S-Allyl-l-cysteine attenuates cerebral ischemic injury by scavenging peroxynitrite and inhibiting the activity of extracellular signal-regulated kinase

Ji Myung Kim; Jae Chul Lee; Namsoo Chang; Hyang Sook Chun; Won Ki Kim

doi:10.1080/10715760600719540

S-Allyl-l-cysteine attenuates cerebral ischemic injury by scavenging peroxynitrite and inhibiting the activity of extracellular signal-regulated kinase

Ji Myung Kim, Jae Chul Lee, Namsoo Chang, Hyang Sook Chun, Won Ki Kim

Research output: Contribution to journal › Article › peer-review

44 Citations (Scopus)

Abstract

S-Allyl-l-cysteine (SAC) has been shown to reduce ischemic injury due to its antioxidant activity. However, the antioxidant property of SAC has been controversial. The present study investigated the neuroprotective mechanism of SAC in cerebral ischemic insults. SAC decreased the size of infarction after transient or global ischemic insults. While it did not alter the N-methyl-d-aspartate excitotoxicity, SAC significantly scavenged the endogenously or exogenously produced ONOO^- and reduced ONOO^- cytotoxicity. In contrast, SAC has much lower scavenging activity against H₂O_2, or NO. Further, SAC inhibited the activity of extracellular signal-regulated kinase (ERK) increased in cultured neurons exposed to oxygen-glucose deprivation or in rat brain tissue after transient middle cerebral artery occlusion. The neuroprotective effect of SAC was mimicked by the ERK inhibitor U0125. The present results indicate that SAC exert its neuroprotective effect by scavenging ONOO^- and inhibiting the ERK signaling pathway activated during initial hypoxic/ischemic insults.

Original language	English
Pages (from-to)	827-835
Number of pages	9
Journal	Free Radical Research
Volume	40
Issue number	8
DOIs	https://doi.org/10.1080/10715760600719540
Publication status	Published - 2006 Aug
Externally published	Yes

Bibliographical note

Funding Information:
This study was supported by a research project on Functional Food Development from the Office for Government Policy Coordination, a grant from the Agriculture R&D Promotion Center, under the Ministry of Agriculture and Forestry, a grant (M103KV010005 03K2201 00510) from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology, and in part a grant from the Korea Health 21 R&D Project (02-PJ1-PG6-AG01-0003) of the Ministry of Health & Welfare, the Republic of Korea.

Keywords

Antioxidant
ERK
Ischemia
Peroxynitrite (ONOO)
S-Allyl-l-cysteine

ASJC Scopus subject areas

Biochemistry

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10.1080/10715760600719540

Cite this

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title = "S-Allyl-l-cysteine attenuates cerebral ischemic injury by scavenging peroxynitrite and inhibiting the activity of extracellular signal-regulated kinase",

abstract = "S-Allyl-l-cysteine (SAC) has been shown to reduce ischemic injury due to its antioxidant activity. However, the antioxidant property of SAC has been controversial. The present study investigated the neuroprotective mechanism of SAC in cerebral ischemic insults. SAC decreased the size of infarction after transient or global ischemic insults. While it did not alter the N-methyl-d-aspartate excitotoxicity, SAC significantly scavenged the endogenously or exogenously produced ONOO- and reduced ONOO- cytotoxicity. In contrast, SAC has much lower scavenging activity against H2O2, or NO. Further, SAC inhibited the activity of extracellular signal-regulated kinase (ERK) increased in cultured neurons exposed to oxygen-glucose deprivation or in rat brain tissue after transient middle cerebral artery occlusion. The neuroprotective effect of SAC was mimicked by the ERK inhibitor U0125. The present results indicate that SAC exert its neuroprotective effect by scavenging ONOO- and inhibiting the ERK signaling pathway activated during initial hypoxic/ischemic insults.",

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author = "Kim, {Ji Myung} and Lee, {Jae Chul} and Namsoo Chang and Chun, {Hyang Sook} and Kim, {Won Ki}",

note = "Funding Information: This study was supported by a research project on Functional Food Development from the Office for Government Policy Coordination, a grant from the Agriculture R&D Promotion Center, under the Ministry of Agriculture and Forestry, a grant (M103KV010005 03K2201 00510) from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology, and in part a grant from the Korea Health 21 R&D Project (02-PJ1-PG6-AG01-0003) of the Ministry of Health & Welfare, the Republic of Korea.",

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AU - Chun, Hyang Sook

AU - Kim, Won Ki

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N2 - S-Allyl-l-cysteine (SAC) has been shown to reduce ischemic injury due to its antioxidant activity. However, the antioxidant property of SAC has been controversial. The present study investigated the neuroprotective mechanism of SAC in cerebral ischemic insults. SAC decreased the size of infarction after transient or global ischemic insults. While it did not alter the N-methyl-d-aspartate excitotoxicity, SAC significantly scavenged the endogenously or exogenously produced ONOO- and reduced ONOO- cytotoxicity. In contrast, SAC has much lower scavenging activity against H2O2, or NO. Further, SAC inhibited the activity of extracellular signal-regulated kinase (ERK) increased in cultured neurons exposed to oxygen-glucose deprivation or in rat brain tissue after transient middle cerebral artery occlusion. The neuroprotective effect of SAC was mimicked by the ERK inhibitor U0125. The present results indicate that SAC exert its neuroprotective effect by scavenging ONOO- and inhibiting the ERK signaling pathway activated during initial hypoxic/ischemic insults.

AB - S-Allyl-l-cysteine (SAC) has been shown to reduce ischemic injury due to its antioxidant activity. However, the antioxidant property of SAC has been controversial. The present study investigated the neuroprotective mechanism of SAC in cerebral ischemic insults. SAC decreased the size of infarction after transient or global ischemic insults. While it did not alter the N-methyl-d-aspartate excitotoxicity, SAC significantly scavenged the endogenously or exogenously produced ONOO- and reduced ONOO- cytotoxicity. In contrast, SAC has much lower scavenging activity against H2O2, or NO. Further, SAC inhibited the activity of extracellular signal-regulated kinase (ERK) increased in cultured neurons exposed to oxygen-glucose deprivation or in rat brain tissue after transient middle cerebral artery occlusion. The neuroprotective effect of SAC was mimicked by the ERK inhibitor U0125. The present results indicate that SAC exert its neuroprotective effect by scavenging ONOO- and inhibiting the ERK signaling pathway activated during initial hypoxic/ischemic insults.

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S-Allyl-l-cysteine attenuates cerebral ischemic injury by scavenging peroxynitrite and inhibiting the activity of extracellular signal-regulated kinase

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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