Department of Pharmacology and Toxicology, KLE College of Pharmacy, KLE Academy of Higher Education and Research (KAHER), Belagavi, Karnataka, India.
Department of Pharmacognosy, KLE College of Pharmacy, KLE Academy of Higher Education and Research (KAHER), Belagavi, Karnataka, India.
J Biophotonics. 2023 Aug;16(8):e202300012. doi: 10.1002/jbio.202300012. Epub 2023 May 5.
The loss and progressive dysfunction of neurons are hallmarks of neurodegenerative diseases. The aim of the current study is to explore the effects of photobiomodulation at 460-660 nm (100-1000 lux units) on the progression of scopolamine-induced cognitive dysfunctions in Wistar male rats. Photobiomodulation (PBM) is defined as "the use of monochromatic or quasi-monochromatic light from a low-power laser or light-emitting diode (LED) source to modify or modulate biological functions." Neuroprotective activity was assessed by in vivo models such as the Morris water maze, the elevated plus maze (EPM), and the T-maze. After using scopolamine (1 mg/kg/day) as a dementia induction model for 21 days, the induction was primarily due to impairments in cholinergic transmission, oxidative stress, and inflammation. The in vitro determinations, including acetylcholinesterase (AChE), butyrylcholinesterase (BChE), reduced glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor-alpha (TNF-α), Interleukin 1 beta (IL-1β), and alkaline phosphatase (ALP), were assessed biochemicals and biomarkers. The structural and morphological integrity of the cortex and hippocampus was investigated through histopathology. In vivo studies of exteroceptive behavior models such as the Morris water maze, the EPM, and the T-maze revealed that administration of scopolamine resulted in enhanced escape latency time (ELT), transfer latency (TL), and decreased percentage alternation, respectively. The levels of AChE, BChE, reduced, GSH, SOD, TNF-α, IL-1β and ALP were increased, while MDA level was decreased. In contrast to normal and control groups with treatment groups, histopathology of the cortex and hippocampus examination revealed the maintenance of structural integrity and densities of CA1 and CA3 neuronal cells. However, network pharmacology predicted Ca modulation of various pathways, among the treatments with red LED light showed highly significant amelioration compared with normal and control groups. Photobiomodulation by hormesis, chromophores in cells, and tissues excitation can influence neuroprotective effect mainly by scavenging of ROS, variation in the level of GSH MDA and SOD mitochondrial electron transfer, the improved abscopal effects on improved in gut microbiome by resembles the of fecal ALP level correlation of intestinal microbiome, cholinergic neurotransmissions, anti-inflammatory, and antioxidant activities.
神经元的丧失和逐渐功能障碍是神经退行性疾病的标志。本研究旨在探讨 460-660nm(100-1000lux 单位)的光生物调节对东莨菪碱诱导的 Wistar 雄性大鼠认知功能障碍进展的影响。光生物调节(PBM)的定义为“使用低功率激光或发光二极管(LED)源的单色或准单色光来修饰或调节生物功能”。神经保护活性通过体内模型进行评估,如 Morris 水迷宫、高架十字迷宫(EPM)和 T 迷宫。使用东莨菪碱(1mg/kg/天)作为痴呆诱导模型 21 天后,诱导主要是由于胆碱能传递、氧化应激和炎症受损。体外测定包括乙酰胆碱酯酶(AChE)、丁酰胆碱酯酶(BChE)、还原型谷胱甘肽(GSH)、丙二醛(MDA)、超氧化物歧化酶(SOD)、肿瘤坏死因子-α(TNF-α)、白细胞介素 1β(IL-1β)和碱性磷酸酶(ALP),评估生物化学和生物标志物。通过组织病理学研究皮质和海马的结构和形态完整性。体内外感受性行为模型,如 Morris 水迷宫、EPM 和 T 迷宫的研究表明,给予东莨菪碱可导致逃避潜伏期时间(ELT)延长、转移潜伏期(TL)延长和百分比交替减少。AChE、BChE、还原型 GSH、SOD、TNF-α、IL-1β和 ALP 水平升高,MDA 水平降低。与正常和对照组相比,治疗组的皮质和海马组织病理学检查显示结构完整性和 CA1 和 CA3 神经元细胞密度得以维持。然而,网络药理学预测了各种途径的钙调节,其中红色 LED 光治疗显示出与正常和对照组相比具有高度显著的改善。光生物调节通过细胞和组织中的生色团的应激反应,主要通过清除 ROS、GSH MDA 和 SOD 线粒体电子传递水平的变化、改善肠道微生物组的旁效应(通过粪便 ALP 水平的相关性)、肠道微生物组、胆碱能神经传递、抗炎和抗氧化活性。