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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

  • Noh, Yoohun (Famenity Biomedical Research Center, Famenity, Inc.) ;
  • Cheon, Seungui (Famenity Biomedical Research Center, Famenity, Inc.) ;
  • Kim, In Hye (Famenity Biomedical Research Center, Famenity, Inc.) ;
  • Kim, Inyong (Research Center for Industrialization of Natural Nutraceuticals, Dankook University) ;
  • Lee, Seung-Ah (Natural Pharmaceutical R&D Center, Naturesense, Inc.) ;
  • Kim, Do-Hee (Natural Pharmaceutical R&D Center, Naturesense, Inc.) ;
  • Jeong, Yoonhwa (Research Center for Industrialization of Natural Nutraceuticals, Dankook University)
  • Received : 2018.04.30
  • Accepted : 2018.06.12
  • Published : 2018.08.31

Abstract

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 $500{\mu}g/ml$, CTE significantly decreased apoptotic cell death and mitochondrial damage induced by $200{\mu}M$ 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.

Keywords

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