Neuroprotective effects of<i>Alpinia katsumadai</i>against experimental ischemic damage via control of oxidative stress

Li, Hua; Park, Joon Ha; Lee, Jae Chul; Yoo, Ki‐Yeon; Hwang, In Koo; Lee, Choong Hyun; Choi, Jung Hoon; Kim, Jong-Dai; Kang, Il‐Jun; Won, Moo‐Ho

doi:10.3109/13880209.2012.716853

Cited by 12 publications

(6 citation statements)

References 48 publications

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“…Some papers have shown that the treatment of exogenous Trx increases expressions of both SOD2 mRNA and its protein level in epithelial cells of the human lens and in microvascular endothelial cells in the human lung . Furthermore, we recently reported that the maintenance or increase of endogenous SODs was closely related with protective effects against ischemia‐induced neuronal death in the gerbil hippocampus . With these findings, therefore, we strongly suggest that the enhanced expression of SOD2 in the ischemic CA1 pyramidal neurons by IPC is related with neuroprotective effect through Trx2 against oxidative stress induced by ischemia‐reperfusion injury.…”

Section: Discussionsupporting

confidence: 54%

Neuroprotection of ischemic preconditioning is mediated by thioredoxin 2 in the hippocampal CA1 region following a subsequent transient cerebral ischemia

et al. 2016

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Preconditioning by brief ischemic episode induces tolerance to a subsequent lethal ischemic insult, and it has been suggested that reactive oxygen species are involved in this phenomenon. Thioredoxin 2 (Trx2), a small protein with redox-regulating function, shows cytoprotective roles against oxidative stress. Here, we had focused on the role of Trx2 in ischemic preconditioning (IPC)-mediated neuroprotection against oxidative stress followed by a subsequent lethal transient cerebral ischemia. Animals used in this study were randomly assigned to six groups; sham-operated group, ischemia-operated group, IPC plus (+) sham-operated group, IPC + ischemia-operated group, IPC + auranofin (a TrxR2 inhibitor) + sham-operated group and IPC + auranofin + ischemia-operated group. IPC was subjected to a 2 minutes of sublethal transient ischemia 1 day prior to a 5 minutes of lethal transient ischemia. A significant loss of neurons was found in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) in the ischemia-operated-group 5 days after ischemia-reperfusion; in the IPC + ischemia-operated-group, pyramidal neurons in the SP were well protected. In the IPC + ischemia-operated-group, Trx2 and TrxR2 immunoreactivities in the SP and its protein level in the CA1 were not significantly changed compared with those in the sham-operated-group after ischemia-reperfusion. In addition, superoxide dismutase 2 (SOD2) expression, superoxide anion radical ( O2-) production, denatured cytochrome c expression and TUNEL-positive cells in the IPC + ischemia-operated-group were similar to those in the sham-operated-group. Conversely, the treatment of auranofin to the IPC + ischemia-operated-group significantly increased cell damage/death and abolished the IPC-induced effect on Trx2 and TrxR2 expressions. Furthermore, the inhibition of Trx2R nearly cancelled the beneficial effects of IPC on SOD2 expression, O2- production, denatured cytochrome c expression and TUNEL-positive cells. In brief, this study shows that IPC conferred neuroprotection against ischemic injury by maintaining Trx2 and suggests that the maintenance or enhancement of Trx2 expression by IPC may be a legitimate strategy for therapeutic intervention of cerebral ischemia.

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Section: Discussionsupporting

confidence: 54%

Neuroprotection of ischemic preconditioning is mediated by thioredoxin 2 in the hippocampal CA1 region following a subsequent transient cerebral ischemia

et al. 2016

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“…[ 32 ] In addition, we demonstrated that the maintenance or increase of intracellular antioxidant enzymes by the administration of some traditional medicinal plant extracts is closely associated with protective effects against ischemia-induced neuronal death in the gerbil hippocampal CA1 region. [ 17 33 34 ] Therefore, it could be postulated that higher and maintained expressions of intracellular antioxidant enzymes in ischemic neurons after treatment with some extracts may be related with neuroprotective effects against ischemic damage.…”

Section: Discussionmentioning

confidence: 99%

Oenanthe Javanica Extract Protects Against Experimentally Induced Ischemic Neuronal Damage via its Antioxidant Effects

