Dera Hussain Al, Alassiri Mohammed, Kahtani Reem Al, Eleawa Samy M, AlMulla Mohammad K, Alamri Abdulhakeem
Department of Basic Medical Sciences, College of Medicine at King Saud, Abdulaziz University for Health Sciences (KSAU-HS), King Abdullah International Medical Research Centre, Ministry of the National Guard Health Affairs, Riyadh, Kingdom of Saudi Arabia.
Department of Basic Sciences, College of Science and Health Professions, King Saud bin Abdulaziz University for Health Sciences (KSAU-HS), King Abdullah International Medical Research Centre, Ministry of the National Guard Health Affairs, Riyadh, Kingdom of Saudi Arabia.
Saudi J Biol Sci. 2022 Apr;29(4):2958-2968. doi: 10.1016/j.sjbs.2022.01.018. Epub 2022 Jan 18.
This study was conducted to examine if modulating transporters like transient receptor potential cation channels, subfamily M, member 7 (TRPM7) underlies the hippocampal neuroprotection afforded by melatonin (Mel) in rats exposed to cerebral hypoperfusion (CHP). Experimental groups included control, Mel-treated (1.87 g/kg), CHP, and CHP + Mel (1.87 g/kg)-treated rats. CHP was induced by the permanent bilateral occlusion of the common carotid arteries (2VO) method and treatments were conducted for 7 days, orally. Mel prevented the damage of the dental gyrus and memory loss in CHP rats and inhibited the hippocampal reactive oxygen species (ROS), lipid peroxidation levels of tumor necrosis factor-α (TNF-α), interleukine-6 (IL-6), interleukine-1 beta (IL-1β), and prostaglandin E2 (PGE2). It also reduced the hippocampal transcription of the TRPM7 channels and lowered levels of calcium (Ca) and zinc (Zn). Mel Also enhanced the levels of total glutathione (GSH) and superoxide dismutase (SOD) in the hippocampus of the control and CHP-treated rats. In conclusion, downregulation of TRPM7 seems to be one mechanism underlying the neuroprotective effect of Mel against global ischemia and is triggered by its antioxidant potential.
本研究旨在探讨调节转运体，如瞬时受体电位阳离子通道M亚家族成员7（TRPM7），是否是褪黑素（Mel）对脑灌注不足（CHP）大鼠海马神经保护作用的基础。实验组包括对照组、Mel处理组（1.87 g/kg）、CHP组和CHP + Mel（1.87 g/kg）处理组大鼠。通过永久性双侧颈总动脉闭塞（2VO）法诱导CHP，并口服给药7天。Mel可预防CHP大鼠齿状回损伤和记忆丧失，并抑制海马活性氧（ROS）、肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）和前列腺素E2（PGE2）的脂质过氧化水平。它还降低了TRPM7通道的海马转录水平，降低了钙（Ca）和锌（Zn）的水平。Mel还提高了对照组和CHP处理组大鼠海马中总谷胱甘肽（GSH）和超氧化物歧化酶（SOD）的水平。总之，TRPM7的下调似乎是Mel对全脑缺血神经保护作用的一种机制，并且是由其抗氧化潜力触发的。
