Downregulation of brain-derived neurotrophic factor (BDNF) in the hippocampus occurs early in the progression of Alzheimer’s disease (AD). Since BDNF plays a critical role in neuronal survival and dendrite growth, BDNF upregulation may contribute to rescue dendrite atrophy and cell loss in AD. Low-level laser therapy (LLLT) has been demonstrated to regulate neuronal function both in vitro and in vivo. In the present study, we found that LLLT rescued neurons loss and dendritic atrophy via the increase of both BDNF mRNA and protein expression. In addition, dendrite growth was improved after LLLT, characterized by upregulation of PSD95 expression, and the increase in length, branching, and spine density of dendrites in hippocampal neurons. Together, these studies suggest that upregulation of BDNF with LLLT can ameliorate Aβ-induced neurons loss and dendritic atrophy, thus identifying a novel pathway by which LLLT protects against Aβ-induced neurotoxicity. Our research may provide a feasible therapeutic approach to control the progression of Alzheimer’s disease.
Low-power laser (He-Ne) irradiation (LPLI) has been found to modulate various biological effects, especially those
involved in promoting cell proliferation and metabolic regulation. However, the underlying mechanisms that LPLI
prevents human cell senescence remain undefined. Herein, we devised a model enabling cell senescence using
D-galactose for two days then treat with or without LPLI(< 15J/cm2), and investigated whether LPLI delays cell
senescent in human dermal fibroblasts cells (HDF-a). First in this study, using SA-β-gal staining, compared with control
cell we detected a lower frequency of SA-β-gal staining under the treatment of LPLI. Moreover, we found the growth
rates of cell with LPLI was higher using CCK-8 analysis. Additionally, we also found LPLI induced HDF-a entered the
irreversible G1 arrest measured by flow cytometry system. Therefore, LPLI may promote cell proliferation by
stimulating cell-cycle progression and delay human cell senescence. Taken together, Low-power laser irradiation delay
HDF-a cells senescence provides new information for the mechanisms of biological effects of LPLI.
Sirtuin type 1 (SIRT1), a NAD+-dependent histone deacetylases, plays a critical role in cellular senescence, aging and
longevity. In general, SIRT1 is localized in nucleus and is believed as a nuclear protein. Though overexpression of
SIRT1 delays senescence, SIRT1-protein levels decline naturally in thymus and heart during aging. In the present
studies, we investigated the subcellular localization of SIRT1 in response to growth factor deprivation in African green
monkey SV40-transformed kidney fibroblast cells (COS-7). Using
SIRT1-EGFP fluorescence reporter, we found that
SIRT1 localized to nucleus in physiological conditions. We devised a model enabling cell senescence via growth factor
deprivation, and we found that SIRT1 partially translocated to cytosol under the treatment, suggesting a reduced level of
SIRT1's activity. We found PI3K/Akt pathway was involved in the inhibition of SIRT1's cytosolic translocation,
because inhibition of these kinases significantly decreased the amount of SIRT1 maintained in nucleus. Taken together,
we demonstrated that growth factor deprivation induces cytosolic translocation of SIRT1, which suggesting a possible
connection between cytoplasm-localized SIRT1 and the aging process.
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