| خلاصه مقاله | Ischemic stroke has remained a principal cause of mortality and neurological disabilities worldwide. Blood flow resumption, reperfusion, in the cerebral ischemia prompts a cascade in the brain characterized by various cellular mechanisms like mitochondrial dysfunction, oxidative stresses, endoplasmic reticulum (ER) stress, and excitotoxicity, finally resulting in programmed cell death. Any changes in the ER-mitochondria axis are probably responsible for both the onset and progression of central nervous system diseases. Melatonin, a neuro-hormone secreted by the pineal gland, has anti-oxidative, anti-inflammatory, and anti-apoptotic properties. Most studies have shown that it exerts neuroprotective effects against ischemic stroke. It has been demonstrated that ER- mitochondrial interactions play critical roles in various physiological and pathophysiological processes. In the ischemic brain, ER-mitochondria crosstalk is involved in multiple cellular functions such as mitochondrial Ca2 + homeostasis, the start of autophagosome formation, cellular apoptosis, lipid transportation, and also mitochondrial fission site determination. Based on the findings of previous studies, melatonin has an improving effect on each organelle function. Melatonin therapy showed that not only reduced mitochondrial dysfunction but also alleviated ER stress and inflammation. Hence, it seems that melatonin may exert a protective role on the crosstalk between the mitochondria and ER stress mechanisms following stroke. Given that stroke leads to mitochondrial and ER dysfunction, and regarding this fact that dysfunction of each organelle aggravates their effects, using appropriate drug intervention that improves the function of ER and mitochondria lonely or in crosstalk connection can be a useful treatment for stroke. Schematic figure shows the ischemic stroke-induced endoplasmic reticulum-mitochondrial Crosstalk and role of melatonin in this cascade |