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 (Aβ 25-35 ) for induction of apoptosis

more »

... re 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 Aβ 25-35 followed by 5 min LPLI treatment, respectively. However, the effect of LPLI activating PKC could be inhibited by Gö 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 Aβ [25] [26] [27] [28] [29] [30][31][32][33][34][35] . Further data show that low fluence of LPLI could reverse the increased level of bax/bcl-xl mRNA ratio caused by Aβ 25-35 treatment. In addition, Gö 6983 could inhibit the decreased level of bax/bcl-xl mRNA ratio. Taken together, these data clearly indicate that LPLI inhibited Aβ 25-35 -induced PC12 cell apoptosis via PKC-mediated regulation of bax/bcl-xl mRNA ratio. Fig. 4. Melting curve analysis of the amplified samples. GAPDH A, bax A and bcl-xl A are samples of the cells treated with 25 µM Aβ 25-35 for 6 h. GAPDH B, bax B and bcl-xl B are samples from the cells without Aβ 25-35 treatment. As a negative, the template RNA was replaced by PCR-grade water.