated. In this study, rats were treated with electroacupuncture (EA) at Baihui (GV20) for 30 min/day for 6 days, ahead of conducting cerebral ischemia–reperfusion (I/R) injury. Infarction volume, Evans blue leakage, and neurological deficits were evaluated at 24 h after I/R injury. Then, the ipsilateral ischemic brain was isolated for RNA sequencing (RNA-Seq) to identify molecular consequences. The results showed that EA pretreatment decreased blood–brain barrier (BBB) permeability, reduced brain infarction volume, and improved neurological outcomes. EA pretreatment could upregulate expression of antivirus and immunity activity-associated genes (such as Ifit1 , Ifit3 , Irf7 , and Oasla) and downregulate expression of matrix disruption-associated genes (Col24a1 , Col11a1 , Col27a1 , etc.) in healthy rats. In addition, it could partially reverse or ameliorate genome-wide transcription changes of the ipsilateral ischemic brain. For the first time, this study provides insight into genomic network modulation of a healthy rat with EA treatment and a EA-preconditioned rat under subsequent I/R injury, which is helpful in explaining acupuncture precondition-induced ischemic tolerance of stroke. It also provides new strategies and targets for the prevention of ischemic stroke. [ABSTRACT FROM AUTHOR]