Evidence Details for Mapk1
PMID Title Journal Year Abstract
23837037 Electroacupuncture at Quchi and Zusanli treats cerebral ischemia-reperfusion injury through activation of ERK signaling. Exp Ther Med. 2013 Jun;5(6):1593-1597. doi: 10.3892/etm.2013.1030. Epub 2013 Mar 26. 2013 Jun The extracellular signal-regulated kinase (ERK) pathway, a critical mediator of cell proliferation, is activated in cerebral ischemia/reperfusion (I/R) injury and is therefore a key target in the treatment of ischemic stroke. Acupuncture has long been used in China to clinically treat stroke. However, the precise mechanism of its neuroprotective activities remains largely unknown. In the present study, a focal cerebral I/R-injured rat model was used to evaluate the in vivo therapeutic efficacy of electroacupuncture (EA) and investigate the underlying molecular mechanisms. EA significantly ameliorated neurological deficits and cerebral infarction in cerebral I/R-injured rats. Moreover, EA significantly increased the phosphorylation levels of ERK, as well as the protein expression levels of Ras, cyclin D1 and cyclin-dependent kinase (CDK)4. Consequently, EA-mediated activation of the ERK pathway resulted in the stimulation of cerebral cell proliferation. The present data suggest that EA at the Quchi and Zusanli acupoints exerts a neuroprotective effect in ischemic stroke via the activation of ERK signaling."

Evidence Sentence: Moreover, EA significantly increased the phosphorylation levels of ERK, as well as the protein expression levels of Ras, cyclin D1 and cyclin-dependent kinase (CDK)4.
Evidence Sentence: To investigate the effect of EA on the ERK pathway, western blotting was performed to examine the expression of Ras and the phosphorylation of ERK in the ischemic cerebral cortex and striatum.
Evidence Sentence: 2, I/R injury increased the Ras protein expression and the phosphorylation level of ERK.
Evidence Sentence: This was consistent with previous studies of the transient focal ischemia model which showed that ERK was activated following I/R and persisted for 24 h. EA at Zusanli and Quchi further upregulated the protein expression of Ras, as well as ERK phosphorylation, whereas the levels of nonphosphorylated ERK remained unchanged in all three animal groups.
Evidence Sentence: ERK activation is important in cell proliferation and therefore, the pro-proliferative activity of EA was investigated using IHC staining for PCNA.
Evidence Sentence: The extracellular signal-regulated kinase (ERK) pathway, a critical mediator of cell proliferation, is activated in cerebral ischemia/reperfusion (I/R) injury and is therefore a key target in the treatment of ischemic stroke.
Evidence Sentence: Consequently, EA-mediated activation of the ERK pathway resulted in the stimulation of cerebral cell proliferation.
Evidence Sentence: EA at the Quchi and Zusanli acupoints activates the ERK pathway in cerebral I/R-injured rats
Evidence Sentence: Electroacupuncture at Quchi and Zusanli treats cerebral ischemia-reperfusion injury through activation of ERK signaling
Evidence Sentence: The present data suggest that EA at the Quchi and Zusanli acupoints exerts a neuroprotective effect in ischemic stroke via the activation of ERK signaling.