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Cell Physiol Biochem. 2008;22(1-4):215-22. doi: 10.1159/000149799. Epub 2008 Jul 25.

Low-power laser irradiation inhibiting Abeta25-35-induced PC12 cell apoptosis via PKC activation.

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1
MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, South China Normal University, Guangzhou, China.

Abstract

Apoptosis is a contributing pathophysiological mechanism of Alzheimer's disease (AD). Recently, low-power laser irradiation (LPLI) has been applied to moderate AD, but the underlying mechanism remains unknown. In this study, the techniques of fluorescence resonance energy transfer (FRET) and real-time quantitative RT-PCR were used to investigate the anti-apoptotic mechanism of LPLI. Rat pheochromocytoma (PC12) cells were treated with amyloid beta 25-35 (Abeta(25-35)) for induction of apoptosis before LPLI treatment. The cell viability assays and morphological examinations show that low fluence of LPLI (0.156 J/cm(2)-0.624 J/cm(2)) could inhibit the cells apoptosis. An increase of PKC activation was dynamically monitored in the cells treated with PMA (specific activator of PKC), LPLI only or Abeta(25-35) followed by 5 min LPLI treatment, respectively. However, the effect of LPLI activating PKC could be inhibited by Go 6983 (specific inhibitor of PKC). Similar results were obtained by using Western blot analysis. Furthermore, LPLI involved an increase in mRNA of the cell survival member bcl-xl and a decrease in the up-regulation of cell death member bax mRNA caused by Abeta(25-35). Further data show that low fluence of LPLI could reverse the increased level of bax/bcl-xl mRNA ratio caused by Abeta(25-35) treatment. In addition, Go 6983 could inhibit the decreased level of bax/bcl-xl mRNA ratio. Taken together, these data clearly indicate that LPLI inhibited Abeta(25-35)-induced PC12 cell apoptosis via PKC-mediated regulation of bax/bcl-xl mRNA ratio.

PMID:
18769048
DOI:
10.1159/000149799
[Indexed for MEDLINE]
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