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Diallyl Disulfide Prevents Cyclophosphamide-Induced Hemorrhagic Cystitis in Rats through the Inhibition of Oxidative Damage, MAPKs, and NF-κB Pathways
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Diallyl Disulfide Prevents Cyclophosphamide-Induced Hemorrhagic Cystitis in Rats through the Inhibition of Oxidative Damage, MAPKs, and NF-κB Pathways

논문 기본 정보

자료유형
학술저널
저자정보
Kim, Sung Hwan (College of Veterinary Medicine, Chonnam National University) Lee, In Chul (College of Veterinary Medicine, Chonnam National University) Ko, Je Won (College of Veterinary Medicine, Chonnam National University) Moon, Changjong (College of Veterinary Medicine, Chonnam National University)
저널정보
한국응용약물학회 Biomolecules & Therapeutics(구 응용약물학회지) Biomolecules & therapeutics 제23권 제2호 KCI Accredited Journals
발행연도
2015.1
수록면
180 - 188 (9page)

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표지
Diallyl Disulfide Prevents Cyclophosphamide-Induced Hemorrhagic Cystitis in Rats through the Inhibition of Oxidative Damage, MAPKs, and NF-κB Pathways
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This 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-${\kappa}B$), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), 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-${\kappa}B$, COX-2, iNOS, TNF-${\alpha}$, 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-${\kappa}B$, COX-2, iNOS, TNF-${\alpha}$, 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-${\kappa}B$ and MAPKs expressions, and its potent anti-oxidative capability through reduction of oxidative DNA damage in the bladder.
#Cyclophosphamide #Hemorrhagic cystitis #Diallyl disulfide #Oxidative damage #MAPKs #NF- ${kappa}B$

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참고문헌 (50)

참고문헌 신청
Beckman, K. B. / 1997 / Oxidative decay of DNA / J. Biol. Chem 272:19633~19666 google schola Berton, T. R. / 1998 / The effect of vitamin E acetate on ultravioletinduced mouse skin carcinogenesis / Mol. Carcinog 23:175~184 google schola Bhatia, K. / 2006 / Aqueous extract of Trigonella foenum-graecum L. ameliorates additive urotoxicity of buthionine sulfoximine and cyclophosphamide in mice / Food Chem. Toxicol 44:1744~1750 google schola Bradford, M. M. / 1976 / A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding / Anal. Biochem 72:248~254 google schola Carlberg, I. / 1986 / Reduction of 2,4,6-trinitrobenzenesulfonate by glutathione reductase and the effect of NADP+on the electron transfer / J. Biol. Chem 261:1629~1635 google schola

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