Evidence Details for Mapk1
PMID Title Journal Year Abstract
30505267 Electroacupuncture Restores Locomotor Functions After Mouse Spinal Cord Injury in Correlation With Reduction of PTEN and p53 Expression. Front Mol Neurosci. 2018 Nov 16;11:411. doi: 10.3389/fnmol.2018.00411. eCollection 2018. 2018 Background: We previously showed that electroacupuncture (EA) at Jiaji points promotes expression of adhesion molecule L1 in spinal cord tissue after mouse spinal cord injury (SCI) and contributes to recovery of neural functions. Objective: We investigated the effects of EA on downstream signaling molecules of L1 and molecules relevant to apoptosis with the aim to understand the underlying molecular mechanisms. Methods: Female C57BL/6 mice were divided into a sham group, injury group, injury+acupuncture (AP) group and injury+EA group. We investigated the changes in cognate L1-triggered signaling molecules after SCI by immunofluorescence staining and immunoblot analysis. Results: Protein levels of phosphatase and tensin homolog (PTEN) and p53 were decreased by EA at different time points after injury, whereas the levels of phosphorylated mammalian target of rapamycin (pmTOR), p-Akt and phosphorylated extracellular signal-regulatedkinase (p-Erk) were increased. Also, levels of myelin basic protein (MBP) were increased by EA. AP alone showed less pronounced changes in expression of the investigated molecules, when compared to EA. Conclusion: We propose that EA contributes to neuroprotection by inhibiting PTEN and p53 expression and by increasing the levels of pmTOR/Akt/Erk and of MBP after SCI. These observations allow novel insights into the beneficial effects of EA via L1-triggered signaling molecules after injury."

Evidence Sentence: Results: Protein levels of phosphatase and tensin homolog (PTEN) and p53 were decreased by EA at different time points after injury, whereas the levels of phosphorylated mammalian target of rapamycin (pmTOR), p-Akt and phosphorylated extracellular signal-regulatedkinase (p-Erk) were increased.
Evidence Sentence: Conclusion: We propose that EA contributes to neuroprotection by inhibiting PTEN and p53 expression and by increasing the levels of pmTOR/Akt/Erk and of MBP after SCI.
Evidence Sentence: AP and EA Increase of p-Erk Levels After SCI
Evidence Sentence: To investigate whether AP and EA affect p-Erk levels, we performed immunoblot analysis at 3, 7, 14 and 28 days after SCI on spinal cord tissue (Figure 2).
Evidence Sentence: p-Erk levels in the injury+AP group were higher than in the injury group at 28 days (means +- SEM are 2.8793 +- 1.1559 and 1.2274 +- 0.3533, t = 2.3289, p = 0.0401).
Evidence Sentence: Even higher levels of p-Erk were observed in the injury+EA group at 3, 14 and 28 days of SCI (means +- SEM are 2.4361 +- 0.2559 and 1.3052 +- 0.4157, t = 2.39, p = 0.0375, means +- SEM are 2.8793 +- 1.156 and 1.0896 +- 0.2245, t = 2.6382, p = 0.0201, and means +- SEM are 1.8894 +- 0.2347 and 1.0325 +- 0.0375, t = 2.8451, p = 0.0239, respectively).
Evidence Sentence: These results indicate that EA promotes p-Erk levels at 3, 14 and 28 days, whereas AP enhances p-Erk levels only at 28 days after SCI.