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硫辛酸可预防兔激素性骨坏死。

Lipoic acid prevents steroid-induced osteonecrosis in rabbits.

机构信息

Department of Orthopedics, Xiangya Hospital, Central-South University, Xiangya Road 87#, Kaifu, Changsha, Hunan, 410008, People's Republic of China.

出版信息

Rheumatol Int. 2012 Jun;32(6):1679-83. doi: 10.1007/s00296-011-1846-6. Epub 2011 Mar 23.

Abstract

The objective of this study was to investigate in vivo effects of lipoic acid (LA) in preventing steroid-induced osteonecrosis and the possible pathway in a rabbit model. Sixty rabbits were divided into 2 groups: rabbits were intraperitoneally injected with LA aqueous solution at 36 mg/kg of body weight per day for 4 weeks in Group A and rabbits were injected with physiologic saline (PS) as a control in Group B. At 2 weeks after starting treatment, they were intramuscularly injected once with 20 mg/kg of methylprednisolone acetate (MPSL). The femora were histopathologically examined for the presence of osteonecrosis. The plasma levels of total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), glutathione (GSH), endothelin (ET) and malondialdehyde (MDA) were assayed at 2 weeks after the injection of MPSL. The incidence of osteonecrosis was significantly higher in Group B (73.1%) than in Group A (20.8%). The GSH level was higher in Group A than in Group B after the LA injection. The plasma MDA and ET levels were lower in Group A than in Group B at 2 weeks after the MPSL administration. Lipoic acid can prevent the development of steroid-induced osteonecrosis in rabbits. Inhibited oxidative stress and amendment of vascular endothelial dysfunction is a possible mechanism for this effect.

摘要

本研究旨在探讨硫辛酸(LA)在预防兔类固醇诱导性骨坏死中的体内作用及其可能的作用途径。60 只兔随机分为 2 组:A 组兔每日腹腔内注射 LA 水溶液 36mg/kg,连续 4 周;B 组兔注射生理盐水作为对照。治疗开始后 2 周,兔一次性肌肉注射 20mg/kg 醋酸甲泼尼龙。观察股骨组织病理学有无骨坏死。注射 MPSL 后 2 周检测总胆固醇(TC)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)、谷胱甘肽(GSH)、内皮素(ET)和丙二醛(MDA)的血浆水平。MPSL 注射后 2 周,B 组(73.1%)骨坏死发生率明显高于 A 组(20.8%)。LA 注射后 A 组 GSH 水平高于 B 组。MPSL 给药后 2 周,A 组血浆 MDA 和 ET 水平低于 B 组。硫辛酸可预防兔类固醇诱导性骨坏死的发生。抑制氧化应激和纠正血管内皮功能障碍可能是其作用机制。

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