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首页> 外文期刊>Clinical and experimental pharmacology & physiology >EFFECTS OF SODIUM FERULATE ON HUMAN OSTEOARTHRITIC CHONDROCYTES AND OSTEOARTHRITIS IN RATS
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EFFECTS OF SODIUM FERULATE ON HUMAN OSTEOARTHRITIC CHONDROCYTES AND OSTEOARTHRITIS IN RATS

机译:阿魏酸钠对大鼠人骨关节炎软骨细胞和骨关节炎的影响

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1. Oxidation, inflammation and apoptosis are involved in the aetiology and pathology of osteoarthritis (OA). Sodium ferulate (SF) has been demonstrated to have anti-oxidant, anti-inflammatory and anti-apoptotic actions in cardiovascular, hepatic and diabetic disorders. These findings suggest that SF may have beneficial effects on OA. Therefore, present study investigated the effects of SF in an in vivo rat OA model, as well as in vitro in human OA chondrocytes.2. Rats were divided into the following groups: (i) an untreated control group; (ii) papain-induced OA; (iii) OA rats treated with 0.1 or 0.5% SF; and (iv) normal rats injected with 0.5% SF intra-articularly. Human chondrocytes from OA patients were cultured before being stimulated with 2 ng/mL interleukin-1beta and subsequently treated with SF (125, 250 and 500 mumol/L). The effects of SF were evaluated both in vivo and in vitro.3. In OA rats, SF treatment dose-dependently reversed pathological changes in OA cartilage, decreased BAX-immunopositive chondrocytes and increased Bcl-2-immunopositive chondrocytes. Both in vivo and in vitro analyses demonstrated a significant decrease in matrix metalloproteinase-l and an increase in tissue-specific inhibitor of metalloproteinase-l. In vitro, SF enhanced chondrocyte proliferation and decreased nitric oxide production and apoptosis.4. The results demonstrate that SF dose-dependently suppresses pathological processes in both in vitro and in vivo OA models. Thus, SF could be a therapeutic strategy for the treatment of OA.
机译:1.氧化,炎症和细胞凋亡与骨关节炎(OA)的病因和病理有关。阿魏酸钠(SF)已被证明在心血管,肝脏和糖尿病疾病中具有抗氧化,抗炎和抗凋亡的作用。这些发现表明,SF可能对OA有有益的作用。因此,本研究探讨了SF在体内大鼠OA模型以及人OA软骨细胞中的作用。2。将大鼠分为以下各组:(i)未治疗的对照组; (ii)木瓜蛋白酶诱导的OA; (iii)用0.1或0.5%SF治疗的OA大鼠; (iv)正常大鼠关节内注射0.5%SF。培养来自OA患者的人软骨细胞,然后用2 ng / mL白细胞介素1beta刺激,然后用SF(125、250和500 mumol / L)处理。在体内和体外评价SF的作用。3。在OA大鼠中,SF治疗剂量依赖性地逆转了OA软骨的病理变化,BAX免疫阳性软骨细胞减少和Bcl-2免疫阳性软骨细胞增加。体内和体外分析均显示基质金属蛋白酶-1的显着减少和金属蛋白酶-1的组织特异性抑制剂的增加。在体外,SF促进软骨细胞增殖,减少一氧化氮的产生和凋亡。4。结果表明,SF在体外和体内OA模型中均剂量依赖性地抑制病理过程。因此,SF可能是OA的一种治疗策略。

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