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Attenuation of nephritis in lupus-prone mice by thalidomide

DC FieldValueLanguage
dc.contributor.author박용범-
dc.contributor.author이상원-
dc.contributor.author이수곤-
dc.contributor.author최규헌-
dc.contributor.author김범석-
dc.contributor.author박규형-
dc.date.accessioned2014-12-19T17:39:09Z-
dc.date.available2014-12-19T17:39:09Z-
dc.date.issued2012-
dc.identifier.issn0080-2727-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/91814-
dc.description.abstractOBJECTIVES: Thalidomide has various effects, such as immune modulation, anti-angiogenicity, anti-inflammation and anti-proliferation. Moreover, thalidomide modulates the activity of NF-κB, which can up-regulate the expression of downstream genes involved in the pathophysiology of LN. Here we investigated the efficacy of thalidomide monotherapy or thalidomide plus prednisolone (PL) on nephritis in NZB/WF1 mice at different doses and compared both with a combination therapy of MMF plus PL. METHODS: Forty-three female NZB/WF1 mice were divided into eight groups (untreated; 1.7, 5 or 10 mg/kg of thalidomide alone; 1.7, 5 or 10 mg/kg of thalidomide plus 1.5 mg/kg of PL and 33.3 mg/kg of MMF plus PL). Proteinuria and histological damage were evaluated. Immune complex deposition and nuclear translocation of NF-κB in kidney tissues were assessed by immunofluorescence staining. Serum concentrations of anti-dsDNA and IgG subclasses were also measured. RESULTS: In comparison with untreated mice, mice treated with 10 mg/kg of thalidomide monotherapy showed a significant decrease in proteinuria and significantly lower glomerular and tubular damage scores, comparable to 5 or 10 mg/kg of thalidomide plus PL or MMF plus PL. Also, treatment with 10 mg/kg of thalidomide significantly decreased immune complex accumulation, reduced the serum concentration of anti-dsDNA, IgG2a and IgG2b and inhibited nuclear translocation of NF-κB in kidney tissues, comparable to standard therapy for LN. CONCLUSION: These data suggest that thalidomide might play an anti-inflammatory role in the pathophysiology of LN, and it could serve as a complementary therapy to standard induction regimens for refractory LN.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfRHEUMATOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHAnti-Inflammatory Agents/administration & dosage-
dc.subject.MESHAnti-Inflammatory Agents/pharmacology*-
dc.subject.MESHAnti-Inflammatory Agents/toxicity-
dc.subject.MESHAntigen-Antibody Complex/metabolism-
dc.subject.MESHDNA/metabolism-
dc.subject.MESHDose-Response Relationship, Drug-
dc.subject.MESHDrug Therapy, Combination-
dc.subject.MESHFemale-
dc.subject.MESHGlomerulonephritis/pathology-
dc.subject.MESHGlomerulonephritis/prevention & control-
dc.subject.MESHImmunoglobulin G/metabolism-
dc.subject.MESHImmunosuppressive Agents/pharmacology-
dc.subject.MESHLupus Nephritis/blood-
dc.subject.MESHLupus Nephritis/pathology-
dc.subject.MESHLupus Nephritis/prevention & control*-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred NZB-
dc.subject.MESHMycophenolic Acid/analogs & derivatives-
dc.subject.MESHMycophenolic Acid/pharmacology-
dc.subject.MESHPrednisolone/administration & dosage-
dc.subject.MESHPrednisolone/pharmacology-
dc.subject.MESHProteinuria/prevention & control-
dc.subject.MESHSurvival Rate-
dc.subject.MESHThalidomide/administration & dosage-
dc.subject.MESHThalidomide/pharmacology*-
dc.subject.MESHThalidomide/toxicity-
dc.titleAttenuation of nephritis in lupus-prone mice by thalidomide-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorSang-Won Lee-
dc.contributor.googleauthorYong-Beom Park-
dc.contributor.googleauthorJaeseok Yang-
dc.contributor.googleauthorKyu-Hyung Park-
dc.contributor.googleauthorSoo-Kon Lee-
dc.contributor.googleauthorKyu Hun Choi-
dc.contributor.googleauthorBeom Seok Kim-
dc.identifier.doi22923758-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01579-
dc.contributor.localIdA02889-
dc.contributor.localIdA04043-
dc.contributor.localIdA00488-
dc.contributor.localIdA01441-
dc.contributor.localIdA02824-
dc.relation.journalcodeJ02624-
dc.identifier.pmid22923758-
dc.identifier.urlhttp://rheumatology.oxfordjournals.org/content/51/12/2131.long-
dc.subject.keywordthalidomide-
dc.subject.keywordNZB/WF1 mice-
dc.subject.keywordLN-
dc.contributor.alternativeNamePark, Yong Beom-
dc.contributor.alternativeNameLee, Sang Won-
dc.contributor.alternativeNameLee, Soo Kon-
dc.contributor.alternativeNameChoi, Kyu Hun-
dc.contributor.alternativeNameKim, Beom Seok-
dc.contributor.alternativeNamePark, Kyu Hyung-
dc.contributor.affiliatedAuthorPark, Yong Beom-
dc.contributor.affiliatedAuthorLee, Soo Kon-
dc.contributor.affiliatedAuthorChoi, Kyu Hun-
dc.contributor.affiliatedAuthorKim, Beom Seok-
dc.contributor.affiliatedAuthorPark, Kyu Hyung-
dc.contributor.affiliatedAuthorLee, Sang Won-
dc.citation.volume51-
dc.citation.number12-
dc.citation.startPage2131-
dc.citation.endPage2140-
dc.identifier.bibliographicCitationRHEUMATOLOGY , Vol.51(12) : 2131-2140, 2012-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers

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