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Conference Paper: Pharmacological induction of Arginase II by C-glucosylated isoflavonone puerarin suppresses nitric oxide-induced mitochondrial dysfunction in differentiated neuronal PC12 cells
Title | Pharmacological induction of Arginase II by C-glucosylated isoflavonone puerarin suppresses nitric oxide-induced mitochondrial dysfunction in differentiated neuronal PC12 cells 葛根素在分化的神經PC12細胞中通過誘導精氨酸酶II以抑制一氧化氮導致的線粒體功能障礙 |
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Authors | |
Issue Date | 2014 |
Citation | The 8th Pong Ding Yuen International Symposium on Traditional Chinese Medicine cum, The 2nd International Chinese Symposium on Free Radical Research & The 6th Symposium for Three Districts of Cross-straits on Free Radical Research, The University of Hong Kong, Hong Kong, 15-16 November 2014. How to Cite? |
Abstract | Aberrant production of nitric oxide (NO) is implicated in the progression of neurodegenerative diseases. The aim of the present study was to explore whether plant natural product puerarin could attenuate nitric oxide (NO)-mediated neurotoxicity via modulating the enzymes in the L-arginine-NO pathway. Neurotoxin 6-hydroxydopamine (6-OHDA) is well known to induce neurodegeneration via a NO-dependent mechanism. We first validated that puerarin protected rat dopamingeric PC12 cells against 6-OHDA-induced neurotoxicity in a concentration-dependent manner. We subsequently profiled the cellular responses to puerarin by a proteomic response fingerprinting approach. A total of sixteen protein spots with > 1.5-fold change of intensity were selected and identified by mass spectrometry. As one of puerarin-upregulated proteins, mitochondrial arginase-2 hydrolyzes L-arginine to L-ornithine, thereby competing with neuronal NOS for substrate L-arginine in mitochondria. Thus, we hypothesize that puerain may attenuate nitric oxide (NO)-mediated mitochondrial injury via increasing arginase-2 expression. Western blot and RT-PCR analyses confirmed that puerarin increased arginase-2 expression in a concentration- and time-dependent manner. Accordingly, puerarin suppressed 6-OHDA-induced NO production and neurotoxicity in PC12 cells and primary rat midbrain neurons. Arginase inhibitor BEC diminished the effect of puerarin on 6-OHDA-induced NO production and neurotoxicity. The activation of arginase-2 by puerarin represents an endogenous mechanism for specific control of NO-mediated mitochondrial damage. Thus, puerarin is useful lead for suppressing NO-mediated neurotoxicity in neurodegenerative diseases. |
Description | Conference Theme: Free Radical, Chinese Medicine and Translational Medicine - 自由基, 中醫藥, 轉化醫學 Parallel Session - Session 4: Young Investigator Oral Presentation: no. YI-02 |
Persistent Identifier | http://hdl.handle.net/10722/213638 |
DC Field | Value | Language |
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dc.contributor.author | Zhao, J | - |
dc.contributor.author | Rong, J | - |
dc.date.accessioned | 2015-08-07T08:32:13Z | - |
dc.date.available | 2015-08-07T08:32:13Z | - |
dc.date.issued | 2014 | - |
dc.identifier.citation | The 8th Pong Ding Yuen International Symposium on Traditional Chinese Medicine cum, The 2nd International Chinese Symposium on Free Radical Research & The 6th Symposium for Three Districts of Cross-straits on Free Radical Research, The University of Hong Kong, Hong Kong, 15-16 November 2014. | - |
dc.identifier.uri | http://hdl.handle.net/10722/213638 | - |
dc.description | Conference Theme: Free Radical, Chinese Medicine and Translational Medicine - 自由基, 中醫藥, 轉化醫學 | - |
dc.description | Parallel Session - Session 4: Young Investigator Oral Presentation: no. YI-02 | - |
dc.description.abstract | Aberrant production of nitric oxide (NO) is implicated in the progression of neurodegenerative diseases. The aim of the present study was to explore whether plant natural product puerarin could attenuate nitric oxide (NO)-mediated neurotoxicity via modulating the enzymes in the L-arginine-NO pathway. Neurotoxin 6-hydroxydopamine (6-OHDA) is well known to induce neurodegeneration via a NO-dependent mechanism. We first validated that puerarin protected rat dopamingeric PC12 cells against 6-OHDA-induced neurotoxicity in a concentration-dependent manner. We subsequently profiled the cellular responses to puerarin by a proteomic response fingerprinting approach. A total of sixteen protein spots with > 1.5-fold change of intensity were selected and identified by mass spectrometry. As one of puerarin-upregulated proteins, mitochondrial arginase-2 hydrolyzes L-arginine to L-ornithine, thereby competing with neuronal NOS for substrate L-arginine in mitochondria. Thus, we hypothesize that puerain may attenuate nitric oxide (NO)-mediated mitochondrial injury via increasing arginase-2 expression. Western blot and RT-PCR analyses confirmed that puerarin increased arginase-2 expression in a concentration- and time-dependent manner. Accordingly, puerarin suppressed 6-OHDA-induced NO production and neurotoxicity in PC12 cells and primary rat midbrain neurons. Arginase inhibitor BEC diminished the effect of puerarin on 6-OHDA-induced NO production and neurotoxicity. The activation of arginase-2 by puerarin represents an endogenous mechanism for specific control of NO-mediated mitochondrial damage. Thus, puerarin is useful lead for suppressing NO-mediated neurotoxicity in neurodegenerative diseases. | - |
dc.language | eng | - |
dc.relation.ispartof | 8th Pong Ding Yuen International Symposium on Traditional Chinese Medicine, 2nd International Chinese Symposium on Free Radical Research & the 6th Symposium for Three Districts of Cross-straits on Free Radical Research | - |
dc.relation.ispartof | 第八屇龐鼎元國際中醫藥研討會暨第二屇世界華人自由基生物學與自由基醫學學術大會及第六屇海峽兩岸三地自由基生物學與自由基醫學研討會 | - |
dc.title | Pharmacological induction of Arginase II by C-glucosylated isoflavonone puerarin suppresses nitric oxide-induced mitochondrial dysfunction in differentiated neuronal PC12 cells | - |
dc.title | 葛根素在分化的神經PC12細胞中通過誘導精氨酸酶II以抑制一氧化氮導致的線粒體功能障礙 | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Rong, J: jrong@hku.hk | - |
dc.identifier.authority | Rong, J=rp00515 | - |
dc.identifier.hkuros | 247198 | - |