Diallyl disulfide prevents cyclophosphamide-induced hemorrhagic cystitis in rats through the inhibition of oxidative damage, MAPKs, and NF-κB pathways

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dc.contributor.authorS H Kim-
dc.contributor.authorIn Chul Lee-
dc.contributor.authorJ W Ko-
dc.contributor.authorC Moon-
dc.contributor.authorS H Kim-
dc.contributor.authorIn Sik Shin-
dc.contributor.authorYoung Won Seo-
dc.contributor.authorHyoung-Chin Kim-
dc.contributor.authorJ C Kim-
dc.date.accessioned2017-04-19T10:02:15Z-
dc.date.available2017-04-19T10:02:15Z-
dc.date.issued2015-
dc.identifier.issn1976-9148-
dc.identifier.uri10.4062/biomolther.2014.126ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/12497-
dc.description.abstractThis study investigated the possible effects and molecular mechanisms of diallyl disulfide (DADS) against cyclophosphamide (CP)-induced hemorrhagic cystitis (HC) in rats. Inflammation response was assessed by histopathology and serum cytokines levels. We determined the protein expressions of nuclear transcription factor kappa-B (NF-κB), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and tumor necrosis factor-α (TNF-α), oxidative stress, urinary nitrite-nitrate, malondialdehyde (MDA), and 8-hydroxy-2’-deoxyguanosine (8-OHdG). Finally, we studied the involvement of mitogen-activated protein kinases (MAPKs) signaling in the protective effects of DADS against CP-induced HC. CP treatment caused a HC which was evidenced by an increase in histopathological changes, proinflammatory cytokines levels, urinary nitrite-nitrate level, and the protein expression of NF-κB, COX-2, iNOS, TNF-α, p-c-Jun N-terminal kinase (JNK), and p-extracellular signal regulated kinase (ERK). The significant decreases in glutathione content and glutathione-S-transferase and glutathione reductase activities, and the significant increase in MDA content and urinary MDA and 8-OHdG levels indicated that CP-induced bladder injury was mediated through oxidative DNA damage. In contrast, DADS pretreatment attenuated CP-induced HC, including histopathological lesion, serum cytokines levels, oxidative damage, and urinary oxidative DNA damage. DADS also caused significantly decreased the protein expressions of NF-κB, COX-2, iNOS, TNF-α, p-JNK, and p-ERK. These results indicate that DADS prevents CP-induced HC and that the protective effects of DADS may be due to its ability to regulate proinflammatory cytokines production by inhibition of NF- κB and MAPKs expressions, and its potent anti-oxidative capability through reduction of oxidative DNA damage in the bladder.-
dc.publisherKorea Soc-Assoc-Inst-
dc.titleDiallyl disulfide prevents cyclophosphamide-induced hemorrhagic cystitis in rats through the inhibition of oxidative damage, MAPKs, and NF-κB pathways-
dc.title.alternativeDiallyl disulfide prevents cyclophosphamide-induced hemorrhagic cystitis in rats through the inhibition of oxidative damage, MAPKs, and NF-κB pathways-
dc.typeArticle-
dc.citation.titleBiomolecules & Therapeutics-
dc.citation.number2-
dc.citation.endPage188-
dc.citation.startPage180-
dc.citation.volume23-
dc.contributor.affiliatedAuthorIn Chul Lee-
dc.contributor.affiliatedAuthorIn Sik Shin-
dc.contributor.affiliatedAuthorYoung Won Seo-
dc.contributor.affiliatedAuthorHyoung-Chin Kim-
dc.contributor.alternativeName김성환-
dc.contributor.alternativeName이인철-
dc.contributor.alternativeName고제원-
dc.contributor.alternativeName문창종-
dc.contributor.alternativeName김성호-
dc.contributor.alternativeName신인식-
dc.contributor.alternativeName서영원-
dc.contributor.alternativeName김형진-
dc.contributor.alternativeName김종춘-
dc.identifier.bibliographicCitationBiomolecules & Therapeutics, vol. 23, no. 2, pp. 180-188-
dc.identifier.doi10.4062/biomolther.2014.126-
dc.subject.keywordCyclophosphamide-
dc.subject.keywordDiallyl disulfide-
dc.subject.keywordHemorrhagic cystitis-
dc.subject.keywordMAPKs-
dc.subject.keywordNF-κB-
dc.subject.keywordOxidative damage-
dc.subject.localCyclophosphamide-
dc.subject.localDiallyl disulfide-
dc.subject.localdiallyl disulfide-
dc.subject.localHemorrhagic cystitis-
dc.subject.localMAPK-
dc.subject.localMAPKs-
dc.subject.localNuclear factor-kappa B-
dc.subject.localnuclear factor κB-
dc.subject.localNf-κb-
dc.subject.localNF-kB-
dc.subject.localnuclear factor kappa B-
dc.subject.localNF-κB (nuclear factor kappa-B)-
dc.subject.localNF-kappaB-
dc.subject.localNuclear factor-κb-
dc.subject.localNF-κ B-
dc.subject.localNF-κB-
dc.subject.localNF-kappa B-
dc.subject.localNuclear factor κB (NF-κB)-
dc.subject.localNuclear factor κB-
dc.subject.localNFκB-
dc.subject.localNf-κB-
dc.subject.localNuclear factor-κB-
dc.subject.localnuclear factorκB-
dc.subject.localNuclear factor (NF)-κB-
dc.subject.localNuclear factor kappa B-
dc.subject.localnuclear factor-κB-
dc.subject.localNF-ΚB-
dc.subject.localNuclear factor-kappa B (NF-κB)-
dc.subject.localNuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB (NF-κB)-
dc.subject.localNFkappaB-
dc.subject.localNuclear factor kappaB-
dc.subject.localOxidative damage-
dc.subject.localoxidative damage-
dc.description.journalClassY-
Appears in Collections:
Jeonbuk Branch Institute > Functional Biomaterial Research Center > 1. Journal Articles
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
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