EGCG treats ICH via up-regulating miR-137-3p and inhibiting Parthanatos
Intracranial hemorrhage (ICH) causes high mortality and disability without effective treatment in the clinical setting. (−)-Epigallocatechin-3-gallate (EGCG) exerts an essential role in the central nervous system and offers a promising therapeutic agent for the treatment of oxidative damage-related...
Ausführliche Beschreibung
Autor*in: |
Wang Jianjun [verfasserIn] Kuang Xuejun [verfasserIn] Peng Zhao [verfasserIn] Li Conghui [verfasserIn] Guo Chengwu [verfasserIn] Fu Xi [verfasserIn] Wu Junhong [verfasserIn] Luo Yang [verfasserIn] Rao Xiaolin [verfasserIn] Zhou Xiangjuan [verfasserIn] Huang Bin [verfasserIn] Tang Weijun [verfasserIn] Tang Yinjuan [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2020 |
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Übergeordnetes Werk: |
In: Translational Neuroscience - De Gruyter, 2015, 11(2020), 1, Seite 371-379 |
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Übergeordnetes Werk: |
volume:11 ; year:2020 ; number:1 ; pages:371-379 |
Links: |
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DOI / URN: |
10.1515/tnsci-2020-0143 |
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Katalog-ID: |
DOAJ085905038 |
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10.1515/tnsci-2020-0143 doi (DE-627)DOAJ085905038 (DE-599)DOAJ6992334a66e446148df174d4d2245f73 DE-627 ger DE-627 rakwb eng RC321-571 Wang Jianjun verfasserin aut EGCG treats ICH via up-regulating miR-137-3p and inhibiting Parthanatos 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Intracranial hemorrhage (ICH) causes high mortality and disability without effective treatment in the clinical setting. (−)-Epigallocatechin-3-gallate (EGCG) exerts an essential role in the central nervous system and offers a promising therapeutic agent for the treatment of oxidative damage-related diseases. MiR-137 can inhibit the oxidative stress and apoptosis to attenuate neuronal injury. However, the role of EGCG in regulating miR-137-3p and neuronal Parthanatos remains to be unclear. In the present study, we build the ICH mice model to investigate the antioxidant effects of EGCG via upregulating miR-137-3p and inhibiting neuronal Parthanatos. We revealed that EGCG upregulated miR-137-3p and inhibited neuronal Parthanatos, and promoted the functional recovery, alleviated ICH-induced brain injury, and reduced oxidative stress in mice following ICH. However, following the inhibition of miR-137-3p and activation of Parthanatos, EGCG was unable to exert neuroprotective roles. These combined results suggest that EGCG may upregulate miR-137-3p and inhibit neuronal Parthanatos to accelerate functional recovery in mice after ICH, laying the foundation for EGCG to be a novel strategy for the treatment of neuronal injuries related to Parthanatos. intracranial hemorrhage (−)-epigallocatechin-3-gallate mir-137-3p parthanatos Neurosciences. Biological psychiatry. Neuropsychiatry Kuang Xuejun verfasserin aut Peng Zhao verfasserin aut Li Conghui verfasserin aut Guo Chengwu verfasserin aut Fu Xi verfasserin aut Wu Junhong verfasserin aut Luo Yang verfasserin aut Rao Xiaolin verfasserin aut Zhou Xiangjuan verfasserin aut Huang Bin verfasserin aut Tang Weijun verfasserin aut Tang Yinjuan verfasserin aut In Translational Neuroscience De Gruyter, 2015 11(2020), 1, Seite 371-379 (DE-627)640087507 (DE-600)2581219-1 20816936 nnns volume:11 year:2020 number:1 pages:371-379 https://doi.org/10.1515/tnsci-2020-0143 kostenfrei https://doaj.org/article/6992334a66e446148df174d4d2245f73 kostenfrei https://doi.org/10.1515/tnsci-2020-0143 kostenfrei https://doaj.org/toc/2081-6936 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2020 1 371-379 |
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10.1515/tnsci-2020-0143 doi (DE-627)DOAJ085905038 (DE-599)DOAJ6992334a66e446148df174d4d2245f73 DE-627 ger DE-627 rakwb eng RC321-571 Wang Jianjun verfasserin aut EGCG treats ICH via up-regulating miR-137-3p and inhibiting Parthanatos 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Intracranial hemorrhage (ICH) causes high mortality and disability without effective treatment in the clinical setting. (−)-Epigallocatechin-3-gallate (EGCG) exerts an essential role in the central nervous system and offers a promising therapeutic agent for the treatment of oxidative damage-related diseases. MiR-137 can inhibit the oxidative stress and apoptosis to attenuate neuronal injury. However, the role of EGCG in regulating miR-137-3p and neuronal Parthanatos remains to be unclear. In the present study, we build the ICH mice model to investigate the antioxidant effects of EGCG via upregulating miR-137-3p and inhibiting neuronal Parthanatos. We revealed that EGCG upregulated miR-137-3p and inhibited neuronal Parthanatos, and promoted the functional recovery, alleviated ICH-induced brain injury, and reduced oxidative stress in mice following ICH. However, following the inhibition of miR-137-3p and activation of Parthanatos, EGCG was unable to exert neuroprotective roles. These combined results suggest that EGCG may upregulate miR-137-3p and inhibit neuronal Parthanatos to accelerate functional recovery in mice after ICH, laying the foundation for EGCG to be a novel strategy for the treatment of neuronal injuries related to Parthanatos. intracranial hemorrhage (−)-epigallocatechin-3-gallate mir-137-3p parthanatos Neurosciences. Biological psychiatry. Neuropsychiatry Kuang Xuejun verfasserin aut Peng Zhao verfasserin aut Li Conghui verfasserin aut Guo Chengwu verfasserin aut Fu Xi verfasserin aut Wu Junhong verfasserin aut Luo Yang verfasserin aut Rao Xiaolin verfasserin aut Zhou Xiangjuan verfasserin aut Huang Bin verfasserin aut Tang Weijun verfasserin aut Tang Yinjuan verfasserin aut In Translational Neuroscience De Gruyter, 2015 11(2020), 1, Seite 371-379 (DE-627)640087507 (DE-600)2581219-1 20816936 nnns volume:11 year:2020 number:1 pages:371-379 https://doi.org/10.1515/tnsci-2020-0143 kostenfrei https://doaj.org/article/6992334a66e446148df174d4d2245f73 kostenfrei https://doi.org/10.1515/tnsci-2020-0143 kostenfrei https://doaj.org/toc/2081-6936 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2020 1 371-379 |
