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Sedum takesimense Protects PC12 Cells against Corticosterone-Induced Neurotoxicity by Inhibiting Neural Apoptosis.
Nutrients. 2020 Nov 30; 12(12)N

Abstract

Neuronal cell death induced by chronic stress in the central nervous system is a cause of neurological dysfunction. We investigated the neuroprotective potential of a water extract of S. takesimense (WEST) against corticosterone-induced apoptosis in PC12 cells and the possible underlying mechanisms. Cells were pretreated with 50 µg/mL of WEST to evaluate its neuroprotective effect based on endoplasmic reticulum (ER) stress inhibition and mitochondrial function improvement. Pretreatment with WEST prevented corticosterone-induced injury in PC12 cells, resulting in increased cell survival, decreased lactate dehydrogenase (LDH) release, and potent apoptosis inhibition by a reduction in apoptotic nuclei demonstrated by Hoechst 33,342 and propidium iodide (PI) double staining, and TUNEL staining. WEST strongly attenuated calcium (Ca2+) elevation, inducing the closure of mitochondrial permeability transition pores (mPTPs), which were opened by corticosterone. It also stabilized mitochondrial membrane potential (MMP) loss and inhibited the corticosterone-induced decrease in adenosine triphosphate (ATP) levels. Furthermore, the increased reactive oxygen species (ROS) production induced by corticosterone was prevented in PC12 cells treated with WEST. WEST also downregulated the expression of glucose-regulated protein 78 (GRP78), growth arrest- and DNA damage-inducible gene 153 (GADD153), the pro-apoptotic protein Bcl-2-associated X (Bax), cytochrome c, cysteine-aspartic protease (caspase)-9, and caspase-3, and upregulated the expression of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2). Thus, WEST exerts a neuroprotective effect by inhibiting the apoptosis pathway in ER stress and the mitochondrial dysfunction induced by corticosterone. These results demonstrate that WEST reduces neuronal damage from the neurotoxicity caused by chronic stress.

Authors+Show Affiliations

Research Center for Industrialization of Natural Nutraceuticals, Dankook University, Cheonan 31116, Korea.Research Center for Industrialization of Natural Nutraceuticals, Dankook University, Cheonan 31116, Korea. Department of Food Science and Nutrition, Dankook University, Cheonan 31116, Korea.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

33266322

Citation

Yun, Hea-Yeon, and Yoonhwa Jeong. "Sedum Takesimense Protects PC12 Cells Against Corticosterone-Induced Neurotoxicity By Inhibiting Neural Apoptosis." Nutrients, vol. 12, no. 12, 2020.
Yun HY, Jeong Y. Sedum takesimense Protects PC12 Cells against Corticosterone-Induced Neurotoxicity by Inhibiting Neural Apoptosis. Nutrients. 2020;12(12).
Yun, H. Y., & Jeong, Y. (2020). Sedum takesimense Protects PC12 Cells against Corticosterone-Induced Neurotoxicity by Inhibiting Neural Apoptosis. Nutrients, 12(12). https://doi.org/10.3390/nu12123713
Yun HY, Jeong Y. Sedum Takesimense Protects PC12 Cells Against Corticosterone-Induced Neurotoxicity By Inhibiting Neural Apoptosis. Nutrients. 2020 Nov 30;12(12) PubMed PMID: 33266322.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sedum takesimense Protects PC12 Cells against Corticosterone-Induced Neurotoxicity by Inhibiting Neural Apoptosis. AU - Yun,Hea-Yeon, AU - Jeong,Yoonhwa, Y1 - 2020/11/30/ PY - 2020/10/12/received PY - 2020/11/25/revised PY - 2020/11/27/accepted PY - 2020/12/3/entrez PY - 2020/12/4/pubmed PY - 2021/5/4/medline KW - ER stress KW - PC12 cells KW - Sedum takesimense KW - apoptosis KW - mitochondrial dysfunction JF - Nutrients JO - Nutrients VL - 12 IS - 12 N2 - Neuronal cell death induced by chronic stress in the central nervous system is a cause of neurological dysfunction. We investigated the neuroprotective potential of a water extract of S. takesimense (WEST) against corticosterone-induced apoptosis in PC12 cells and the possible underlying mechanisms. Cells were pretreated with 50 µg/mL of WEST to evaluate its neuroprotective effect based on endoplasmic reticulum (ER) stress inhibition and mitochondrial function improvement. Pretreatment with WEST prevented corticosterone-induced injury in PC12 cells, resulting in increased cell survival, decreased lactate dehydrogenase (LDH) release, and potent apoptosis inhibition by a reduction in apoptotic nuclei demonstrated by Hoechst 33,342 and propidium iodide (PI) double staining, and TUNEL staining. WEST strongly attenuated calcium (Ca2+) elevation, inducing the closure of mitochondrial permeability transition pores (mPTPs), which were opened by corticosterone. It also stabilized mitochondrial membrane potential (MMP) loss and inhibited the corticosterone-induced decrease in adenosine triphosphate (ATP) levels. Furthermore, the increased reactive oxygen species (ROS) production induced by corticosterone was prevented in PC12 cells treated with WEST. WEST also downregulated the expression of glucose-regulated protein 78 (GRP78), growth arrest- and DNA damage-inducible gene 153 (GADD153), the pro-apoptotic protein Bcl-2-associated X (Bax), cytochrome c, cysteine-aspartic protease (caspase)-9, and caspase-3, and upregulated the expression of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2). Thus, WEST exerts a neuroprotective effect by inhibiting the apoptosis pathway in ER stress and the mitochondrial dysfunction induced by corticosterone. These results demonstrate that WEST reduces neuronal damage from the neurotoxicity caused by chronic stress. SN - 2072-6643 UR - https://www.unboundmedicine.com/medline/citation/33266322/Sedum_takesimense_Protects_PC12_Cells_against_Corticosterone_Induced_Neurotoxicity_by_Inhibiting_Neural_Apoptosis_ L2 - https://www.mdpi.com/resolver?pii=nu12123713 DB - PRIME DP - Unbound Medicine ER -