Buddhachat Kittisak, Siengdee Puntita, Chomdej Siriwadee, Soontornvipart Kumpanart, Nganvongpanit Korakot
Animal Bone and Joint Research Laboratory, Department of Veterinary Biosciences and Public Health, Faculty of Veterinary Medicine, Chiang Mai University, Chiang Mai, 50100, Thailand.
Department of Biology, Faculty of Science, Naresuan University, Phitsanulok, 65000, Thailand.
In Vitro Cell Dev Biol Anim. 2017 May;53(5):448-457. doi: 10.1007/s11626-016-0125-y. Epub 2017 Jan 11.
Our purpose was to evaluate the protective effect of three marine omega-3 sources, fish oil (FO), krill oil (KO), and green-lipped mussel (GLM) against cartilage degradation. Canine cartilage explants were stimulated with either 10 ng/mL interleukin-1β (IL-1β) or IL-1β/oncostatin M (10 ng/mL each) and then treated with various concentrations of docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA; 3 and 30 μg/mL), FO, KO, or GLM (250, 500, and 1000 μg/mL) for 28 days. Gene expression was then investigated in primary canine chondrocytes. Our results showed that DHA and EPA as well as omega-3 sources could suppress matrix degradation in cytokine-induced cartilage explants by significantly reducing the increase of sulfated glycosaminoglycans (s-GAGs) and preserving uronic acid and hydroxyproline content (except GLM). These agents were not able to reduce IL-1β-induced IL1B and TNFA expression but were able to down-regulate the expression of the catabolic genes MMP1, MMP3, and MMP13 and up-regulate the anabolic genes AGG and COL2A1; FO and KO were especially effective. Our findings indicated that FO and KO were superior to GLM for their protective effect against proteoglycan and collagen degradation. Hence, FO and KO could serve as promising sources of chondroprotective agents.
我们的目的是评估三种海洋ω-3来源,即鱼油(FO)、磷虾油(KO)和绿唇贻贝(GLM)对软骨降解的保护作用。用10 ng/mL白细胞介素-1β(IL-1β)或IL-1β/制瘤素M(各10 ng/mL)刺激犬软骨外植体,然后用不同浓度的二十二碳六烯酸(DHA)、二十碳五烯酸(EPA;3和30 μg/mL)、FO、KO或GLM(250、500和1000 μg/mL)处理28天。随后在原代犬软骨细胞中研究基因表达。我们的结果表明,DHA、EPA以及ω-3来源可通过显著减少硫酸化糖胺聚糖(s-GAGs)的增加并保留糖醛酸和羟脯氨酸含量(GLM除外)来抑制细胞因子诱导的软骨外植体中的基质降解。这些药物不能降低IL-1β诱导的IL1B和TNFA表达,但能够下调分解代谢基因MMP1、MMP3和MMP13的表达并上调合成代谢基因AGG和COL2A1的表达;FO和KO尤其有效。我们的研究结果表明,FO和KO在保护蛋白聚糖和胶原蛋白降解方面优于GLM。因此,FO和KO可作为有前景的软骨保护剂来源。