peptic ulceration
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EBioMedicine ◽  
2021 ◽  
Vol 74 ◽  
pp. 103728
Author(s):  
Stephane Bourgeois ◽  
Daniel F. Carr ◽  
Crispin O. Musumba ◽  
Alexander Penrose ◽  
Celestine Esume ◽  
...  

2021 ◽  
Vol 89 ◽  
pp. 104720
Author(s):  
Omolbanin Feili ◽  
Seyedeh Zahra Bakhti ◽  
Saeid Latifi-Navid ◽  
Saber Zahri ◽  
Abbas Yazdanbod

Author(s):  
PRASANT KUMAR SABAT

Objective: To evaluate the curative protects activity of electrohomeopathic drug Cancerous15 (C15) against Indomethacin (IND)-induced gastric ulcer in albino rats. None of the data have been reported on antiulcer activity of C15 drug. Hence, the present study focuses on the scientific investigation of antiulcer activity of C15 against Indomethacin-induced peptic ulceration of rat models. Methods: A total number of 35 albino rats were divided into five groups equally. Pure water was given to Group 1 (normal). IND was given orally to Group 2 (ulcerated control). Cancerous15 third dilution was given to Group 3. IND was given to Group 4 and Group 5 animals, thereafter pretreatment with Esomeprazole (ESM) and C15-third dilution, respectively. The pretreatments were treated in each day’s interval for 21 days before IND administration. There was provision of food and water throughout the experimental period. On the 23rd day, the stomachs of the sacrificed rats were removed, and (1) ulcer index, (2) percentage of ulcer inhibition, (3) gastric volume, (4) pH, (5) pepsin activity, (6) mucin content, (7) malondialdehyde (MDA) concentration, and (8) stearidonic acid activity were studied. Results: The pre-treated animals with ESM and C15 shown as significantly decreases in ulcer index, gastric volume, pepsin activity and MDA concentration, and significant increase in the percentage ulcer inhibition, pH value, mucin content, and superoxide dismutase activity concentration in comparison to ulcer-induced rats. Conclusion: The study shows the significant ulcer protective activity of the C15 drug against IND-induced peptic ulceration in rats.


Author(s):  
Leela Hugar ◽  
Ramesh H.

Background: Most important adverse effect of NSAID is peptic ulceration. Even though H2 blockers and proton pump inhibitors are effective in preventing NSAID associated peptic ulceration, they are not without side effects. Hence there is a need for drugs which are effective in preventing NSAID induced peptic ulcer without producing side effects. Two plant products Aloe vera leaf extract and Aegle marmalos leaves are commonly used in Indian traditional medicine for treatment of peptic ulcers. Hence this study is undertaken to assess the antiulcerogenic potential of combination of these two drugs in comparison with ranitidine in preventing NSAID induced peptic ulcers.Methods: 18 albino rats were divided into 3 groups of 6 rats each. Group A: received ulcerogen only. Group B: pretreated with ranitidine before exposing to ulcerogen. Group C: pretreated with combination of Aloe vera and Aegle marmelos before exposing to ulcerogen. Two doses of indomethacin were administered at an interval of 15 hrs. Animals were sacrificed 6 hrs after the second dose of Indomethacin. Number of ulcers was noted, and ulcer index was calculated.Results: There was significant reduction in total score, mean score and ulcer index in ranitidine pretreated group and test compound group as compared to control group. Even though the total score and ulcer index in test group were lesser as compared to standard control group, it was not statistically significant.Conclusions: Combination of Aloe vera leaf extract and Aegle marmelos leaf extract produced very significant protection against indomethacin induced gastric ulcer.


Author(s):  
Mark Beattie

This chapter covers Helicobacter pylori infection and other causes of peptic ulceration. The section on Helicobacter pylori infection includes section on pathophysiology, investigation, and management.


2017 ◽  
Vol 232 (3) ◽  
pp. F1-F5 ◽  
Author(s):  
George Fink

Hans Selye in a note to Nature in 1936 initiated the field of stress research by showing that rats exposed to nocuous stimuli responded by way of a ‘general adaptation syndrome’ (GAS). One of the main features of the GAS was the ‘formation of acute erosions in the digestive tract, particularly in the stomach, small intestine and appendix’. This provided experimental evidence for the view based on clinical data that gastro-duodenal (peptic) ulcers could be caused by stress. This hypothesis was challenged by Marshall and Warren’s Nobel Prize (2005)-winning discovery of a causal association between Helicobacter pylori and peptic ulcers. However, clinical and experimental studies suggest that stress can cause peptic ulceration in the absence of H. pylori. Predictably, the etiological pendulum of gastric and duodenal ulceration has swung from ‘all stress’ to ‘all bacteria’ followed by a sober realization that both factors play a role, separately as well as together. This raises the question as to whether stress and H. pylori interact, and if so, how? Stress has also been implicated in inflammatory bowel disease (IBD) and related disorders; however, there is no proof yet that stress is the primary etiological trigger for IBD. Central dopamine mechanisms seem to be involved in the stress induction of peptic ulceration, whereas activation of the sympathetic nervous system and central and peripheral corticotrophin-releasing factor appears to mediate stress-induced IBD.


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