The deposition and accumulation of amyloid-β-peptide (Aβ) in the brain are considered a pathological hallmark of
Alzheimer's disease(AD). Apoptosis is a contributing pathophysiological mechanism of AD. Low-power laser
irradiation (LPLI), a non-damage physical therapy, which has been used clinically for decades of years, is shown to
promote cell proliferation and prevent apoptosis. Recently, low-power laser irradiation (LPLI) has been applied to
moderate AD. In this study, Rat pheochromocytoma (PC12) cells were treated with amyloid beta 25-35 (Aβ25-35) for
induction of apoptosis before LPLI treatment. We measured cell viability with CCK-8 according to the manufacture's
protocol, the cell viability assays show that low fluence of LPLI (2 J/cm2 ) could inhibit the cells apoptosis. Then using
statistical analysis of proportion of apoptotic cells by flow cytometry based on Annexin V-FITC/PI, the assays also
reveal that low fluence of LPLI (2 J/cm2 ) could inhibit the Aβ-induced cell apoptosis. Taken together, we demonstrated
that low fluence of LPLI (2 J/cm2 ) could inhibit the Aβ-induced cell apoptosis, these results directly point to a
therapeutic strategy for the treatment of AD through LPLI.
Protein kinase C delta (PKCδ) mediates apoptosis downstream of many apoptotic stimuli. However, whether PKCδ is
involved in high fluence low-power laser irradiation (HF-LPLI)-induced cell apoptosis is still not understood. In this
study, we investigated the activity of PKCδ in response to HF-LPLI treatment in human breast adenocarcinoma cells
(MCF-7). Cells were transiently transfected pGFP-PKCδ and irradiated with a He-Ne laser for 10 minutes under a
fluence of 120 J/cm2 after 36 hours expression. Nuclear staining with Hoechst 33258 and analysis of flow cytometry
based on Annexin V-FITC/PI revealed that overexpression of PKCδ promoted the apoptotic effect of HF-LPLI. Taken
together, we demonstrated that PKCδ promoted cell apoptosis caused by HF-LPLI, providing a new insight of
mechanisms of HF-LPLI.
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