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首页> 外文期刊>Calcified Tissue International >Estrogen and Testosterone Attenuate Extracellular Matrix Loss in Collagen-Induced Arthritis in Rats
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Estrogen and Testosterone Attenuate Extracellular Matrix Loss in Collagen-Induced Arthritis in Rats

机译:雌激素和睾丸激素减轻胶原诱导的关节炎大鼠细胞外基质的损失。

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摘要

Rheumatoid arthritis (RA) is a sexually dimorphic, autoimmune inflammatory disorder affecting the joints. Joint disability in RA results primarily from loss of matrix components (collagen and glycosoaminoglycan) in the cartilage and synovium. This study was carried out to understand the effect of physiological levels of testosterone, estrogen, and progesterone on oxidative stress-induced changes in matrix composition in rat synovium in arthritis. Arthritis induction in castrated and ovariectomized rats resulted in enhanced oxidative stress and this was assessed by lipid peroxidation levels and depletion of antioxidants. This, in turn, led to significantly (p < 0.01) increased levels of TNF-α and matrix metalloproteinase-2 (MMP-2), subsequently resulting in loss of collagen, elastin, and glycosoaminoglycan (GAG) and disorganization of reticulin as evidenced by biochemical quantitation and also by staining for collagen, reticulin, and elastin. Treatment with physiological doses of dihydrotestosterone (25 mg topically) and estrogen (5 μg/0.1 ml subcutaneously) restored the antioxidant levels significantly (p < 0.05) and reduced the levels of TNF-α and MMP-2, with estrogen exhibiting a higher potency. This, in turn, attenuated the damage to reticulin organization as well as the loss of collagen and GAG in the articular tissues. However, elastin loss could not be attenuated by either treatment. Progesterone (2 mg/0.1 ml subcutaneously) was not shown to have any significance in disease modification, and on the contrary, it inhibited the protective effects of estrogen. However, progesterone contributed to increased collagen levels in the tissues.
机译:类风湿关节炎(RA)是一种性二形,自身免疫性炎症疾病,会影响关节。 RA的关节残疾主要是由于软骨和滑膜中的基质成分(胶原蛋白和糖胺基聚糖)流失所致。进行这项研究以了解生理水平的睾丸激素,雌激素和孕激素对关节炎大鼠滑膜中氧化应激诱导的基质组成变化的影响。去势和去卵巢大鼠的关节炎诱导导致氧化应激增强,这可以通过脂质过氧化水平和抗氧化剂的消耗来评估。反过来,这导致TNF-α和基质金属蛋白酶2(MMP-2)的水平显着(p <0.01)升高,随后导致胶原蛋白,弹性蛋白和糖胺聚糖(GAG)丢失以及网状蛋白紊乱通过生化定量以及胶原蛋白,网状蛋白和弹性蛋白染色。生理剂量的二氢睾丸激素(局部25 mg)和雌激素(皮下5μg/ 0.1 ml)治疗显着恢复了抗氧化剂水平(p <0.05),并降低了TNF-α和MMP-2的水平,雌激素表现出更高的效力。反过来,这减弱了对网状蛋白组织的损害以及关节组织中胶原蛋白和GAG的损失。但是,两种治疗都不能减轻弹性蛋白的损失。黄体酮(皮下注射2 mg / 0.1 ml)未显示对疾病改变有任何意义,相反,它抑制了雌激素的保护作用。但是,孕酮有助于增加组织中的胶原蛋白水平。

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