KMID : 0624620180510080400
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BMB Reports 2018 Volume.51 No. 8 p.400 ~ p.405
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The protective effects of ethanolic extract of Clematis terniflora against corticosterone-induced neuronal damage via the AKT and ERK1/2 pathway
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Noh Yoo-Hun
Cheon Seung-Ui Kim In-Hye Kim In-Yong Lee Seung-Ah Kim Do-Hee Jeong Yoon-Hwa
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Abstract
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Chronic stress induces neuronal cell death, which can cause nervous system disorders including Parkinson¡¯s disease and Alzheimer¡¯s disease. In this study, we evaluated the neuroprotective effects of Clematis terniflora extract (CTE) against corticosterone-induced apoptosis in rat pheochromocytoma (PC12) cells, and also investigated the underlying molecular mechanisms. At concentrations of 300 and 500 ¥ìg/ml, CTE significantly decreased apoptotic cell death and mitochondrial damage induced by 200 ¥ìM corticosterone. CTE decreased the expression levels of endoplasmic reticulum (ER) stress proteins GRP78, GADD153, and mitochondrial damage-related protein BAD, suggesting that it downregulates ER stress evoked by corticosterone. Furthermore, our results suggested that these protective effects were mediated by the upregulation of p-AKT and p-ERK1/2, which are involved in cell survival signaling. Collectively, our results indicate that CTE can lessen neural damage caused by chronic stress.
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KEYWORD
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Chronic stress, Clematis terniflora, Corticosterone, ER stress, Neuroprotective effect
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