The inhibitory effects of Boswellia serrata (BW) extracts on degenerative osteoarthritis were investigated in primary-cultured rat cartilage cells and a monosodium-iodoacetate (MIA)-induced osteoarthritis rat model. To identify the protective effects of BW extract against H2O2 (800 μM, 2 hr) in vitro, cell survival was measured by MTT assay. Cell survival after H2O2 treatment was elevated by BW extract at a concentration of 20 μg/mL. In addition, BW extract treatment significantly reduced and normalized the productions of pro-inflammatory factors, nuclear transcription factor κB, cyclooxygenase-2, tumor necrosis factor-α, and interleukin-6 at a concentration of 20 μg/mL. Treatment of chondrocytes with BW extract significantly reduced 5-lipoxygenase activity and production of prostaglandin E2, especially at a concentration of 10∼20 μg/mL. For the in vivo animal study, osteoarthritis was induced by intra-articular injection of MIA into knee joints of rats. Consumption of a diet containing BW extract (100 and 200 mg/kg) for 35 days significantly inhibited the development and severity of osteoarthritis in rats. To determine the genetic expression of arthritic factors in articular cartilage, real-time PCR was applied to measure matrix metalloproteinases (MMP-3, MMP-9, and MMP-13), collagen type I, collagen type II, and aggrecan, and BW extract had protective effects at a concentration of 200 mg/kg. In conclusion, BW extract was able to inhibit articular cartilage degeneration by preventing extracellular matrix degradation and chondrocyte injury. One can consider that BW extract may be a potential therapeutic treatment for degenerative osteoarthritis.

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The object of this study was to investigate the inhibitory effects of chios mastic gum (MG) on gastric acid secretion in an ethanol-induced SD rat model and primary parietal cells. Rats were randomly divided into four groups: Vehicle (normal group), Control (treated with ethanol), MG50 (treated with ethanol and mastic gum at 50 mg/kg b.w), MG100 (treated with ethanol and mastic gum at 100 mg/kg b.w). Groups treated with both MG50 and MG100 showed attenuation of gastric mucosal injury, sub-epithelial loss, hemorrhaging, and gastric juice secretion. We also examined the acidity of gastric juice during gastric injury. Oral administration of both MG50 and MG100 significantly decreased acidity of gastric juice by % and %, respectively. To examine the stimulatory factors related to gastric acid secretion, mRNA expression levels of H2r, M3r, CCK2r, and H + /K + ATPase were measured by real-time PCR. Compared with a vehicle group, mRNA expression levels of H2r, CCK2r, and H + /K + ATPase clearly increased in the control group. However, levels of H2r, CCK2r, and H + /K + ATPase slightly but significantly decreased in MG-treated groups compared with control. Blood level of histamine significantly decreased in MG-treated groups, which indicates the involvement of MG on in histamine-related acid secretion. To identify the mode of action of MG in regulating histamine-related pathways, intracellular level of cAMP and mRNA levels of H2r, M3r, CCK2r, and H + /K + ATPase were measured in primary parietal cells. While mRNA levels of M3r and CCK2r remained unchanged, levels of H2r and H + /K + ATPase significantly decreased upon MG treatment. Subsequently, intracellular levels of cAMP decreased. These results suggest that mastic gum has the ability to inhibit gastric acid secretion by regulating a histamine-related pathway.Key words: mastic gum, gastric acid, histamine, cAMP, proton pump

We investigated the inhibitory effect of Canavalia gladiata water extract (CGW) on ethanol‐induced gastric inflammation, specifically on gastric acid secretion and gastric mucosal damage in Sprague‐Dawley (SD) rats. The possible mechanisms of CGW actions via ROS was also further determined for antioxidant effects. Rats were divided into four groups : saline(G1), gastric inflammation plus saline(G2), gastric inflammation plus Lansoprazole 30mg/kg b.w(G3), gastric inflammation plus CGW 250mg/kg b.w(G4), gastric inflammation plus CGW 500mg/kg b.w(G5). After oral administration of either saline, Lansoprazole or CGW for 7 days, acute gastric inflammation was induced by oral administration of 1mL of 70% ethanol and 0.15M HCl at groups G2,G3,G4 and G5. After 1h on ethanol administration, all animals were sacrificed. Gastric acid secretion and gastric mucosal injury were significantly decreased in G3 when compared to that of G2. And groups pretreated with CGW (G4, G5) caused a significant decrease in gastric acid secretion and gastric mucosal injury in a dose dependant manner. To examine the regulatory factors related inflammation, NF‐kB, COX‐1, COX‐2 and cytokines were measured by immuno‐histochemistry and ELISA. The expression of NF‐kB, COX‐1 and COX‐2 were clearly decreased in G3 and G5 compared with the G2. Additionally, cytokines was significantly decreased in G3 and G5. We next examined the levels of MDA and SOD activity related in antioxidative effects. Oral administration of CGW significantly decreased levels of MDA and SOD activity was dramatically increased. In conclusion, our data show that CGW has inhibitory effects on gastric inflammation induced by acute ethanol treatment in SD rat. Although the exact mechanism underlying these actions is unclear, the effects on acute gastric lesions suggest a multifactorial mechanism probably involving the antioxidant properties of CGW.

The immune system protects the body against harmful substances and infectious agents. Normally, the body can maintain a state of immune homeostasis. However, failure of immune homeostasis results in severe diseases when the immune system is defective. We investigated the immunomodulatory effect of Curcuma longa L.