Background: Ankaferd blood stopper (ABS) is a herbal extract that enhances mucosal healing. It has therapeutic potential in the management of external hemorrhage and controlling gastrointestinal bleeding associated with various benign lesions refractory to conventional antihemorrhagic measures. The aim of this experimental study was to assess the effects of ABS on hemorrhagic lesions and compare them with omeprazole.
Methods: The study was conducted on 30 rats. Rats were divided into five groups: group A (only indomethacin), group B (ABS administration 60 min before indomethacin-induced injury), group C (ABS administration 30 min after indomethacin-induced injury), group D (omeprazole administration 60 min before indomethacin-induced injury), group E (omeprazole administration 30 min after indomethacin-induced injury). Gastric mucosal lesions were produced by indomethacin in all three groups. The effect was studied morphologically 6 h after oral administration of the drug. Subsequently, affected tissue was examined histologically.
Results: Based on the number and the total size of hemorrhagic lesions, the hemorrhagic lesion scores were significantly better in Group C compared to other groups (p < 0.05). The hemorrhagic lesion score of Group B was significantly better than Group D and Group A (p < 0.05). Omeprazole groups (Group D, Group E) did not show significant improvement as indicated by macroscopic scores. There was no significant difference between the groups with respect to microscopic scores.
Conclusion: These results indicate that ABS has a potent inhibitory action on indomethacin-induced gastric bleeding and mucosal lesions and it is useful in the treatment of acute gastric mucosal lesions.
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http://dx.doi.org/10.1007/s00508-015-0762-2 | DOI Listing |
Med J Islam Repub Iran
September 2024
Communicable Diseases Research Center, Alborz University of Medical Sciences, Karaj, Iran.
Background: The role of histamine H3 receptors (H3Rs) in gastric protection and anti-inflammatory function is controversial. In this study, we investigated the gastroprotective effect of a histamine H3 receptor antagonist drug, betahistine, on cytokine-induced neutrophil chemoattractant (CINC) gene expression in a rat model of indomethacin-induced gastric mucosal injury.
Methods: In this experiment, rats were divided into four groups; the control group received no treatment, group 2 was treated with indomethacin at a dose of 25 mg/kg, group 3 pre-treated with famotidine at a dose of 50 mg/kg, and group 4 pre-treated with betahistine (as a reference drug) at a dose of 50 mg/kg.
J Mol Histol
December 2024
Faculty of Pharmacy, Department of Biochemistry, Ataturk University, Erzurum, 25240, Turkey.
A peptic ulcer is a stomach lesion. It is generally caused by malnutrition, the use of anti-inflammatory medications, and an imbalance between mucosal defense systems. In fishes, the lubricous substance that called mucus secreted from the skin, prevents the entry of microorganisms that can enter the body through the skin.
View Article and Find Full Text PDFFront Mol Biosci
November 2024
Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Tianjin, China.
Introduction: AKK-derived outer membrane vesicles (AKK-OMVs) have shown potential in modulating intestinal mucosal immunity by increasing the number of intestinal goblet cells. However, it remains unclear whether AKK-OMVs can directly regulate MUC2 secretion in goblet cells exposed to indomethacin and the underlying mechanisms involved.
Methods: The abnormal mucin secretion model in LS174T cells was established using indomethacin, with treatment including (AKK) supernatant, AKK-OMVs, and extracellular vesicle removal supernatant.
Sci Rep
November 2024
Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Korea.
J Mol Med (Berl)
September 2024
Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-Ku, Fukuoka, 812-8582, Japan.
EP prostanoid receptor (EPR) contributes to the intestinal epithelial Cl secretion, and inhibition of prostaglandin E (PGE) production by non-steroidal anti-inflammatory drugs (NSAIDs) plays a central role in NSAID-induced enteropathy. Although M muscarinic acetylcholine receptor (MR) also contributes to the intestinal epithelial Cl secretion, it remains unclear whether MR is involved in NSAID-induced enteropathy due to a lack of selective agents. The present study explored how MR is involved in the regulation of the intestinal epithelial Cl secretion and its pathophysiological role in NSAID-induced enteropathy.
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