[Blue light regulates the expression of brain derived neurotrophic factor in the habenula nucleus of depression-like rats induced by light deprivation].

Objective: To investigate the regulatory effect of blue light on the expression of brain derived neurotrophic factor (BDNF) in the habenula nucleus of depression-like rats induced by light deprivation. Methods: male SD rats were exposed to white light (white light control group, 20 rats) and constant darkness (depression model group, 60 rats), respectively. 18 days later rats in depression model group were randomly divided into three groups: depression model group (treated with constant darkness), blue light group (treated with blue light) and red light group (treated with red light). Rats in white light control group were kept in white light. All rats exposed to light were in a standard 12∶12 h Light/Dark condition at 20 lx for 36 days. Sucrose preference test was applied to evaluate depression-like symptoms of rats. The c-fos+cells in the habenula nucleus, intergeniculate leaflet and ventral lateral geniculate nucleus were detected. The phosphoylation of cAMP-response element binding protein (CREB) and the relative BDNF protein level in the habenula nucleus were measured. Results: Sucrose intake per kg body weight increased in rats exposed to blue light and returned to the level of control group (P>0.05). Sucrose intake per kg body weight in red light group and depression model group were lower than control group (P<0.05). More c-fos+cells were detected in the habenula nucleus, intergeniculate leaflet and ventral lateral geniculate nucleus from blue light group than those from depression model group (P<0.05). The relative BDNF protein level and the phosphoylation of CREB in the habenula nucleus from blue light group were higher than those from depression model group (P<0.05). Conclusion: Blue light could relieve depression-like symptoms in light-deprived rats. Exposure to blue light could activate neurons in the habenula nucleus to which intrinsically photosensitive retinal ganglion cells projected. Blue-light-mediated antidepressant effect might involve in the activation of CREB/BDNF signal transduction pathways in the habenula nucleus.

0.95 W high-repetition-rate, picosecond 335 nm laser based on a frequency quadrupled, diode-pumped Nd:YVO(4) MOPA system.

An efficient all-solid-state picosecond (ps) ultraviolet (UV) laser at 335 nm was demonstrated based on frequency quadrupling of a mode-locked 1342 nm MOPA system. An output power of 0.95 W was obtained under a fundamental wave power of 16.38 W, corresponding to a conversion efficiency of 5.8% from infrared to UV. The repetition rate and pulse duration were 77 MHz and 20.2 ps, respectively. The beam quality factor M(2) was measured to be 1.56. This is, to the best of our knowledge, the highest output power at 335 nm.

MiR-31 aggravates inflammation and apoptosis in COPD rats via activating the NF-κB signaling pathway.

OBJECTIVE: To study the effect of micro ribonucleic acid (miR)-31 on rats with chronic obstructive pulmonary disease (COPD) by activating the nuclear factor-κB (NF-κB) signaling pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly divided into normal group (n=12), model group (n=12) and miR-31 mimics group (n=12). The rats were fed normally in normal group. In model group, the COPD model was first established, followed by intervention using normal saline. In miR-31 mimics group, the COPD model was also first established, followed by intervention using miR-31 mimics. The expression of NF-κB was detected via immunohistochemistry. Protein expressions of B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) were determined through Western blotting. Serum levels of interleukin-6 (IL-6), IL-18 and tumor necrosis factor-α (TNF-α) were measured via enzyme-linked immunosorbent assay (ELISA). Moreover, the apoptosis was examined via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, and the relative expression of miR-31 was detected by means of quantitative polymerase chain reaction (qPCR). RESULTS: The immunohistochemistry results showed that the positive expression of NF-κB was significantly higher in the other two groups than that in normal group (p<0.05), while it was also remarkably higher in miR-31 mimics group than that in model group (p<0.05). The results of Western blotting revealed that the relative protein expression of Bax significantly increased, while that of Bcl-2 notably declined in the other two groups compared with those in normal group (p<0.05). Similarly, the relative protein expression of Bax was upregulated, while that of Bcl-2 was distinctly reduced in miR-31 mimics group compared with those in model group (p<0.05). It was found via ELISA that the model group and miR-31 mimics group had evidently higher levels of IL-6, IL-18 and TNF-α than those in normal group (p<0.05), while miR-31 mimics group also had prominently higher levels than those in model group (p<0.05). In addition, according to the TUNEL assay, the apoptosis rate remarkably increased in the other two groups in comparison with that in normal group (p<0.05), while it remarkably rose in miR-31 mimics group compared with that in model group (p<0.05). Finally, a significantly higher expression of miR-31 was observed in the other two groups than that in normal group via qPCR (p<0.05), and such a higher expression was also found in miR-31 mimics group than that in model group (p<0.05). CONCLUSIONS: MiR-31 aggravates inflammation and apoptosis in COPD rats by activating the NF-κB signaling pathway.