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In the present study, the gastroprotective effects of arctigenin of Fructus Arctii were evaluated and the possible underlying mechanisms of action were elucidated. Arctigenin (high-performance liquid chromatography purity, >99.0%) was isolated and purified from the seeds of Arctium lappa L. The anti-ulcerogenic activity of arctigenin against ulcers induced by absolute ethanol and acetic acid was evaluated in a Sprague-Dawley rat model. In addition, the antioxidant activity was assessed by measuring malondialdehyde (MDA) levels in an ethanol-induced model and the anti-inflammatory effects were assessed by measuring five factors in an acetic acid-induced model. In the ethanol-induced model, arctigenin inhibited gastric lesions in a dose-dependent manner, by 53.04, 53.91 and 64.43% at doses of 0.05, 0.15 and 0.45 mg/kg, respectively. In addition, arctigenin reduced MDA (P<0.01) and increased superoxide dismutase (P<0.01) levels in serum when compared with the vehicle group. The lesion index induced by acetic acid was significantly inhibited by all doses of arctigenin (0.05, 0.15 and 0.45 mg/kg; P<0.01) in comparison to the vehicle group and in a dose-dependent manner. In addition, it was shown that the expression levels of tumor necrosis factor-α, interleukin-6 (IL-6), IL-10 and C-reactive protein were significantly decreased (P<0.05) in the arctigenin group compared with the vehicle group. Thus, the current study indicated that arctigenin exerted anti-ulcer activity, which may be associated with its reduction in oxidative and inflammatory damage. All the results indicate that arctigenin may be used as an effective therapeutic agent to prevent gastric ulcers. [ABSTRACT FROM AUTHOR]

There is increasing evidence showing that inflammation occurs in atherosclerosis and contributes to the formation of atherosclerotic plaques. As important inflammatory peptides, kinins are increased in inflammation, eliciting vasodilation, increasing vascular permeability and recruiting inflammatory cells to the injury sites by activating specific receptors, B1 and B2. The two receptors have been reported to increase in inflammation, but their expressions remain to be defined in human carotid atherosclerotic plaques (CAP). In order to assess the gene expression of kinin receptors in human CAP, 47 CAP specimens were collected from patients undergoing endarterectomy and classified into stable and unstable plaque groups, respectively, with 10 mesenteric arteries used as controls. Total mRNA of B1R and B2R was extracted from CAPs and their levels were determined using reverse transcription-polymerase chain reaction. The expression of B1R and B2R mRNA was significantly upregulated in human CAPs compared to the control arteries. In the unstable plaques, the ratios of B1R to the β-actin mRNA level were significantly increased relative to the stable plaques. However, no notable differences were observed in the ratios of B2R to β-actin in mRNA expression between the stable and unstable plaques. The present study suggests that kinin-mediated inflammation involves the formation of atherosclerotic plaque and B1R plays an important role in plaque instability, indicating that kinin receptors can be used as potential targets for future therapeutic interventions. [ABSTRACT FROM AUTHOR]