细胞凋亡
蛋白激酶R
小干扰RNA
肺
EIF-2激酶
蛋白激酶A
信号转导
程序性细胞死亡
激酶
癌症研究
化学
转染
医学
分子生物学
生物
细胞生物学
内科学
生物化学
细胞周期蛋白依赖激酶2
基因
作者
Yunen Liu,Dehong Tan,Changci Tong,Haohuan Li,Ying Xu,Xinwei Liu,Yan Gao,Mingxiao Hou
标识
DOI:10.1016/j.cbi.2015.11.001
摘要
The purpose of this study was to explore the effect of blueberry anthocyanins (BA) on radiation-induced lung injury and investigate the mechanism of action. Seven days after BA(20 and 80 mg/kg/d)administration, 6 weeks old male Sprague–Dawley rats rats were irradiated by LEKTA precise linear accelerator at a single dose of 20 Gy only once. and the rats were continuously treated with BA for 4 weeks. Moreover, human pulmonary alveolar epithelial cells (HPAEpiC) were transfected with either control-siRNA or siRNA targeting protein kinase R (PKR). Cells were then irradiated and treated with 75 μg/mL BA for 72 h. The results showed that BA significantly ameliorated radiation-induced lung inflammation, lung collagen deposition, apoptosis and PKR expression and activation. In vitro, BA significantly protected cells from radiation-induced cell death through modulating expression of Bcl-2, Bax and Caspase-3. Suppression of PKR by siRNA resulted in ablation of BA protection on radiation-induced cell death and modulation of anti-apoptotic and pro-apoptotic proteins, as well as Caspase-3 expression. These findings suggest that BA is effective in ameliorating radiation-induced lung injury, likely through the PKR signaling pathway.
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