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RC321-571 EGCG treats ICH via up-regulating miR-137-3p and inhibiting Parthanatos intracranial hemorrhage (−)-epigallocatechin-3-gallate mir-137-3p parthanatos |
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EGCG treats ICH via up-regulating miR-137-3p and inhibiting Parthanatos |
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Intracranial hemorrhage (ICH) causes high mortality and disability without effective treatment in the clinical setting. (−)-Epigallocatechin-3-gallate (EGCG) exerts an essential role in the central nervous system and offers a promising therapeutic agent for the treatment of oxidative damage-related diseases. MiR-137 can inhibit the oxidative stress and apoptosis to attenuate neuronal injury. However, the role of EGCG in regulating miR-137-3p and neuronal Parthanatos remains to be unclear. In the present study, we build the ICH mice model to investigate the antioxidant effects of EGCG via upregulating miR-137-3p and inhibiting neuronal Parthanatos. We revealed that EGCG upregulated miR-137-3p and inhibited neuronal Parthanatos, and promoted the functional recovery, alleviated ICH-induced brain injury, and reduced oxidative stress in mice following ICH. However, following the inhibition of miR-137-3p and activation of Parthanatos, EGCG was unable to exert neuroprotective roles. These combined results suggest that EGCG may upregulate miR-137-3p and inhibit neuronal Parthanatos to accelerate functional recovery in mice after ICH, laying the foundation for EGCG to be a novel strategy for the treatment of neuronal injuries related to Parthanatos. |
abstractGer |
Intracranial hemorrhage (ICH) causes high mortality and disability without effective treatment in the clinical setting. (−)-Epigallocatechin-3-gallate (EGCG) exerts an essential role in the central nervous system and offers a promising therapeutic agent for the treatment of oxidative damage-related diseases. MiR-137 can inhibit the oxidative stress and apoptosis to attenuate neuronal injury. However, the role of EGCG in regulating miR-137-3p and neuronal Parthanatos remains to be unclear. In the present study, we build the ICH mice model to investigate the antioxidant effects of EGCG via upregulating miR-137-3p and inhibiting neuronal Parthanatos. We revealed that EGCG upregulated miR-137-3p and inhibited neuronal Parthanatos, and promoted the functional recovery, alleviated ICH-induced brain injury, and reduced oxidative stress in mice following ICH. However, following the inhibition of miR-137-3p and activation of Parthanatos, EGCG was unable to exert neuroprotective roles. These combined results suggest that EGCG may upregulate miR-137-3p and inhibit neuronal Parthanatos to accelerate functional recovery in mice after ICH, laying the foundation for EGCG to be a novel strategy for the treatment of neuronal injuries related to Parthanatos. |
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Intracranial hemorrhage (ICH) causes high mortality and disability without effective treatment in the clinical setting. (−)-Epigallocatechin-3-gallate (EGCG) exerts an essential role in the central nervous system and offers a promising therapeutic agent for the treatment of oxidative damage-related diseases. MiR-137 can inhibit the oxidative stress and apoptosis to attenuate neuronal injury. However, the role of EGCG in regulating miR-137-3p and neuronal Parthanatos remains to be unclear. In the present study, we build the ICH mice model to investigate the antioxidant effects of EGCG via upregulating miR-137-3p and inhibiting neuronal Parthanatos. We revealed that EGCG upregulated miR-137-3p and inhibited neuronal Parthanatos, and promoted the functional recovery, alleviated ICH-induced brain injury, and reduced oxidative stress in mice following ICH. However, following the inhibition of miR-137-3p and activation of Parthanatos, EGCG was unable to exert neuroprotective roles. These combined results suggest that EGCG may upregulate miR-137-3p and inhibit neuronal Parthanatos to accelerate functional recovery in mice after ICH, laying the foundation for EGCG to be a novel strategy for the treatment of neuronal injuries related to Parthanatos. |
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(−)-Epigallocatechin-3-gallate (EGCG) exerts an essential role in the central nervous system and offers a promising therapeutic agent for the treatment of oxidative damage-related diseases. MiR-137 can inhibit the oxidative stress and apoptosis to attenuate neuronal injury. However, the role of EGCG in regulating miR-137-3p and neuronal Parthanatos remains to be unclear. In the present study, we build the ICH mice model to investigate the antioxidant effects of EGCG via upregulating miR-137-3p and inhibiting neuronal Parthanatos. We revealed that EGCG upregulated miR-137-3p and inhibited neuronal Parthanatos, and promoted the functional recovery, alleviated ICH-induced brain injury, and reduced oxidative stress in mice following ICH. However, following the inhibition of miR-137-3p and activation of Parthanatos, EGCG was unable to exert neuroprotective roles. 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