Evidence Details for Pten
PMID Title Journal Year Abstract
36440366 Electroacupuncture Activates Neuroplasticity in the Motor Cortex and Corticospinal Tract via the mTOR Pathway in a Rat P-MCAO Model. Biomed Res Int. 2022 Nov 14;2022:3470685. doi: 10.1155/2022/3470685. eCollection 2022. 2022 Electroacupuncture (EA) combines traditional Chinese medicine acupuncture theory with modern scientific technology. It is a promising therapy for the treatment of cerebrovascular diseases such as cerebral infarction. A large number of clinical studies have shown that EA promotes recovery of neurological function after cerebral infarction, however, the underlying mechanisms behind its effects remain unclear. We tested whether EA stimulation of the Zusanli (ST36) and Neiguan (PC6) acupoints activates neuroplasticity in rats with ischemic stroke and whether this involves the regulation of axonal regeneration through the mTOR pathway. 24 h after permanent middle cerebral artery occlusion (p-MCAO) in rats, EA treatment was started for 20 min, daily, for 14 days. We found that EA significantly reduced Modified Neurological Severity Scores (mNSS), cerebral infarct volume, and apoptosis of neuronal cells. EA also significantly increased the expression of the neuroplasticity-associated proteins GAP-43 and SYN and upregulated the phosphorylation levels of AKT, mTOR, S6, and PTEN to promote CST axon sprouting in the spinal cord at C1-C4 levels. The positive effects of EA were blocked by the administration of the mTOR inhibitor Rapamycin. In short, we found that EA of the Zusanli (ST36) and Neiguan (PC6) acupoints in p-MCAO rats induced neuroprotective and neuroplastic effects by regulating the mTOR signaling pathway. It promoted neuroplasticity activated by axon regeneration in the contralateral cortex and corticospinal tract. Activation of such endogenous remodeling is conducive to neurological recovery and may help explain the positive clinical effects seen in patients with infarcts."

Evidence Sentence: To test how EA affects the mTOR and PTEN pathways after ischemic stroke, we used Western blotting to detect total AKT (t-AKT), phosphorylated AKT (p-AKT), total mTOR (t-mTOR), phosphorylated mTOR (p-mTOR), total S6 (t-S6), phosphorylated S6 (p-S6), total PTEN (t-PTEN), and phosphorylated PTEN (p-PTEN) expression (Figure 6(a)).
Evidence Sentence: EA also significantly increased the expression of the neuroplasticity-associated proteins GAP-43 and SYN and upregulated the phosphorylation levels of AKT, mTOR, S6, and PTEN to promote CST axon sprouting in the spinal cord at C1-C4 levels.
Evidence Sentence: PTEN is a negative regulator of the mTOR pathway.
Evidence Sentence: Using Western blot analysis (Figure 6(e)) we found that the level of PTEN phosphorylation (p-PTEN/t-PTEN) was significantly higher in the EA than in the p-MCAO group after EA.
Evidence Sentence: The activity of PTEN is known to be inhibited after phosphorylation.
Evidence Sentence: This indicates that EA can alter the negative regulatory effect of PTEN on the mTOR pathway and produce further mTOR pathway activation by inhibiting the PTEN protein.
Evidence Sentence: EA Activates mTOR and PTEN Pathways in the P-MCAO Healthy Cortex