1. Department of Pathophysiology, College of Basic Medical Science, China Medical University;
2. Department of Pharmacology, Liaoning Medical University;
3. Department of Urology, the Forth Affiliated Hospital, China Medical University;
4. Tanaka Memorial Laboratory, Nikken Sohonsha Corporation;
5. International Education School, China Medical University;
6. Department of ethnopharmacology, School of Pharmaceutical Sciences, China Medical University
* Luning Sun and Ying Jin equally contributed at this work.
Stroke is a major cause of mortality and the leading cause of permanent disability. In this study, we adopted the classic middle cerebral artery occlusion(MCAO) stroke model to observe the therapeutic effects of coccomyxa gloeobotrydiformis(CGD) on ischemic stroke, and discuss the underlying mechanisms. Low dose (50 mg/kg.day) and high dose (100 mg/kg.day) concentrations of the drug CGD were intragastrically administrated separately for 8 weeks. Infarct volumes, neurologic deficits and degree of stroke-induced brain edema were measured 24 hours after reperfusion. Furthermore, oxidative stress related factors (SOD and MDA), mitochondrial membrane potential, and apoptosis regulatory factors (mitochondrial Cyt-C, Bcl-2, Bax, and caspase-3) were all investigated in this research. We found that CGD attenuated cerebral infarction, brain edema and neurologic deficits; CGD maintained the mitochondrial membrane potential and decreased mitochondrial swelling. It also prevented oxidative damage by reducing MDA and increasing SOD. In addition, CGD could effectively attenuate apoptosis by restoring the level of mitochondrial Cyt C and regulating the expression of Bcl-2, Bax and caspase 3. These results revealed that CGD has a therapeutic effect on ischemic stroke, possibly by inducing mitochondrial protection and anti-apoptotic mechanisms.
Keywords: Coccomyxa gloeobotrydiformis (CGD), ischemic stroke, apoptosis, mitochondrion