大鼠佐剂性关节炎脂质过氧化及其吲哚美辛的抑制作用。

Journal of applied biochemistry Pub Date : 1983-12-01
T Yoshikawa, H Tanaka, M Kondo
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引用次数: 0

摘要

通过注射结核分枝杆菌诱导大鼠佐剂性关节炎,根据足、尾、耳的宏观表现对其严重程度进行评分。同时给予吲哚美辛(1.5 mg/kg/d)时,平均得分较低。吲哚美辛可明显抑制白蛋白/球蛋白比值的降低。注射佐剂后,酸性磷酸酶和β -葡糖醛酸酶水平升高,但给予吲哚美辛后,它们有一定程度的降低。注射佐剂后2周血清和滑膜中硫代巴比妥酸(TBA)反应性物质水平升高,随后下降。给予1.5 mg/kg吲哚美辛的大鼠,血清和滑膜TBA反应物水平的升高均被显著抑制。这些观察结果表明,佐剂性关节炎的加重可能与脂质过氧化有关,而吲哚美辛可能在一定程度上通过防止脂质过氧化引起的滑膜损伤来发挥其抗炎作用。
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Lipid peroxidation in rat adjuvant arthritis and its inhibition by indomethacin.

Adjuvant arthritis was induced in rats by the injection of Mycobacterium tuberculosis, and its severity was scored according to the macroscopic findings of the legs, tails, and ears. The average score so obtained was lower when the rats also received indomethacin (1.5 mg/kg/day). The depression of the albumin/globulin ratio was inhibited significantly by the administration of indomethacin. The levels of acid phosphatase and beta-glucuronidase were elevated after the injection of an adjuvant, but they decreased to some extent in rats administered indomethacin. The levels of thiobarbituric acid (TBA)-reactive substances in the sera and synovia were elevated at 2 weeks after the injection of adjuvant and decreased thereafter. In rats administered 1.5 mg/kg of indomethacin, the increase in both serum and synovial levels of TBA reactants was inhibited significantly. These observations suggest that the aggravation of adjuvant arthritis may be associated with lipid peroxidation and that indomethacin may, in part, exert its anti-inflammatory effect by preventing lipid peroxide-induced damage of the synovial membrane.

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