Kwon Han Ol, Lee Minhee, Kim Ok-Kyung, Ha Yejin, Jun Woojin, Lee Jeongmin
Department of Medical Nutrition, Kyung Hee University, 1732, Deogyeong-daero, Giheung-gu, Yongin 17104, Korea.
Division of Food and Nutritional Science, Chonnam National University, Gwangju 61186, Korea.
Nutr Res Pract. 2016 Jun;10(3):265-73. doi: 10.4162/nrp.2016.10.3.265. Epub 2016 Apr 1.
BACKGROUND/OBJECTIVES: The inhibitory effect of Hijikia fusiforme (HF) extracts on degenerative osteoarthritis was examined in primary cultured rat cartilage cells and a monosodium iodoacetate (MIA)-induced osteoarthritis rat model.
MATERIALS/METHODS: In vitro, cell survival and the expression of matrix metalloproteinases (MMPs), collagen type I, collagen type II, aggrecan, and tissue inhibitor of metalloproteinases (TIMPs) was measured after H2O2 (800 µM, 2 hr) treatment in primary chondrocytes. In vivo animal study, osteoarthritis was induced by intra-articular injection of MIA into knee joints of rats, and then RH500, HFE250 and HFE500 were administered orally once a day for 28 days. To determine the anti-inflammatory effects of HFE, nitric oxide (NO), prostaglandin E2 (PGE2) expression were measured. In addition, real-time PCR was performed to measure the genetic expression of MMPs, collagen type I, collagen type II, aggrecan, and TIMPs.
In the in vitro assay, cell survival after H2O2 treatment was increased by HFE extract (20% EtOH). In addition, anabolic factors (genetic expression of collagen type I, II, and aggrecan) were increased by HFE extract (20% EtOH). However, the genetic expression of MMP-3 and 7, known as catabolic factors were significantly inhibited by treatment with HFE extract (20% EtOH). In the in vivo assay, anabolic factors (genetic expression of collagen type I, II, aggrecan, and TIMPs) were increased by oral administration of HFE extract. However, the genetic expression of MMP-3 and 7, known as catabolic factors, and production of NO and PGE2 were significantly inhibited by treatment with oral administration of HFE extract.
HFE extract inhibited articular cartilage degeneration through preventing extracellular matrix degradation and chondrocyte injury.
背景/目的:在原代培养的大鼠软骨细胞和碘乙酸钠(MIA)诱导的骨关节炎大鼠模型中,研究了羊栖菜(HF)提取物对退行性骨关节炎的抑制作用。
材料/方法:在体外,用H2O2(800 μM,2小时)处理原代软骨细胞后,检测细胞存活率以及基质金属蛋白酶(MMPs)、I型胶原、II型胶原、聚集蛋白聚糖和金属蛋白酶组织抑制剂(TIMPs)的表达。在体内动物研究中,通过向大鼠膝关节内注射MIA诱导骨关节炎,然后每天口服一次RH500、HFE250和HFE500,持续28天。为了确定HFE的抗炎作用,检测了一氧化氮(NO)、前列腺素E2(PGE2)的表达。此外,进行实时PCR以检测MMPs、I型胶原、II型胶原、聚集蛋白聚糖和TIMPs的基因表达。
在体外试验中,HFE提取物(20%乙醇)提高了H2O2处理后的细胞存活率。此外,HFE提取物(20%乙醇)增加了合成代谢因子(I型、II型胶原和聚集蛋白聚糖的基因表达)。然而,作为分解代谢因子的MMP-3和7的基因表达被HFE提取物(20%乙醇)处理显著抑制。在体内试验中,口服HFE提取物增加了合成代谢因子(I型、II型胶原、聚集蛋白聚糖和TIMPs的基因表达)。然而,作为分解代谢因子的MMP-3和7的基因表达以及NO和PGE2的产生被口服HFE提取物处理显著抑制。
HFE提取物通过防止细胞外基质降解和软骨细胞损伤来抑制关节软骨退变。