Melatonin attenuates cerebral hypoperfusion-induced hippocampal damage and memory deficits in rats by suppressing TRPM7 channels

• Published in: Saudi journal of biological sciences 2022-04, Vol.29 (4), p.2958-2968
• Main Authors: Dera, Hussain Al, Alassiri, Mohammed, Kahtani, Reem Al, Eleawa, Samy M., AlMulla, Mohammad K., Alamri, Abdulhakeem
• Format: Article
• Language: English
• Subjects: Calcium; Cerebral hypoperfusion; Hippocampus; Ischemia; Melatonin; Memory; Original; Oxidative stress; TRPM7
• ISSN: 1319-562X; 2213-7106
• DOI: 10.1016/j.sjbs.2022.01.018

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 (Ca2+) and zinc (Zn2+). 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.