抗氧化剂对骨关节炎大鼠模型炎症和氧化应激标志物的影响:扫描电镜观察

E. H. A. Heidar, FareedF Al Faya, W. N. Hassan, R. Eid, M. Haidara
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引用次数: 7

摘要

骨关节炎(OA)的特点是基质降解和关节软骨破坏。关节软骨细胞单独负责细胞外基质的产生和维持。因此,软骨细胞破坏与软骨变性有关。大量研究表明,抗氧化治疗是OA病例中有希望的治疗方法。本研究旨在研究维生素E是否能保护大鼠软骨细胞免受炎症标志物和氧化应激增加的影响,并防止单碘乙酸诱导的骨关节炎模型大鼠软骨破坏。数据显示,骨关节炎组炎症标志物肿瘤坏死因子-α (TNF-α)(38±1 ng/mL)、白细胞介素-6 (IL-6)(253±15 ng/mL)和氧化应激标志物超氧化物歧化酶(SOD)(14±1 ng/mL)分别较对照组(18±1 ng/mL)、(121+/-23 ng/mL)和(8±1 ng/mL)显著升高。维生素E组则相反,TNF-α(27±2 ng/mL)和SOD(10±1 ng/mL)明显下降。电镜检查证实了上述结果,并显示服用维生素e后膝关节得到改善。这项研究支持了OA是一种多因素并发症的观点,由炎症和氧化应激增加引起。在急性关节炎动物模型中,维生素E可降低炎症和氧化应激标志物,改善膝关节超微结构。然而,需要进一步的工作来验证在患有骨关节炎的人类患者中的可靠性。
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THE IMPACT OF ANTIOXIDANTS ON INFLAMMATION AND OXIDATIVE STRESS MARKERS IN OSTEOARTHRITIS RAT MODEL: SCANNING ELECTRON MICROSCOPE INSIGHTS
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.
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