[Near-infrared light therapy ameliorates depression-induced intestinal dysfunction in rats possibly by activating...

To investigate the effect of near-infrared (NIR) light therapy on depression-induced intestinal dysfunction in rats and explore the possible mechanism.

Thirty-two male SD rats were randomly divided into control group, model group, low-dose NIR light group and high-dose NIR light group. All the rats except for those in the control group were subjected to chronic restrained stress (CRS) for 4 weeks, and NIR light therapy of the head was administered in the two NIR light groups. The depression- like behaviors, intestinal functions, fecal water content and number of fecal pellets of the rats were evaluated. HE staining was used for detecting histopathological changes in the hippocampus and colon, and hippocampal expressions of BDNF, Nrf2 and PGC-1α were detected with Western blotting.

The rats in the CRS model group showed significantly increased immobility time and visceral sensitivity in the behavioral tests, decreased fecal pellets and fecal water content, and lowered expressions of BDNF, Nrf2, and PGC-1α in the hippocampus (P<0.05). Histopathological examination of the CRS rats revealed loosely arranged hippocampal pyramidal cells, obvious neuronal damages, and obvious inflammatory cell infiltration in the colon with irregularly arranged mucosal glands and a high pathological score. High-dose NIR light therapy significantly lowered the immobility time and visceral sensitivity, increased the number of fecal pellets and fecal water content (P<0.05), and enhanced hippocampal expressions of BDNF, Nrf2, and PGC-1α (P<0.05) of the depressive rats. The rats receiving high-dose NIR light therapy also exhibited close arrangement of the hippocampal pyramidal cells with significantly reduced neuronal damage and colonic inflammatory cell infiltration, neatly arranged mucosal glands, and lowered pathological score.

NIR light therapy can significantly improve depression-like behavior and intestinal function in rats possibly by ameliorating oxidative stress via the PGC-1α/Nrf2 signaling pathway and increasing BDNF level in the hippocampus.