BACKGROUND/OBJECTIVESThe 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/METHODSIn 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.RESULTSIn 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.CONCLUSIONSHFE extract inhibited articular cartilage degeneration through preventing extracellular matrix degradation and chondrocyte injury.

We have provided a protocol for establishing an atopic dermatitis (AD) in vitro model, and evaluated the effects of Costaria costata (CC) extracts on AD in an in vitro model using keratinocytes and splenocytes from AD-induced mice and mast cells. HaCaT cells were each treated with 200 μg/mL of CC water extract (CCW), CC 10% ethanol extract (CCE10%), and CC 70% ethanol extract (CCE70%), immediately followed by stimulation with 20 ng/mL tumor necrosis factor (TNF)-α, and 20 ng/mL interferon (IFN)-γ for inflammation. The splenocytes from AD-induced mice were each treated with 200 μg/mL of CCW, CCE10%, and CCE70%, followed by stimulation with 5 μg/mL ConA or lipopolysaccharide (LPS), to induce T cell or B-cell activation, and 5 μg/mL LPS and 50 ng/mL interleukin-4, to induce immunoglobulin (Ig) E production. We investigated the effects of CCW, CCE10%, and CCE70% on the production of histamine in PMA, and A23187-stimulated MC/9 cells. We found that treatments with CC extracts decreased the production of proinflammatory cytokines in TNF-α and IFN-γ-stimulated HaCaT cells, and the suppression of the imbalance of Th1/Th2 cytokines and IgE production on primary splenocytes. In addition, CC extracts resulted in a decrease in histamine release in the PMA and A23187-simulated MC/9 cells. According to our present results, we can conclude that CC extracts may be effective for the treatment of other allergy diseases, and AD, via the attenuation of allergic reactions.

We investigated the potential effects of Costaria costata (CC) on atopic dermatitis (AD) development in chloro-2,4-dinitrobenzene (DNCB)-treated NC/Nga mice. CC is a brown alga distributed across the seas of Korea, China, and Japan. A total of 40 mice were randomly assigned to 5 groups with 8 mice per group: untreated Balb/c mice, AD control (0.1% w/v DNCB-treated NC/Nga mice), positive control (i.e., DNCB-treated NC/Nga mice fed a dietary supplement of 66.6 mg/kg of body weight [b.w.] of CJLP133), DNCB-treated NC/Nga mice fed a dietary supplement of 100 mg/kg b.w. of CCE10 (CCE10 100), and DNCB-treated mice fed a dietary supplement of 300 mg/kg b.w. of CCE10 (CCE10 300) groups. The CCE10 100 and CCE10 300 treatment groups suppressed AD development including clinical and histopathological changes and a reduction in skin hydration induced by DNCB. In addition, Th2 cytokine production in primary splenocytes, serum IgE and histamine production, and mast cell infiltration into the skin were suppressed in the CCE10 300 mice compared to the CCE10 100 mice. Our finding demonstrated an inhibitory effect of CCE10 in AD development by means of improving the Th1/Th2 cytokine balance and anti-inflammatory effect in an in vivo model.

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