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Inflammation ; 2020 Mar 20.
Artigo em Inglês | MEDLINE | ID: mdl-32198725


The therapeutic effect of electroacupuncture (EA) on inflammatory pain has been well recognized clinically, but the mechanism is unclear. Interleukin-10 (IL-10), which is produced by regulatory T (Treg) cell, is a key anti-inflammatory cytokine for relieving inflammatory pain. Therefore, the aim of this study is to investigate whether EA could inhibit CFA-induced pain and attenuate inflammation progression by regulating the activation of immunocyte and inducing the expression of IL-10. In this study, mice were treated with EA (2/100 Hz, 2 mA) for five consecutive days after 1 day of CFA injection. The behavioral tests were measured and analyzed after the daily EA treatment; then, hind paw, spinal cord, and spleen tissues were prepared for assessment. The results showed that EA treatment significantly increased the mechanical threshold and thermal latency after CFA injection and boosted the expression of IL-10 in paw and spinal cord tissues. EA treatment promoted Treg cells; suppressed macrophage and neutrophils cells; reduced the expression of IL-1ß, NLRP3, and TNF-α; and ultimately relieved inflammatory pain. The findings suggested that the analgesic and anti-inflammatory effect of EA treatment could be partially associated with suppression of pro-inflammatory cytokines mediated by induction of IL-10.

Zhongguo Zhen Jiu ; 39(5): 501-6, 2019 May 12.
Artigo em Chinês | MEDLINE | ID: mdl-31099221


OBJECTIVE: To observe the effects of electroacupuncture (EA) on sympathetic nerve-related substance in myocardial tissue in mice with myocardial ischemia (MI), and to explore its possible mechanism. METHODS: Thirty adult male C57BL/6 mice were randomly divided into a sham operation group, a model group and an EA group, 10 mice in each one. The model of MI was established in the model group and EA group by ligating the left anterior descending branch of coronary artery. The mice in the sham operation group were not treated with ligating at left anterior descending branch of coronary artery, but the remaining procedure was similar with the model group. The mice in the EA group were treated with EA at "Neiguan" (PC 6) with 2 Hz/100 Hz of frequency and 2 mA of intensity, 20 min per treatment, once a day for totally 5 days. No EA was given for model group and sham operation group. The electrocardiogram was recorded and △ST value was calculated to evaluate the model. TTC staining was applied to evaluate the infarct size. Immunohistochemical (IHC) method was applied to evaluate the positive nerve fiber density in myocardial tissue. Western blot method was applied to test the protein expression levels of neuregulin-1 (NRG-1), tyrosine hydroxylase (TH), growth associated protein-43 (GAP-43). RESULTS: The electrocardiogram (lead II) results indicated compared with the sham operation group, the S-T segments in the model group and EA group were increased obviously (both P<0.01), indicating the MI model was established successfully. The TTC staining results indicated compared with sham operation group, the infarction size was significantly increased in the model group (P<0.01); compared with the model group, the infarction size in the EA group was significantly reduced (P<0.01). The IHC results indicated compared with the sham operation group, the positive nerve fiber density in myocardial was increased in the model group (P<0.01); compared with the model group, the positive nerve fiber density in myocardial was reduced in the EA group (P<0.05). The Western blot results indicated compared with the sham operation group, the expression levels of TH, NRG-1 and GAP-43 were significantly increased in the model group (P<0.01); compared with the model group, the expression level of TH and GAP-43 were significantly reduced (P<0.01) and that of NRG-1 was increased in the EA group (P<0.05). CONCLUSION: EA could increase the expression of NRG-1 and reduce the expression of TH and GAP-43 in myocardial tissues in MI mice, which could suppress sympathetic nerve hyperexcitability after infarction to achieve myocardial protection effect.

