Electroacupuncture improves neurological deficits and enhances proliferation and differentiation of endogenous nerve stem cells in rats with focal cerebral ischemia

Tao, Jing; Xue, Xiehua; Chen, Lidian; Yang, Shanli; Jiang, Min; Gao, Youliang; Wang, Xiang-Bin

doi:10.1179/174313209x414506

Cited by 51 publications

(42 citation statements)

References 26 publications

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“…Focal cerebral ischemia-reperfusion was administered as previously reported [25][26]. Briefly, an 18-22 mm of nylon monofilament (Jialing-bio, China) with a rounded tip was inserted into the left common external carotid artery (ECA), which advanced through the internal carotid until the origin of the middle cerebral artery (MCA) was blocked.…”

Section: Induction Of Cerebral Ischemia and Reperfusion Injurymentioning

confidence: 99%

Electroacupunctre improves motor impairment via inhibition of microglia-mediated neuroinflammation in the sensorimotor cortex after ischemic stroke

Wang²,

Yang

et al. 2016

Life Sciences

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Section: Induction Of Cerebral Ischemia and Reperfusion Injurymentioning

confidence: 99%

Electroacupunctre improves motor impairment via inhibition of microglia-mediated neuroinflammation in the sensorimotor cortex after ischemic stroke

Wang²,

Yang

et al. 2016

Life Sciences

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“…The C57BL/6 J mice were housed in an environmentally controlled room under a 12h light/dark cycle with free access to food and water ad libitum. Ischemic stroke mouse model was induced by MCAO, as described previously [27]. Briefly, the mice were anesthetized with pentobarbital sodium and the left common carotid artery (CCA) and left external carotid arteries (ECA) were exposed and ligated through a ventral midline neck incision.…”

Section: Methodsmentioning

confidence: 99%

Down-Regulation of Lncrna MALAT1 Attenuates Neuronal Cell Death Through Suppressing Beclin1-Dependent Autophagy by Regulating Mir-30a in Cerebral Ischemic Stroke

Guo¹,

Ma²,

Yan³

et al. 2017

Cell Physiol Biochem

158

102

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Background/Aims: LncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was reported to be highly expressed in an in vitro mimic of ischemic stroke conditions. However, the exact biological role of MALAT1 and its underlying mechanism in ischemic stroke remain to be elucidated. Methods: The roles of MALAT1 and miR-30a on cell death and infarct volume and autophagy were evaluated in experimental ischemic stroke. The relationships between miR-30a and MALAT1, Beclin1 were confirmed by luciferase reporter assay. The autophagy inhibitor 3-methyadenine (3-MA) was used to examine the impact of autophagy on ischemic injury. Results: We found that MALAT1, along with the levels of conversion from autophagy-related protein microtubule-associated protein light chain 3-I (LC3-I) to LC3-phosphatidylethanolamine conjugate (LC3-II), as well as Beclin1 were up-regulated and miR-30a was down-regulated in cerebral cortex neurons after oxygen-glucose deprivation (OGD) and mouse brain cortex after middle cerebral artery occlusion-reperfusion (MCAO). Down-regulation of MALAT1 suppressed ischemic injury and autophagy in vitro and in vivo. Furthermore, MALAT1 may serve as a molecular sponge for miR-30a and negatively regulate its expression. In addition, MALAT1 overturned the inhibitory effect of miR-30a on ischemic injury and autophagy in vitro and in vivo, which might be involved in the derepression of Beclin1, a direct target of miR-30a. Mechanistic analyses further revealed that autophagy inhibitor 3-methyadenine (3-MA) markedly suppressed OGD-induced neuronal cell death and MCAO-induced ischemic brain infarction. Conclusion: Taken together, our study first revealed that down-regulation of MALAT1 attenuated neuronal cell death through suppressing Beclin1-dependent autophagy by regulating miR-30a expression in cerebral ischemic stroke. Besides, our study demonstrated a novel lncRNA-miRNA-mRNA regulatory network that is MALAT1-miR-30a-Beclin1 in ischemic stroke, contributing to a better understanding the pathogenesis and progression of ischemic stroke.

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“…Altered evoked potential 49 54 and cell proliferation in cerebral ischaemia by acupuncture needling alone [50][51][52][53] support the effect of acupuncture. Proliferation of nestin(+) neural stem cells 34 52-56 and reduction in infarction volume by EA 51 suggest that effect may not be mediated by electrical stimulation alone.…”

Section: Discussionmentioning

confidence: 99%

“…45 46 49 In addition, acupuncture promotes cell proliferation after transient cerebral ischaemia. [47][48][49][50][51][52][53][54] Like acupuncture, EA also induces proliferation of neural stem cells in the subependymal zone and hippocampus with nestin expression. 21 34 49-55 This proliferation effect resulted in reduced infarction volume.…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture Enhances Motor Recovery Performance with Brain-Derived Neurotrophic Factor Expression in Rats with Cerebral Infarction

et al. 2012

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Objective Electroacupuncture (EA) is a traditional medicine in patients with post-stroke rehabilitation. Brain-derived neurotrophic factor (BDNF) is a potent growth factor involved in recovery following cerebral injury. The aim of the present study was to investigate whether EA increases BDNF levels and facilitates functional recovery. Methods Occlusion of the middle cerebral artery was performed in rats (N=12) followed by reperfusion. EA was applied at the GV20 (Baihui) acupoint. Motor and sensory functions were monitored on the Garcia scale for 2 weeks. Expressions of BDNF and receptor tyrosine kinase B (trkB) were determined by immunoblotting and immunohistochemistry. Results Improvement of Garcia scores, particularly in motor performance, were noted in the group with EA stimulation (p<0.05). With EA application, BDNF was elevated in the ischaemic hemisphere with increased numbers of BDNF(+) cells. Increased expression of trkB was also detected. Conclusion These results indicate that EA at GV20 improves motor recovery and stimulates BDNF/trkB expression in rats with cerebral ischaemia.

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Electroacupuncture improves neurological deficits and enhances proliferation and differentiation of endogenous nerve stem cells in rats with focal cerebral ischemia

Cited by 51 publications

References 26 publications

Electroacupunctre improves motor impairment via inhibition of microglia-mediated neuroinflammation in the sensorimotor cortex after ischemic stroke

Electroacupunctre improves motor impairment via inhibition of microglia-mediated neuroinflammation in the sensorimotor cortex after ischemic stroke

Down-Regulation of Lncrna MALAT1 Attenuates Neuronal Cell Death Through Suppressing Beclin1-Dependent Autophagy by Regulating Mir-30a in Cerebral Ischemic Stroke

Electroacupuncture Enhances Motor Recovery Performance with Brain-Derived Neurotrophic Factor Expression in Rats with Cerebral Infarction

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