Abstract:Electroacupuncture (EA) treatment has been widely used for stroke-like disorders in traditional Chinese medicine. However, the underlying mechanisms remain unclear. Our previous studies showed that single-time EA stimulation at “Baihui” (GV 20) and “Shuigou” (GV 26) after the onset of ischemia can protect the brain against ischemic injury in rats with middle cerebral artery occlusion (MCAO). Here, we further investigated the differential effects between multiple EA and single-time EA stimulation on ischemic in… Show more
“…These data suggest that MEK1 is activated in the hippocampus contralateral to the nerve injury side following four times of EA intervention, and this increase in MEK1 activity may initiate a cumulative effect of EA treatment. Previously reported gene screening results suggest that the discrepancy between the effects of multiple and single EA treatments on brain ischemia/reperfusion are possibly caused by their differential modulation on gene expression, such as brain-derived neurotrophic factor and signal transducer-related genes [4]. This proposal is consistent with our data.…”
Section: Discussionsupporting
confidence: 92%
“…Acupuncture therapy, a method of traditional Chinese medicine, has received worldwide attention as a strategy to relieve pain [1–3]. Clinical practice demonstrates that multiple sessions of acupuncture treatment (not a single session) may induce an obvious analgesic effect [4–6]. However, the number of acupuncture treatment sessions required for effective pain relief is unclear.…”
BackgroundElectroacupuncture (EA) intervention can relieve a variety of pain; however, optimal EA protocols have not been clearly determined. In addition, although central mitogen-activated protein kinase kinase (MEK) signaling has been shown to be involved in the antinociceptive effect of acupuncture stimulation, its characteristics at different time-points of EA intervention have not been fully elucidated. Therefore, the present study investigated the relationship between the effects of different numbers of EA intervention sessions and the activation of MEK1 in the hippocampus and hypothalamus in a rat model of neuropathic pain.MethodsAfter ligation of the left sciatic nerve, which induces chronic constriction injury (CCI), the acupoints Zusanli (ST36) and Yanglingquan (GB34) were applied. The thermal withdrawal latency of the hind paw was used to evaluate the effect of EA on pain thresholds. Intra-hippocampus microinjection of PD98059, a MEK inhibitor, was performed to validate the involvement of MEK in EA analgesia. The hippocampus and hypothalamus were harvested to examine the phosphorylation levels of MEK (pMEK) by western blotting.ResultsIn CCI rats, the thermal pain threshold of the affected hind paw decreased significantly relative to the control. Following subsequent daily EA interventions, CCI-induced ipsilateral hyperalgesia was markedly improved from day 4 and the analgesic effect of EA lasted 3 days after cessation of EA. Four sessions of EA markedly suppressed CCI-induced decrease of hippocampal pMEK1 (normalized to the total MEK level). In contrast, successive sessions of EA intervention gradually down-regulated the CCI-induced up-regulation of hypothalamic pMEK1 along with the increase numbers of EA intervention. However, EA did not exert the same analgesic effect after microinjection of PD98059 into the contralateral hippocampus during the first 3 days of EA intervention.ConclusionsEA intervention can induce time-dependent cumulative analgesia in neuropathic pain rats after 4 successive sessions of daily EA intervention, which is at least in part related to the activation of hippocampal MEK1.
“…These data suggest that MEK1 is activated in the hippocampus contralateral to the nerve injury side following four times of EA intervention, and this increase in MEK1 activity may initiate a cumulative effect of EA treatment. Previously reported gene screening results suggest that the discrepancy between the effects of multiple and single EA treatments on brain ischemia/reperfusion are possibly caused by their differential modulation on gene expression, such as brain-derived neurotrophic factor and signal transducer-related genes [4]. This proposal is consistent with our data.…”
Section: Discussionsupporting
confidence: 92%
“…Acupuncture therapy, a method of traditional Chinese medicine, has received worldwide attention as a strategy to relieve pain [1–3]. Clinical practice demonstrates that multiple sessions of acupuncture treatment (not a single session) may induce an obvious analgesic effect [4–6]. However, the number of acupuncture treatment sessions required for effective pain relief is unclear.…”
BackgroundElectroacupuncture (EA) intervention can relieve a variety of pain; however, optimal EA protocols have not been clearly determined. In addition, although central mitogen-activated protein kinase kinase (MEK) signaling has been shown to be involved in the antinociceptive effect of acupuncture stimulation, its characteristics at different time-points of EA intervention have not been fully elucidated. Therefore, the present study investigated the relationship between the effects of different numbers of EA intervention sessions and the activation of MEK1 in the hippocampus and hypothalamus in a rat model of neuropathic pain.MethodsAfter ligation of the left sciatic nerve, which induces chronic constriction injury (CCI), the acupoints Zusanli (ST36) and Yanglingquan (GB34) were applied. The thermal withdrawal latency of the hind paw was used to evaluate the effect of EA on pain thresholds. Intra-hippocampus microinjection of PD98059, a MEK inhibitor, was performed to validate the involvement of MEK in EA analgesia. The hippocampus and hypothalamus were harvested to examine the phosphorylation levels of MEK (pMEK) by western blotting.ResultsIn CCI rats, the thermal pain threshold of the affected hind paw decreased significantly relative to the control. Following subsequent daily EA interventions, CCI-induced ipsilateral hyperalgesia was markedly improved from day 4 and the analgesic effect of EA lasted 3 days after cessation of EA. Four sessions of EA markedly suppressed CCI-induced decrease of hippocampal pMEK1 (normalized to the total MEK level). In contrast, successive sessions of EA intervention gradually down-regulated the CCI-induced up-regulation of hypothalamic pMEK1 along with the increase numbers of EA intervention. However, EA did not exert the same analgesic effect after microinjection of PD98059 into the contralateral hippocampus during the first 3 days of EA intervention.ConclusionsEA intervention can induce time-dependent cumulative analgesia in neuropathic pain rats after 4 successive sessions of daily EA intervention, which is at least in part related to the activation of hippocampal MEK1.
“…Protein samples (15 μ g/lane) from different groups were electrophoresed on 10% SDS–polyacrylamide gel and transferred to the polyvinyl difluoride membrane (Bio‐Rad, Hercules, CA, USA) as the method described . Peroxidase activity was visualized with an enhanced chemiluminescence substrate system (ECL; Santa Cruz Biotechnology, Santa Cruz, CA, USA).…”
Intranasal delivery of hNSCs could prevent HI-induced brain injury and improve neurobehavioral outcomes in neonatal HI rats, which is possibly related to the modulation of NF-κB signaling.
“…EA intervention is reported to suppress ischemia-elicited astrocyte activation and reduce the expression of GMF. Thus, it is speculated that EA might inhibit astroglial activation via decreasing GMF (Wang et al, 2014) (as shown in Table 1).…”
Stroke is one of the main causes of death all over the world. As the combination of acupuncture and electric stimulation, electroacupuncutre is a safe and effective therapy, which is commonly applied in ischemic stroke therapy in both experimental studies and clinical settings. The review was performed via searching for related articles in the databases of OVID, PUBMED, and ISI Web of Science from their respective inceptions to May 2018. In this review, we summarized the mechanism of EA for ischemic stroke via a series of factors, consisting of apoptosis related-factors, inflammatory factors, autophagy-related factors, growth factors, transcriptional factors, cannabinoid CB1 receptors, and other factors. In summary, EA stimulation may effectively alleviate ischemic brain injury via a series of signal pathways and various other factors.
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