Original articles
DONG Huafeng, LIU Bing, CHEN Xiaobing, LIU Weiwei, XIE Fang, ZHAO Yun, SUN Zhaowei, WANG Xue, QIAN Lingjia
Objective To find out whether photobiomodulation （PBM） can mitigate cognitive dysfunction caused by chronic stress by affecting levels of adenosine triphosphate （ATP） and adenosine receptors. Methods Twenty-four C57BL/6J mice were randomly divided into a control group, a stress group, and a treatment group. Chronic unpredictable mild stress was used to establish a mouse model of stress. Six weeks into modeling, the treatment group was subjected to one week of PBM interventions. Behavioral tests were conducted to observe behavioral changes in the mice. Western blotting （WB） was used to detect the expressions of A1, A2B, and A3 adenosine receptors in the hippocampus and prefrontal cortex of mice in the three groups. Twelve C57BL/6J mice were randomly divided into a control group and an intervention group. The intervention group received a week of PBM interventions and underwent behavioral testing. WB was used to detect the expression changes of A1, A2B, and A3 adenosine receptors in the hippocampus and prefrontal cortex in both groups. Immunofluorescence assay was adopted to detect the expression of c-Fos in the hippocampus of mice in the two groups. The ATP assay kit made by Beyotime Biotechnology Co., Ltd. was used to measure changes in ATP contents in the hippocampus and prefrontal cortex tissues of mice. Cell experiments were conducted to verify the effect of PBM on intracellular ATP contents. Results Mice in the stress group covered a similar distance to the control group, but finished far fewer platform crossings. There was no significant difference between the treatment group and the control group in the number of times of platform crossings, but compared favorably with the stress group where the levels of adenosine receptors in the hippocampus and prefrontal cortex were lower, but were increased by PBM. After PBM interventions in normal mice, platform crossings were increased significantly compared to the control group. PBM also raised adenosine receptor levels and ATP contents in the hippocampus and prefrontal cortex, and increased hippocampal c-Fos expressions. In vitro, PBM elevated intracellular ATP levels. Conclusion PBM may improve chronic stress-induced cognitive dysfunction by regulating ATP levels and adenosine receptor expressions, thereby modulating neuronal responsiveness in the hippocampus.
