Aluminum chloride-induced amyloidβ accumulation and endoplasmic reticulum stress in rat brain are averted by melatonin.
Food Chem Toxicol. 2020 Oct 29 ;146:111829. Epub 2020 Oct 29. PMID: 33130240
Accumulation of aluminium (Al) in the brain is known to be a toxic insult that result in neurodegenerative diseases and melatonin is known to have neuroprotective role. The present study was designed to investigate the neuroprotective effects of melatonin for aluminium chloride (AlCl)-induced neurotoxicity in rats. Twelve-week old male Wistar rats were orally received 175 mg/kg AlClwith or without 5 mg/kg melatonin intraperitoneal pretreatment. Group 3 intraperitoneally recieved 5 mg/kg melatonin and group 4 rats were orally treated with saline solution for 8 weeks. A series of behavioral tests, biochemical analysis and expression of AD-associated proteins in the brain were determined after7 weeks of all treatments. Our results indicated that AlCltreatment tends to induce memory and cognitive impairment. However, melatonin treatment attenuated amyloid beta (Aβ) (1-42) level by decreasing β-secretase, augmented low-density lipoprotein receptor-related protein 1, and neprilysin protein expression. Moreover, AlCl-induced endoplasmic reticulum (ER) stress and oxidative stress was attenuated by melatonin supplementation. In conclusion, these findings demonstrate a protective role of melatonin against Aβ peptide accumulation, ER stress and oxidative stress in the AlCl-treated AD model. Hence, the melatonin supplement might be an alternative way to alleviate the development of AD.