Evidence Details for Gfap
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: Abundant expression of A53T alpha-syn was seen in the GFAP-positive astrocytes as demonstrated by co-staining of alpha-syn with GFAP in the SN (Fig.
Evidence Sentence: We then assessed the rate of astrogliosis by analyzing expression of GFAP in A53T mice.
Evidence Sentence: Immunofluorescent staining revealed a larger number of GFAP-positive astrocytes in the SN of A53T mice (Fig.
Evidence Sentence: EA (100 Hz) decreased the number of GFAP-immunoreactive astrocytes (Fig.
Evidence Sentence: Similarly, in immunoblot assays, EA effectively alleviated the excessive expression of GFAP in the SN of A53T mice (Fig.
Evidence Sentence: Of note, the level of GFAP in the EA-treated A53T mice still remained higher than that seen in control nTg mice.
Evidence Sentence: In addition, GFAP mRNA expression was probed using quantitative RT-PCR.
Evidence Sentence: We found that GFAP mRNA expression was elevated in the midbrain (Fig.
Evidence Sentence: However, unlike GFAP proteins, GFAP mRNA levels in these regions remained at a higher control level after EA treatment.
Evidence Sentence: The fact that EA limited the protein although no mRNA expression of GFAP in astrocytes of A53T mice indicates that EA may primarily inhibit reactive astrogliosis.