Evidence Details for Nfe2l2
PMID Title Journal Year Abstract
26016857 Electroacupuncture remediates glial dysfunction and ameliorates neurodegeneration in the astrocytic alpha-synuclein mutant mouse model. J Neuroinflammation. 2015 May 28;12:103. doi: 10.1186/s12974-015-0302-z. 2015 May 28 BACKGROUND: The acupuncture or electroacupuncture (EA) shows the therapeutic effect on various neurodegenerative diseases. This effect was thought to be partially achieved by its ability to alleviate existing neuroinflammation and glial dysfunction. In this study, we systematically investigated the effect of EA on abnormal neurochemical changes and motor symptoms in a mouse neurodegenerative disease model. METHODS: The transgenic mouse which expresses a mutant alpha-synuclein (alpha-syn) protein, A53T alpha-syn, in brain astrocytic cells was used. These mice exhibit extensive neuroinflammatory and motor phenotypes of neurodegenerative disorders. In this study, the effects of EA on these phenotypic changes were examined in these mice. RESULTS: EA improved the movement detected in multiple motor tests in A53T mutant mice. At the cellular level, EA significantly reduced the activation of microglia and prevented the loss of dopaminergic neurons in the midbrain and motor neurons in the spinal cord. At the molecular level, EA suppressed the abnormal elevation of proinflammatory factors (tumor necrosis factor-alpha and interleukin-1beta) in the striatum and midbrain of A53T mice. In contrast, EA increased striatal and midbrain expression of a transcription factor, nuclear factor E2-related factor 2, and its downstream antioxidants (heme oxygenase-1 and glutamate-cysteine ligase modifier subunits). CONCLUSIONS: These results suggest that EA possesses the ability to ameliorate mutant alpha-syn-induced motor abnormalities. This ability may be due to that EA enhances both anti-inflammatory and antioxidant activities and suppresses aberrant glial activation in the diseased sites of brains."

Evidence Sentence: EA modulated expression of Nrf2, HO-1, and GCLM proteins in A53T mice
Evidence Sentence: It is well known that Nrf2 suppresses neurodegeneration via a mechanism involving the inhibition of oxidative stress and gliosis.
Evidence Sentence: In A53T mice, Nrf2 protein levels were dramatically reduced in the midbrain and striatum compared to nTg mice (Fig.
Evidence Sentence: EA stimulation substantially increased Nrf2 proteins in the midbrain to a level higher than that in nTg control mice (Fig.
Evidence Sentence: EA also increased Nrf2 expression in the striatum (Fig.
Evidence Sentence: Meanwhile, EA markedly elevated the Nrf2 mRNA level in the midbrain of A53T mice compared to untreated-mice (Fig.
Evidence Sentence: In contrast, EA increased striatal and midbrain expression of a transcription factor, nuclear factor E2-related factor 2, and its downstream antioxidants (heme oxygenase-1 and glutamate-cysteine ligase modifier subunits).