壳聚糖和卵磷脂改善碘乙酸盐诱导的大鼠骨关节炎症状。
Chitosan and Lecithin Ameliorate Osteoarthritis Symptoms Induced by Monoiodoacetate in a Rat Model.
机构信息
Department of Biology, College of Sciences, Taif University, P.O. Box 11099, Taif 21944, Saudi Arabia.
Department of Zoology, Faculty of Science, Zagazig University, Zagazig 44519, Egypt.
出版信息
Molecules. 2020 Dec 4;25(23):5738. doi: 10.3390/molecules25235738.
The present work aimed to assess the chondroprotective influence of chitosan and lecithin in a monoiodoacetate (MIA)-induced experimental osteoarthritis (OA) model. Forty male rats weighing 180-200 g were randomly distributed among the following five experimental groups (eight per group): control, MIA-induced OA, MIA-induced OA + chitosan, MIA-induced OA + lecithin, and MIA-induced OA + chitosan + lecithin. The levels of TNF-α, IL6, RF, ROS, and CRP, as well as mitochondrial markers such as mitochondrial swelling, cytochrome C oxidase (complex IV), MMP, and serum oxidative/antioxidant status (MDA level) (MPO and XO activities) were elevated in MIA-induced OA. Also, SDH (complex II) activity in addition to the levels of ATP, glutathione (GSH), and thiol was markedly diminished in the MIA-induced OA group compared to in control rats. These findings show that mitochondrial function is associated with OA pathophysiology and suggest that chitosan and lecithin could be promising potential ameliorative agents in OA animal models. Lecithin was more effective than chitosan in ameliorating all of the abovementioned parameters.
本研究旨在评估壳聚糖和卵磷脂在单碘乙酸（MIA）诱导的实验性骨关节炎（OA）模型中的软骨保护作用。40 只体重为 180-200g 的雄性大鼠随机分为以下五组（每组 8 只）：对照组、MIA 诱导的 OA 组、MIA 诱导的 OA+壳聚糖组、MIA 诱导的 OA+卵磷脂组和 MIA 诱导的 OA+壳聚糖+卵磷脂组。在 MIA 诱导的 OA 组中，TNF-α、IL6、RF、ROS 和 CRP 水平以及线粒体标记物（如线粒体肿胀、细胞色素 C 氧化酶（复合物 IV）、MMP 和血清氧化/抗氧化状态（MDA 水平）（MPO 和 XO 活性）升高。此外，与对照组大鼠相比，MIA 诱导的 OA 组中 SDH（复合物 II）活性以及 ATP、谷胱甘肽（GSH）和巯基水平显著降低。这些发现表明线粒体功能与 OA 病理生理学有关，并表明壳聚糖和卵磷脂可能是 OA 动物模型中很有前途的潜在改善剂。与壳聚糖相比，卵磷脂在改善上述所有参数方面更有效。
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