Qiang Hui, Liu Huitong, Ling Ming, Wang Kunzheng, Zhang Chen
The Second Department of Orthopaedics, Shaanxi Provincial People's Hospital, The Third Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710068, China.
The Second Department of Orthopaedics, Shaanxi Provincial People's Hospital, The Third Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710068, China ; The First Department of Orthopaedics, Fuzhou Second Hospital of Xiamen University, Fuzhou, Fujian 350007, China.
Evid Based Complement Alternat Med. 2015;2015:719370. doi: 10.1155/2015/719370. Epub 2015 Mar 16.
Background. This study was aimed at investigating the pathogenesis of oxidative stress in steroid-induced avascular necrosis of the femoral head (SANFH) and at exploring the mechanism and protective effects of Panax notoginseng saponins (PNS) on early SANFH. Methods. 80 adult New Zealand rabbits were randomly divided into control group, model group, and PNS group. In model group, equine serum was injected into auricular vein; then methylprednisolone was injected into gluteus. In PNS group, PNS was applied for 14 consecutive days before methylprednisolone management. At different time points, serum and femoral heads were prepared for T-AOC, SOD, GSH-PX, ·OH, and MDA determination. Two weeks after steroid management, all femoral heads were assessed with MRI and HE staining. Results. Typical early osteonecrosis symptoms were observed in model group. Our results showed that PNS could significantly ameliorate the decrease of T-AOC level, improve SOD and GSH-PX activity, suppress ·OH ability, and augment MDA level. Besides, PNS improved MRI and pathological changes of the femoral head, markedly reducing the incidence of osteonecrosis. Conclusion. Based on our research, we found oxidative stress played a positive role in the occurrence of SANFH where reactive oxygen species was the direct cause. PNS could protect rabbits against early steroid-induced osteonecrosis of femoral head by its antioxidative effect.
背景。本研究旨在探讨激素性股骨头缺血性坏死(SANFH)中氧化应激的发病机制,并探索三七总皂苷(PNS)对早期SANFH的作用机制及保护作用。方法。80只成年新西兰兔随机分为对照组、模型组和PNS组。模型组于耳静脉注射马血清,然后于臀肌注射甲基强的松龙。PNS组在甲基强的松龙处理前连续14天应用PNS。在不同时间点,制备血清和股骨头用于测定总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、羟自由基(·OH)和丙二醛(MDA)。激素处理两周后,对所有股骨头进行磁共振成像(MRI)和苏木精-伊红(HE)染色评估。结果。模型组观察到典型的早期骨坏死症状。我们的结果表明,PNS可显著改善T-AOC水平的降低,提高SOD和GSH-PX活性,抑制·OH生成能力,并降低MDA水平。此外,PNS改善了股骨头的MRI表现和病理变化,显著降低了骨坏死的发生率。结论。基于我们的研究,我们发现氧化应激在SANFH的发生中起积极作用,其中活性氧是直接原因。PNS可通过其抗氧化作用保护兔免受早期激素性股骨头坏死的影响。