The present work examined the effect exerted by tectoridin preventing oxygen glucose deprivation/reoxygenation (OGD/R) damage within PC12 cell. We incubated PC12 cells with Na2S2O4 (10 mM) for 2 h, and tectoridin at different concentrations was then added; based on methyl-thiazolyl-tetrazolium (MTT) and lactate dehydrogenase (LDH) tests, the protection impact was tested. 2',7'-dicholorofluorescein diacetate (DCFH-DA), Fluo-3AM, and 5, 5', 6, 6' -tetrachloro-1, 1', 3, 3' -tetraethyl-imidacarbocyanine iodide (JC-1) staining, and Western blotting were used for determining reactive oxygen species (ROS) level, intracellular Ca2+ content, mitochondrial membrane potential (MMP) and the related proteins contents. As a result, tectoridin could improve the cell viability and inhibit the release of LDH. In-depth studies demonstrated that tectoridin limited the overproduction of ROS and intracellular Ca2+ content and increased MMP, which showed a close association with ROS-mediated mitochondrial function. Moreover, tectoridin hindered apoptosis based on the up-regulation of the expressions of p-AKT, Bcl-2/Bax and p-mTOR. Furthermore, the level of Nrf2 was also improved by treatment of tectoridin. In addition, the expression of Bcl-2/Bax, p-Akt, p-mTOR, Nrf2, HO-1, NQO1 and GCLM were reduced by LY294002 and the protective role of tectoridin was limited by LY294002. The results unambiguously suggested that tectoridin reduced OGD/R-caused damage to PC12 cells and might ensure neuroprotection by stimulating the PI3K/AKT signaling channel.
Keywords: OGD/R; PI3K/AKT signaling channel; Stroke; Tectoridin.
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