Park

Cho

Kim

et al. 2015

Chinese Medical Journal

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Background:Water dropwort (Oenanthe javanica) as a popular traditional medicine in Asia shows various biological properties including antioxidant activity. In this study, we firstly examined the neuroprotective effect of Oenanthe javanica extract (OJE) in the hippocampal cornus ammonis 1 region (CA1 region) of the gerbil subjected to transient cerebral ischemia.Methods:Gerbils were established by the occlusion of common carotid arteries for 5 min. The neuroprotective effect of OJE was estimated by cresyl violet staining. In addition, 4 antioxidants (copper, zinc superoxide dismutase [SOD], manganese SOD, catalase, and glutathione peroxidase) immunoreactivities were investigated by immunohistochemistry.Results:Pyramidal neurons in the CA1 region showed neuronal death at 5 days postischemia; at this point in time, all antioxidants immunoreactivities disappeared in CA1 pyramidal neurons and showed in many nonpyramidal cells. Treatment with 200 mg/kg, not 100 mg/kg, OJE protected CA1 pyramidal neurons from ischemic damage. In addition, 200 mg/kg OJE treatment increased or maintained antioxidants immunoreactivities. Especially, among the antioxidants, glutathione peroxidase immunoreactivity was effectively increased in the CA1 pyramidal neurons of the OJE-treated sham-operated and ischemia-operated groups.Conclusion:Our present results indicate that treatment with OJE can protect neurons from transient ischemic damage and that the neuroprotective effect may be closely associated with increased or maintained intracellular antioxidant enzymes by OJE.

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“…It is, thus, applied for gastric pain and distended abdomen. Neuro-protection effect of A. katsumadai for ischemic damage has been observed through antioxidants [1,2]. Choi et al [3] showed that extracts of A. katsumadai attenuate phenylbenzoquinone-induced writhing and carrageenan-induced hyperalgesia, and they found that this effect was independent of opioid receptor but involved in COX-2 pathway, suggesting potential role of A. katsumadai on inflammatory nociception.…”

Section: Introductionmentioning

confidence: 99%

Cardamonin, a Novel Antagonist of hTRPA1 Cation Channel, Reveals Therapeutic Mechanism of Pathological Pain

et al. 2016

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Abstract:The increasing demand for safe and effective treatments of chronic pain has promoted the investigation of novel analgesic drugs. Some herbals have been known to be able to relieve pain, while the chemical basis and target involved in this process remained to be clarified. The current study aimed to find anti-nociceptive candidates targeting transient receptor potential ankyrin 1 (TRPA1), a receptor that implicates in hyperalgesia and neurogenic inflammation. In the current study, 156 chemicals were tested for blocking HEK293/TRPA1 ion channel by calcium-influx assay. Docking study was conducted to predict the binding modes of hit compound with TRPA1 using Discovery Studio. Cytotoxicity in HEK293 was conducted by Cell Titer-Glo assay. Additionally, cardiotoxicity was assessed via xCELLigence RTCA system. We uncovered that cardamonin selectively blocked TRPA1 activation while did not interact with TRPV1 nor TRPV4 channel. A concentration-dependent inhibitory effect was observed with IC 50 of 454 nM. Docking analysis of cardamonin demonstrated a compatible interaction with A-967079-binding site of TRPA1. Meanwhile, cardamonin did not significantly reduce HEK293 cell viability, nor did it impair cardiomyocyte constriction. Our data suggest that cardamonin is a selective TRPA1 antagonist, providing novel insight into the target of its anti-nociceptive activity.

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Neuroprotective effects ofAlpinia katsumadaiagainst experimental ischemic damage via control of oxidative stress

Abstract: Won (2013) Neuroprotective effects of Alpiniakatsumadai against experimental ischemic damage via control of oxidative stress,

Cited by 12 publications

References 48 publications

Neuroprotection of ischemic preconditioning is mediated by thioredoxin 2 in the hippocampal CA1 region following a subsequent transient cerebral ischemia

Neuroprotection of ischemic preconditioning is mediated by thioredoxin 2 in the hippocampal CA1 region following a subsequent transient cerebral ischemia

Oenanthe Javanica Extract Protects Against Experimentally Induced Ischemic Neuronal Damage via its Antioxidant Effects

Cardamonin, a Novel Antagonist of hTRPA1 Cation Channel, Reveals Therapeutic Mechanism of Pathological Pain

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