J Appl Biomed 16:126-132, 2018 | DOI: 10.1016/j.jab.2017.11.004

Inotodiol protects PC12 cells against injury induced by oxygen and glucose deprivation/restoration through inhibiting oxidative stress and apoptosis

Yan Li^a, Wenting Zhang^b, Chun Chen^a, Chunping Zhang^a, Jingyu Duan^a, Huankai Yao^a,*, Qunli Wei^a, Aiguo Meng^b,*, Jun Shi^b

^a Xuzhou Medical University, School of Pharmacy and Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou, Jiangsu, China

^b North China University of Science and Technology, Affiliated Hospital and School of Clinical Medicine, Tangshan, Hebei, China

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; PC12 cells; Oxygen and glucose deprivation; Apoptosis; Oxidative stress

Received: August 8, 2016; Revised: September 19, 2017; Accepted: November 23, 2017; Published: May 1, 2018  Show citation