title: Red photon treatment inhibits apoptosis via regulation of bcl-2 proteins and ROS levels, alleviating hypoxic-ischemic brain damage.
abstract: Therapeutic options for hypoxic-ischemic brain damage (HIBD) are scarce and inefficient. Recently, many studies have demonstrated that red photon plays an important role in anti-inflammatory processes as well as apoptosis, the main trait of HIBD. In this study, we investigated whether red photon can protect from HIBD in SD rats and oxygen-glucose deprivation (OGD) in PC12 cells. Apoptosis, mitochondrial transmembrane potential (MMP), and reactive oxygen species (ROS) rates were assessed in PC12 cells. We found that 6-h irradiation resulted in decreased MMP, ROS and apoptosis rates, although these changes were reversible with prolonged irradiation. Importantly, these effects were sustained for 2-8h upon quenching of the red photon. Similar trends were observed for protein and mRNA expression of bax and bcl-2, with short-term irradiation (6h) inhibiting apoptosis in PC12 Cells. However, long-term (>6h) irradiation caused cell damage. In vivo experiments, bax mRNA and protein levels were reduced after 7days in HIBD model rats treated with red photon, in contrast to bcl-2. Furthermore, we found that bax and bcl-2 were mainly expressed in pyramidal cells of the hippocampus CA1 and CA3. Importantly, Morris Water Maze test results revealed an improvement in learning ability and spatial memory in rats after irradiation. Overall, our data showed that short-term irradiation with red photon in the acute phase inhibits the mitochondrial apoptotic pathway via regulation of bcl-2-related proteins and reduction of ROS levels, thereby decreasing apoptosis in nerve cells and improving the neurological prognosis of HIBD.
authors.affiliation: Rehabilitation Centers, Children's Hospital of Chongqing Medical University, Chongqing 400014, China; Children Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing 400014, China.
authors.forename: W
authors.initials: W
authors.lastname: Jiang
authors.affiliation: Rehabilitation Centers, Children's Hospital of Chongqing Medical University, Chongqing 400014, China; Children Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing 400014, China; Department of Pediatrics, University-Town Hospital of Chong Qing Medical University, Chongqing 401331, China.
authors.forename: L
authors.initials: L
authors.lastname: Chen
authors.affiliation: Children Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing 400014, China.
authors.forename: X J
authors.initials: XJ
authors.lastname: Zhang
authors.affiliation: Children Nutrition Research Center, Children's Hospital of Chongqing Medical University, Chongqing 400014, China; Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Developmental Diseases in Childhood, Ministry of Education Key Laboratory of Child Development and Disorders, Key Laboratory of Pediatrics in Chongqing, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Chongqing 400014, China.
authors.forename: J
authors.initials: J
authors.lastname: Chen
authors.affiliation: Biological Engineering Institute of Chongqing University, Chongqing 400014, China.
authors.forename: X C
authors.initials: XC
authors.lastname: Li
authors.affiliation: Biological Engineering Institute of Chongqing University, Chongqing 400014, China.
authors.forename: W S
authors.initials: WS
authors.lastname: Hou
authors.affiliation: Rehabilitation Centers, Children's Hospital of Chongqing Medical University, Chongqing 400014, China; Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Developmental Diseases in Childhood, Ministry of Education Key Laboratory of Child Development and Disorders, Key Laboratory of Pediatrics in Chongqing, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Chongqing 400014, China. Electronic address: xiaonongwl@163.com.
authors.forename: N
authors.initials: N
authors.lastname: Xiao
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology / Q000528:radiation effects*; D056547:CA1 Region, Hippocampal / Q000503:physiopathology / Q000528:radiation effects; D056654:CA3 Region, Hippocampal / Q000503:physiopathology / Q000528:radiation effects; D004195:Disease Models, Animal; D015870:Gene Expression / Q000528:radiation effects; D020925:Hypoxia-Ischemia, Brain / Q000503:physiopathology* / Q000628:therapy*; D018782:Maze Learning / Q000528:radiation effects; D053078:Membrane Potential, Mitochondrial / Q000528:radiation effects; D016716:PC12 Cells; D010789:Phototherapy / Q000379:methods*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D017966:Pyramidal Cells / Q000503:physiopathology / Q000528:radiation effects; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013997:Time Factors; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein
keywords: ROS; apoptosis; bax; bcl-2; hypoxic–ischemic brain damage; red photon