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Inotodiol protects PC12 cells against injury induced by oxygen and glucose deprivation/restoration through inhibiting oxidative stress and apoptosis
Yan Li, Wenting Zhang, Chun Chen, Chunping Zhang, Jingyu Duan, Huankai Yao, Qunli Wei, Aiguo Meng, Jun Shi
Language English Country Czech Republic
- 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
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.
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Literatura
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- $a 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.
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