Doença da Artéria Coronariana , Eletroacupuntura , Isquemia Miocárdica , Animais , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Miocárdio
Zhen Ci Yan Jiu ; 44(4): 302-6, 2019 Apr 25.
Artigo em Chinês | MEDLINE | ID: mdl-31056886


The inflammatory reaction induced by ischemic myocardial injury (IMI) is divided into three phases, i.e. the inflammatory phase, the fibrous proliferative phase and the stable phase. The appropriate inflammatory reaction effectively removes the fragments of myocardial cells, which is the essential phase in the pathological progression of myocardial ischemia (MI). However, the excessive inflammatory reaction may aggravate the myocardial injury. For this reason, the immediate control of the post-injury inflammatory reaction is the principal therapeutic measure and the research hotspot at the present. Acupuncture intervention has been demonstrated to have positive roles in relieving MI and inflammatory reaction by suppressing myocardial inflammatory cytokines (suppressing IL-1ß, TNF-α, IL-8, etc.), adjusting inflammatory reaction pathway (NF-κB signaling, TGF-ß, etc.)and activating cholinergic anti-inflammatory pathway. Therefore, it is feasible to explore the underlying mechanism of acupuncture therapy in protecting ischemic myocardium based on anti-inflammatory efficacy.

Terapia por Acupuntura , Inflamação , Anti-Inflamatórios , Humanos , Interleucina-1beta , NF-kappa B
Zhen Ci Yan Jiu ; 43(5): 314-8, 2018 May 25.
Artigo em Chinês | MEDLINE | ID: mdl-29888568


OBJECTIVE: To observe the effect of electroacupuncture (EA) on insulin signaling pathway in liver tissues of central neuronal specific signal transduction and activator of transcription 5 conditional-knockout (Stat 5 NKO) mice, so as to explore its mechanism underlying improvement of insulin resistance (IR).. METHODS: Twenty-four male Stat 5 NKO mice were randomly divided into model and EA groups (n=12 mice/group), and 12 Stat 5 fl/fl mice were used as the normal control group. EA (2 Hz/15 Hz, 0.8-1.0 mA) was alternatively applied to ipsilateral "Zusanli" (ST 36) and "Neiting" (ST 44) for 20 min, once a day, 6 times a week for 4 weeks. The glucose tolerance test (GTT) and insulin tolerance test (ITT) were performed, and the values of fasting plasma glucose (FPG) and fasting insulin (FINS) were measured by glucometer and ELISA, separately. The insulin sensitivity index (ISI) was calculated. The phosphorylation protein expressions of insulin receptor substrate 1 (IRS 1), insulin receptor ß (IRß) and protein kinases B (Akt) in the liver tissues were detected by Western blot. RESULTS: In Stat 5 NKO mice (model group), FPG level and glucose area under the curve (GAUC) of ITT and GTT were significantly increased (P<0.01, P<0.05, P<0.001), while the ISI was notably down-regulated in comparison with the Stat 5 fl/fl mice (normal group, P<0.01), suggesting an impairment of both glucose tolerance (GT) and insulin tolerance (IT) in mice of the model group. After the EA treatment, the increased FPG and GAUC levels and the decreased ISI were reversed markedly (P<0.05, P<0.01, P<0.001). No significant differences were found in FINS among the three groups (P>0.05). Compared with the normal group, the protein expression levels of liver p-IRS 1 and p-IRß were significantly up-regulated (P<0.001), and the p-Akt expression was significantly down-regulated (P<0.01) in the model group. Following EA treatment, the increased p-IRS 1 and p-IRß protein expression and the decreased p-Akt expression were apparently reversed in the EA group relevant to the model group (P<0.001, P<0.01).. CONCLUSION: EA can improve the IR induced by central neuronal Stat 5-knockout in mice, which may contribute to its effectiveness in regulating hepatic IRß/IRS 1/Akt signaling pathway.

Eletroacupuntura , Resistência à Insulina , Pontos de Acupuntura , Animais , Proteínas Substratos do Receptor de Insulina , Fígado , Masculino , Camundongos , Camundongos Knockout , Proteínas Proto-Oncogênicas c-akt , Transdução de Sinais