1,725,560 research outputs found
Augmenting Effect of DA-9601 on Ghrelin in an Acute Gastric Injury Model
No full textBackground/Aims: Acute gastric injury by alcohol or indomethacin has been reported to be prevented by DA-9601, an extract of the herb Artemisia asiatica. Ghrelin, an endogenously produced gastrointestinal peptide hormone, has also been demonstrated to play a role in gastric mucosal defense. The aim of this study was to investigate the effects of DA-9601 on ghrelin in an acute gastric injury model induced by alcohol or indomethacin. Methods: A total of 140 Sprague-Dawley rats were divided into two groups, a placebo group and a DA-9601-pretreated group. Thirty minutes later, half of the rats in each group received ethanol injury and the other half received indomethacin injury. Levels of serum ghrelin and gastric mucosal ghrelin mRNA were measured by ELISA and RT-PCR, respectively. Results: Immediately after ethanol administration, ghrelin increased in both groups pretreated with DA-9601 and placebo. However, the increase occurred more rapidly and was higher in the DA-9601-pretreated rats than in the controls that did not receive DA-9601-pretreatment. Similarly, from 30 minutes to 2 hours after indomethacin administration, the DA-9601-pretreated rats showed a significant increase in serum and gastric mucosal ghrelin concentrations, whereas placebo-pretreated rats showed only a mild increase. Conclusions: DA-9601 potentiates the endogenous production and secretion of ghrelin in acute gastric injury models induced by ethanol or indomethacin. (Gut Liver 2011;5:52-56
Augmenting Effect of DA-9601 on Ghrelin in an Acute Gastric Injury Model
No full textBackground/Aims: Acute gastric injury by alcohol or indomethacin has been reported to be prevented by DA-9601, an extract of the herb Artemisia asiatica. Ghrelin, an endogenously produced gastrointestinal peptide hormone, has also been demonstrated to play a role in gastric mucosal defense. The aim of this study was to investigate the effects of DA- 9601 on ghrelin in an acute gastric injury model induced by alcohol or indomethacin. Methods: A total of 140 Sprague- Dawley rats were divided into two groups, a placebo group and a DA-9601-pretreated group. Thirty minutes later, half of the rats in each group received ethanol injury and the other half received indomethacin injury. Levels of serum ghrelin and gastric mucosal ghrelin mRNA were measured by ELISA and RT-PCR, respectively. Results: Immediately after ethanol administration, ghrelin increased in both groups pretreated with DA-9601 and placebo. However, the increase occurred more rapidly and was higher in the DA-9601-pretreated rats than in the controls that did not receive DA-9601-pretreatment. Similarly, from 30 minutes to 2 hours after indomethacin administration, the DA-9601-pretreated rats showed a significant increase in serum and gastric mucosal ghrelin concentrations, whereas placebo-pretreated rats showed only a mild increase. Conclusions: DA-9601 potentiates the endogenous production and secretion of ghrelin in acute gastric injury models induced by ethanol or indomethacin. (Gut Liver 2011;5:52-56
DA-9601 suppresses 2, 4-dinitrochlorobenzene and dust mite extract-induced atopic dermatitis-like skin lesions
No full textDA-9601 (Stillen (TM)) is a novel anti-peptic formulation prepared from the ethanol extracts of Artemisia asiatica possessing anti-oxidative, anti-allergic and anti-inflammatory activities. However, their effect on atopic dermatitis (AD) has not been studied yet. In this study, we report that topical application of DA-9601 suppressed house dust mite extract (Dermatophagoides farinae extract. DFE) and 2, 4-dinitrochlorobenzene (DNCB)-induced AD-like skin lesions in BALB/c mice model. We established atopic dermatitis model in BALB/c mice by repeated local exposure of DFE/DNCB to the ears. Repeated alternative treatment of DFE/DNCB caused AD-like lesions. DA-9601 reduced AD-like skin lesions based on ear thickness and histopathological analysis, and serum IgE levels. DA-9601 inhibited mast cell infiltration into the ear and elevation of serum histamine in AD model. In addition, DA-9601 suppressed DFE/DNCB-induced expression of IL-4, IL-13, IL-31, and TNF-alpha in the ears. Taken together, our results showed that topical application of DA-9601 exerts beneficial effects in animal model of AD, suggesting that DA-9601 might be a candidate for the treatment of AD. (C) 2011 Elsevier B.V. All rights reserved.FALSEsciescopu
DA-9601 Decreases Immediate-Type Allergic Reaction and Tumor Necrosis Factor-.ALPHA. Production
