The Possible Mechanism Of Red Photon Protect Against Hypoxic Ischemic Brain Damage

Objective: In this study, we investigated the optimal irradiation time redphoton can protect against hypoxic ischemic brain damage models on PC12cells. Methods: A developed ischemic model using oxygen-glucosedeprivation (OGD) model, red photon group were given durationirradiating with wavelength660nm, energy density30mw/cm2LED at thebeginning of the OGD. And then, we got the PC12cells at4h,6h,8h,10h,14h:1) By using flow cytometry we tested the apoptosis rates,mitochondrial membrane potential (MMP), active oxygen species (ROS).2)Real-time PCR and Western blot were used to test the expression of mRNA and protein of bax and bcl-2. Results: after6h irradiating, the apoptosisrates，MMP and ROS were decreased, then reversed later with continuousirradiating. The same changes happened on the expression of protein andmRNA of pro-apoptotic factor bax, and anti-apoptotic factor bcl-2was onthe contrast. Conclusion: In both cases, short-term irradiation (<6h)produced protective effect of PC12Cells. On the other hand, long-term(>6h) irradiation resulted in a damage effect. We demonstrated6h is theoptimal treatment time, it could decrease the apoptosis rate, to inhibit thedeath of PC12in the acute phase. Objective: To investigated whether red photon can protect against hypoxicischemic brain damage models on PC12cells and the the possiblemechanism. Methods: A developed ischemic model using oxygen-glucosedeprivation (OGD) model, red photon group were given durationirradiating with wavelength660nm, energy density30mw/cm2LED at thebeginning of the OGD for6h. And then, we got the PC12cells at6h+2h,6h+8h:1) By using flow cytometry we tested the apoptosis rates,mitochondrial membrane potential (MMP), active oxygen species (ROS).2)Real-time PCR and Western blot were used to test the expression of mRNAand protein of bax and bcl-2. Results: After6h irradiating, the MMP, ROSand apoptosis rates was significantly decreased. The same changeshappened on the expression of protein and mRNA of bax, and bcl-2on theopposite, but there was no significantly difference at6h+8h. Conclusion:Combined with the treatment effect short-term irradiating in the acutephase we demonstrated that red photon could decrease the apoptosis, toinhibit the death of PC12in the acute phase. We can get a short term effective therapy. And it might decreased the ROS level, inhibit theexpression of bax and increase the bcl-2, to main the stability ofmitochondrial membrane potential, and then decreased the nerve cellsapoptosis, improve the prognosis of HIBD. Objective: To investigate the effect and the possible mechanism of redphoton on hypoxic-ischemic brain damage on acute phase in neonatal rats.Methods:75seven days old Sprague Dawley rats were randomly dividedinto CON group, HIBD group, RP group. HIBD group were induced usingRice-Vannueci model. RP rats were irradiated on scalp by red photonimmediately after HIBD,30min per day, lasted7days.1) Random10ratsof each group were sacrificed by cervical dislocation and the lefthippocampus was rapidly isolated and snap-frozen in liquid nitrogen foruse in mRNA and protein examination, on the7day.2) Random10ratswas used for moriss water maze to test the learning and memory function28days after HIBD;3) Random5rats was used for immunofluorescence toevaluate the expression of bax and bcl-2in the localization and semiquantitative. Results: The mRNA and protein of bax and bcl-2in lefthippocampus of rats were respectively higher expression of HIBD group than CON group on7day (P<0.05). After irradiated by red light, themRNA and protein expression of bax of RP group was significantly lowerthan HIBD group, and bcl-2on contrast. The moriss water maze at35dshowed escape latency was significantly shorter of RP group than HIBDgroup on4-6d. And there was a a significant shorter on path length on3-6dof RP group than HIBD group and passing times increased on7d. In theCA1field and CA3field, the bax staining in RP group were evidentedlower level than HIBD group. And the bcl-2was higher than HIBD rats.Conclusion: Red photon can decrease the expression of pro-apoptosisfactor of bax and increase the anti-apoptosis factor bcl-2of hypoxicischemic brain damage in acute phase, and decrease the neural cellsapoptosis, to achieve the purpose of treatment on hypoxic-ischemic braindamage.