Melatonin modulates the aggravation of pyroptosis, necroptosis, and neuroinflammation following cerebral ischemia and reperfusion injury in obese rats

This study aimed to investigate the roles of melatonin on pyroptosis, necroptosis, and pro-inflammatory pathways occurring in the I/R brain of obese rats. Male Wistar rats were given a high-fat diet for 16 weeks to induce the obese condition, and then were divided into 4 groups: Sham-operated, I/R treated with vehicle, I/R treated with melatonin (10 mg/kg), and I/R treated with glycyrrhizic acid (10 mg/kg). All drugs were administered via intraperitoneal injection at the onset of reperfusion. The development of neurological deficits, cerebral infarction, histological changes, neuronal death, and glial cell hyperactivation were investigated. This study revealed that melatonin effectively improved these detrimental parameters. Furthermore, the processes of pyroptosis, necroptosis, and inflammation were all diminished by melatonin treatment. A summary of the findings is that melatonin effectively reduces ischemic brain pathology and thereby improves post-stroke outcomes in obese rats by modulating pyroptosis, necroptosis, and inflammation.PMID:37302429 | DOI:10.1016/j.bbadis.2023.166785
Source: Biochimica et Biophysica Acta - Category: Biochemistry Authors: Source Type: research