No full textThe immediate-type allergic reaction is involved in many allergic diseases such as asthma, allergic rhinitis, and sinusitis. The discovery of drugs for the treatment of immediate-type allergic disease is a very important subject in human health. The formulated ethanol extract of Artemisia asiatica Nakai (DA-9601) has been reported to have anti-oxidative and anti-inflammatory activities. In this report, we investigated the effect of DA-9601 on the immediate-type allergic reaction and studied its possible mechanisms of action, focusing on the mast cell-mediated allergic reaction. DA-9601 inhibited compound 48/80-induced systemic anaphylactic reactions and serum histamine release in mice. DA-9601 decreased the IgE-mediated passive cutaneous anaphylaxis, the model of local allergic reaction in vivo. DA-9601 dose-dependently reduced histamine release from mast cells activated by compound 48/80 or IgE. Furthermore, DA-9601 decreased the gene expression and production of tumor necrosis factor (TNF)-alpha in phorbol 12-myristate 13-acetate plus A23187-stimulated mast cells. These findings provide evidence that DA-9601 could be a candidate as an anti-allergic agent.TRUEsciescopu
Protective Effect of DA-9601, an Artemisiae Herba Extract, on Radiation-induced Colitis in Wistar Rats
No full textThis study was performed to examine the effects of DA-9601, a novel antiulcer agent extracted from Artemisiae Herba, on radiation colitis in the rat. Female Wistar rats received a 30 Gy dose of irradiation to the 2 cm of distal colon in length using an intrarectal applicator system. 30 mg/kg or 100 mg/kg of DA9601 was administered orally 30 min before and 4 h after radiation on day 1. And the same dose of DA-9601 was given to the animals twice a day from day 2 to 14. As a reference control, sucralfate suspension (100 or 300 mg/head) was given as an enema based on the same treatment schedule of DA-9601. Body weight change and the frequency of diarrhea were recorded during the observation period as markers of radiationinduced injury. All animals were sacrificed on day 15 for evaluation of macro- and microscopic findings and mucosal myeloperoxidase (MPO) activity. Radiated animals showed diarrhea, mucosal redness and histologic changes characterized by edema and eosinophilic infiltration of the periglandular lamina propria with loss of colonic epithelium. Radiation also significantly increased mucosal MPO activity of affected colon (P<0.05). However, most of these changes were completely protected by oral administration with DA-9601. DA-9601 reduced radiation-induced histologic alteration significantly in a dose-related manner (P<0.05). In addition, mucosal MPO activity in rats receiving high dose of DA 9601 decreased significantly when compared with that in radiated control. High. dose. of sucralfate (300 mg/head) alleviated radiation-induced histologic lesion, but failed to reach statistical significance. The results of this study suggest that DA-9601 can be useful for the prevention of acute clinical symptoms of radiation proctocolitis and that decrease of mucosal MPO by DA9601 plays a role in its protective mechanism(s), at least in part
DA-9601, Artemisia Asiatica Herbal Extract, Ameliorates Airway Inflammation of Allergic Asthma in Mice
No full textWe previously reported that DA-9601, ethanol herbal extract of Artemisia asiatica, inhibited histamine and leukotriene releases in guinea pig lung mast cells activated with specific antigen/antibody reaction. This study aimed to evaluate the inhibitory effect of DA-9601 on the OVA-induced airway inflammation in allergic asthma mouse model. BALB/c mice were sensitized and challenged with OVA. DA-9601 was administered orally 1 h before every local OVA-challenge. OVA-specific serum IgE was measured by ELISA, recruitment of inflammatory cells in BAL fluids and lung tissues by Diff-Quik and H&E staining, respectively, the expressions of CD40, CD40L and VCAM-1 by immunohistochemistry, goblet cell hyperplasia by PAS staining, activities of MMPs by gelatin zymography, expressions of mRNA and proteins of cytokines by RT-PCR and ELISA, activities of MAP kinases by western blot, and activity of NF-KappaB by EMSA. DA-9601 reduced IgE level, recruitment of inflammatory cells into the BAL fluid and lung tissues, expressions of CD40, CD40L and VCAM-1 molecules, goblet cell hyperplasia, MMPs activity, expressions of mRNA and productions of various cytokines, activities of MAP kinases and NK-KappaB increased from OVA-challenged mice. These data suggest that DA-9601 may be developed as a clinical therapeutic agent in allergic diseases due to suppressing the airway allergic inflammation via regulation of various cellular molecules expressed by MAP kinases/NF-KappaB pathway.ope
Sequence-based typing identifies a novel HLA-DPB1 allele, DPB1*9601
No full textIn this report we describe the identification of a novel HLA-DPB1 allele, DPB1*9601, found in a Caucasian individual sample named ucla#356. The new allele was detected in the DNA of ucla#356 during routine HLA sequence-based typing (SBT) of samples participating in the UCLA International HLA DNA Exchange (number 55) for HLA DNA Proficiency Testing. DPB1*9601 was identical to DPB1*3901 except for a single nucleotide substitution 'G'-->'C' in previously constant position 277 (position 177, respectively, counting only exon 2). This nucleotide change causes an amino acid substitution from aspartic acid in DPB1*3901 to histidine at codon 64 in the novel allele. This new allele has been submitted to the EMBL database and has been assigned the accession number AJ514871. The WHO Nomenclature Committee has officially assigned the name DPB1*9601
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