Host: The Japanese Pharmacological Society
Name : The 97th Annual Meeting of the Japanese Pharmacological Society
Number : 97
Location : [in Japanese]
Date : December 14, 2023 - December 16, 2023
Cerebral ischemia is a lethal disease that causes irreversible neuronal damage and severe sequelae worldwide. Reperfusion therapy is performed after cerebral ischemia but induces further injury with mitochondrial dysfunction. Minimizing ischemia-reperfusion injury and improving prognosis may benefit from mitochondrial protection. In the present study, we investigated the effects of Mitochonic acid -5 (MA-5), which activates mitochondria and increases the efficiency of adenosine triphosphate production, on neuronal cell damage using in vivo and in vitro experimental models. Male ddY mice were subjected to transient cerebral ischemia by reperfusion 2 hours after middle cerebral artery occlusion (MCAO). Immediately after reperfusion, MA-5 was administered intracerebroventricularly at 0.66 or 0.066 μg. The human neuroblastoma cell line, SH-SY5Y was exposed to oxygen-glucose deprivation followed by reoxygenation (OGD/R). MA-5 significantly reduced infarct volume and improved neurological deficits 24 hours after MCAO. MA-5 suppressed cell death and reactive oxygen species (ROS) production in SH-SY5Y cells after OGD/R. In conclusion, MA-5 has a neuroprotective effect against cerebral ischemia/reperfusion injury, and it might contribute to the improvement of prognosis as a novel therapeutic drug.
