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Protective effects of 6‐gingerol on 6‐hydroxydopamine‐induced apoptosis in PC12 cells through modulation of SAPK/JNK and survivin activation
Due to many therapeutic effects, Ginger (Zingiber officinale) is the most widely used spice around the world, including in Iran. Due to its potent anti‐inflammatory and antioxidant effects, ginger may protect against neurodegenerative disorders. Here, we investigated the effects of 6‐gingerol (the m...
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Published in: | Journal of biochemical and molecular toxicology 2022-02, Vol.36 (2), p.e22956-n/a |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Due to many therapeutic effects, Ginger (Zingiber officinale) is the most widely used spice around the world, including in Iran. Due to its potent anti‐inflammatory and antioxidant effects, ginger may protect against neurodegenerative disorders. Here, we investigated the effects of 6‐gingerol (the main bioactive compound in ginger) on 6‐hydroxydopamine (6‐OHDA)‐induced cell death in PC12 cells. Cell viability, cell apoptosis, and stress‐activated protein kinase/c‐Jun N‐terminal kinase (SAPK/JNK), and survivin expression were measured using resazurin, propidium iodide (PI) and flow cytometry, and western blot analysis. 6‐OHDA (100 μM) reduced the cell viability, increased apoptosis, increased the active form of SAPK/JNK, and decreased survivin protein level in PC12 exposed cells in a dose and time‐dependent manner. Pretreatment with 6‐gingerol significantly increased the viability and reduced apoptosis (2.5 and 5 µM). Also, pretreatment with 6‐gingerol at 2.5 and 5 µM increased survivin whereas, 6‐gingerol at 2.5 µM reduced (P‐SAPK/JNK):(SAPK/JNK) levels to a level near that of the related control. According to the results, 6‐gingerol blocks 6‐OHDA‐induced cell damage by suppressing oxidative stress and anti‐apoptotic activity. Thus, 6‐gingerol may process beneficial protective effects in slowing the progression of Parkinson's disease. |
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ISSN: | 1095-6670 1099-0461 |
DOI: | 10.1002/jbt.22956 |