E. H. A. Heidar, FareedF Al Faya, W. N. Hassan, R. Eid, M. Haidara
{"title":"THE IMPACT OF ANTIOXIDANTS ON INFLAMMATION AND OXIDATIVE STRESS MARKERS IN OSTEOARTHRITIS RAT MODEL: SCANNING ELECTRON MICROSCOPE INSIGHTS","authors":"E. H. A. Heidar, FareedF Al Faya, W. N. Hassan, R. Eid, M. Haidara","doi":"10.3844/AJPTSP.2014.157.167","DOIUrl":null,"url":null,"abstract":"Osteoarthritis (OA) is characterized by degradation of matrix and destruction of articular cartilage. Articular chondrocytes are solely responsible for t he production and maintenance of the extracellular matrix. Therefore, chondrocyte disruption is implic ated in cartilage degeneration. Numerous studies have shown that antioxidant treatments are promisin g therapeutics in cases of OA. This study was designedto examine whether vitamin E protects rat a rticular chondrocytes against increased inflammatory markers and oxidative stress and preve nts cartilage destruction in mono-iodoacetateinduced osteoarthritis rat model. Data showed that osteoarthritis group showed a significant increase in inflammatory markers, Tumor Necrosis Factor-α (TNF-α) (38±1 ng/mL), Interlukin-6 (IL-6) (253±15 ng/mL) and oxidative stress marker, Super Oxide Dis mutase (SOD) (14±1 ng/mL) compared to control (18±1 ng/mL), (121+/-23 ng/mL) and (8±1 ng/mL) respectively. Opposite trend was found when animals were treated with vitamin E where TNF-α (27±2 ng/mL) and SOD (10±1 ng/mL) declined significantly. Electro-microscopic examination docu mented the above results and showed improvement of knee joint after administration of v itamin E. This study supported the notion that OA is a multi factorial complication, caused by inflam mation and increased oxidative stress. Administration of vitamin E decreased the markers o f inflammation and oxidative stress as well asimproved ultra-structure of the knee jointin acut e OA animal model. However, further work id needed to validate reliability in human patients su ffering from osteoarthritis.","PeriodicalId":7769,"journal":{"name":"American Journal of Pharmacology and Toxicology","volume":"444 1","pages":"157-167"},"PeriodicalIF":0.0000,"publicationDate":"2014-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"7","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"American Journal of Pharmacology and Toxicology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3844/AJPTSP.2014.157.167","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 7
Abstract
Osteoarthritis (OA) is characterized by degradation of matrix and destruction of articular cartilage. Articular chondrocytes are solely responsible for t he production and maintenance of the extracellular matrix. Therefore, chondrocyte disruption is implic ated in cartilage degeneration. Numerous studies have shown that antioxidant treatments are promisin g therapeutics in cases of OA. This study was designedto examine whether vitamin E protects rat a rticular chondrocytes against increased inflammatory markers and oxidative stress and preve nts cartilage destruction in mono-iodoacetateinduced osteoarthritis rat model. Data showed that osteoarthritis group showed a significant increase in inflammatory markers, Tumor Necrosis Factor-α (TNF-α) (38±1 ng/mL), Interlukin-6 (IL-6) (253±15 ng/mL) and oxidative stress marker, Super Oxide Dis mutase (SOD) (14±1 ng/mL) compared to control (18±1 ng/mL), (121+/-23 ng/mL) and (8±1 ng/mL) respectively. Opposite trend was found when animals were treated with vitamin E where TNF-α (27±2 ng/mL) and SOD (10±1 ng/mL) declined significantly. Electro-microscopic examination docu mented the above results and showed improvement of knee joint after administration of v itamin E. This study supported the notion that OA is a multi factorial complication, caused by inflam mation and increased oxidative stress. Administration of vitamin E decreased the markers o f inflammation and oxidative stress as well asimproved ultra-structure of the knee jointin acut e OA animal model. However, further work id needed to validate reliability in human patients su ffering from osteoarthritis.