Ischemic stroke is a severe cause of disability and death all over the world. To search for effective therapy for ischemic stroke, PC12 cells damaged by oxygenation and glucose deprivation/restoration were employed to assess the protective effects of inotodiol. As a result, inotodiol can improve the cell viability and attenuate the leakage of lactate dehydrogenase. Meanwhile, inotodiol can prevent oxidative stress by reducing reactive oxygen species generation, decreasing the content of malonic dialdehyde, and increasing the activity of superoxide dismutase. In addition, the dysfunction of mitochondria induced by oxygenation and glucose deprivation/restoration was ameliorated through decreasing the level of intracellular calcium and increasing the mitochondrial membrane potential. At the same time, inotodiol can inhibit PC12 cells apoptosis through downregulation of Caspase-3 and Bax as well as upregulation of Bcl-2. These results reveal inotodiol can protect PC12 cells against the injury induced by oxygenation and glucose deprivation/restoration. This investigation gives promising evidences for the therapy of ischemic stroke.

• Keywords
• inotodiol,
• MeSH
• Apoptosis MeSH
• PC12 Cells * pathology   drug effects   MeSH
• Stroke * drug therapy   MeSH
• Glucose MeSH
• Caspase 3 MeSH
• Rats MeSH
• Oxygen MeSH
• Lactate Dehydrogenases metabolism   MeSH
• Lanosterol analogs & derivatives   pharmacology   MeSH
• Membrane Potential, Mitochondrial drug effects   MeSH
• Oxidative Stress drug effects   MeSH
• Reactive Oxygen Species metabolism   MeSH
• Calcium Signaling drug effects   MeSH
• Blotting, Western MeSH
• Check Tag
• Rats MeSH