scholarly journals Gastroprotective and ulcer healing effects of camel milk and urine in HCl/EtOH, non-steroidal anti-inflammatory drugs (indomethacin), and water-restraint stress-induced ulcer in rats

2017 ◽  
Vol 13 (52) ◽  
pp. 559 ◽  
Author(s):  
PatrickNwabueze Okechukwu ◽  
Zijuan Hu ◽  
Xiaoman Chang ◽  
Qing Pan ◽  
Kebin Gu
2000 ◽  
Vol 32 (7) ◽  
pp. 583-594 ◽  
Author(s):  
T. Brzozowski ◽  
P.Ch. Konturek ◽  
S.J. Konturek ◽  
Z. Sliwowski ◽  
D. Drozdowicz ◽  
...  

10.1038/70995 ◽  
1999 ◽  
Vol 5 (12) ◽  
pp. 1418-1423 ◽  
Author(s):  
Michael K. Jones ◽  
Hongtao Wang ◽  
Brigitta M. Peskar ◽  
Ellis Levin ◽  
Rabiha M. Itani ◽  
...  

1997 ◽  
Vol 25 (4) ◽  
pp. 190-195 ◽  
Author(s):  
Y Matsukawa ◽  
Y Tomita ◽  
S Nishinarita ◽  
T Horie ◽  
K Kato ◽  
...  

Beyond the obvious step of limiting use of non-steroidal anti-inflammatory drugs (NSAIDs), the treatment of ulcers induced by NSAIDs remains controversial. We evaluated the efficacy of the proton-pump inhibitor lansoprazole on NSAID-induced ulcers. Ulcers were endoscopically diagnosed in 47 NSAID users. These patients received 30 mg/day lansoprazole, orally, for 6 or 8 weeks (6 weeks for duodenal ulcers and 8 weeks for other ulcers). Ulcer healing was assessed using an established classification system. The presence of immunoglobulin G antibody against Helicobacter pylori was also evaluated. The antibody was present in the sera of 51% of patients (24/47). Most of the ulcers reached scarring stages S1 (healing) or S2 (good healing), and the S2 healing rate was 35%. Two H. pylori seropositive patients did not reach these stages; their ulcers were improved by H. pylori eradication therapy, followed, in one case, by medication with misoprostol. Lansoprazole seemed to be useful for most patients with NSAID-induced ulcers, but a few needed additional treatments.


2008 ◽  
Vol 88 (4) ◽  
pp. 1547-1565 ◽  
Author(s):  
John L. Wallace

Except in rare cases, the stomach can withstand exposure to highly concentrated hydrochloric acid, refluxed bile salts, alcohol, and foodstuffs with a wide range of temperatures and osmolarity. This is attributed to a number of physiological responses by the mucosal lining to potentially harmful luminal agents, and to an ability to rapidly repair damage when it does occur. Since the discovery in 1971 that prostaglandin synthesis could be blocked by aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), there has been great interest in the contribution of prostaglandins to gastric mucosal defense. Prostaglandins modulate virtually every aspect of mucosal defense, and the importance of this contribution is evident by the increased susceptibility of the stomach to injury following ingestion of an NSAID. With chronic ingestion of these drugs, the development of ulcers in the stomach is a significant clinical concern. Research over the past two decades has helped to identify some of the key events triggered by NSAIDs that contribute to ulcer formation and/or impair ulcer healing. Recent research has also highlighted the fact that the protective functions of prostaglandins in the stomach can be carried out by other mediators, in particular the gaseous mediators nitric oxide and hydrogen sulfide. Better understanding of the mechanisms through which the stomach is able to resist injury in the presence of luminal irritants is helping to drive the development of safer anti-inflammatory drugs, and therapies to accelerate and improve the quality of ulcer healing.


1989 ◽  
Vol 17 (01n02) ◽  
pp. 51-56 ◽  
Author(s):  
M.A. Al-Yahya ◽  
S. Rafatullah ◽  
J.S. Mossa ◽  
A.M. Ageel ◽  
N.S. Parmar ◽  
...  

The cytoprotective and gastric anti-ulcer studies of ginger have been carried out in albino rats. Cytodestruction was produced by 80% ethanol, 0.6M HC1, 0.2M NaOH and 25% NaC1. Whereas gastric ulcers were produced by ulcerogenic agents including indomethacin, aspirin and reserpine, beside hypothermic restraint stress and by pylorus ligated Shay rat technique. The results of this study demonstrate that the extract in the dose of 500 mg/kg orally exert highly significant cytoprotection against 80% ethanol, 0.6M HC1, 0.2M NaOH and 25% NaC1 induced gastric lesions. Th extract also prevented the occurrence of gastric ulcers induced by non-steroidal anti-inflammatory drugs (NSAIDs) and hypothermic restraint stress. These observations suggest cytoprotective and anti-ulcerogenic effect of the ginger.


Sign in / Sign up

Export Citation Format

Share Document