Light emitting diode irradiation inhibits the amyloid beta 25-35 induced pc12 apoptosis in vitro
Por Ling Zhu (Autor), Timon Cheng-y Liu (Autor), Rui Duan (Autor), Xiao-yang Xu (Autor), Xiao-guang Liu (Autor), Shu-Xun Deng (Autor).
Integra
Introduction
Chronic traumatic brain injury (CTBI) associated with boxing occurs in approximately 20% of professional boxers [1], which shares many characteristics with Alzheimer’s disease (AD) (i.e., neurofibrillary triangles, diffuse amyloid plaques, acetylcholine deficiency, and/or tau immunoreactivity). The findings of Sumitani et al [2] suggested that severe long-term exercise might damage hippocampal neurons. As beta-amyloid (A beta) induced apoptosis is a leading hypothesis of the cause of AD [3], PC12 is a widely-used cell model of neurons and the photobiomodulation of light emitting diode (LED) irradiation has attracted wide attention [4], the photobiomodulation of LED irradiation on A beta induced PC12 apoptosis was studied in this paper.
Methods
Monolayer cell cultures of PC12 were subjected to A beta 25-35 or/and GaAlAs LED irradiation (640±15nm) at various intensity from 0.5W/m2 to 10W/m2 with the irradiation time was from 30 min to 60 min, respectively. Cell apoptosis was confirmed by morphological criteria, DNA fragmentation assay, and FAScan flow cytometer assay.
Results
Treatment of the cells with LED irradiation significantly diminished A beta induced apoptosis within 24 hours.
Discussion / Conclusions
The GaAlAs LED irradiation (640±15nm), when utilized at power of 0.9 W/m2 and 60 minutes, has significantly diminished A beta induced apoptosis of PC12 cells. This finding suggested that LED might be used to develop a green treatment of AD, CTBI or severe long-term exercise induced neuron damage, which have not been effectively treated yet.
References
[1]. Jordan BD. (2000). Chronic traumatic brain injury associated with boxing. Semin Neurol. 20(2):179-85.
[2]. Sumitani K, Miyamoto O, Yamagami S, Okada Y, Itano T, Murakami T, Negi T. (2002). The influence of severe long-term exercise on the mouse hippocampus. Nippon Seirigaku Zasshi. 64(7-8):152-8.
[3]. Hardy JA, Higgins GA. (1992). Alzheimer’s disease: the amyloid cascade hypothesis. Science. 256(5054):184-5
[4]. Eells JT, Henry MM, Summerfelt P, Wong-Riley MT, Buchmann EV, Kane M, Whelan NT, Whelan HT. (2003). Therapeutic photobiomodulation for methanol-induced retinal toxicity. Proc Natl Acad Sci U S A. 100(6):3439-44.