Role of Abrus precatorius Linn. in indomethacin induced gastric ulcer in rats

2014 ◽  
Vol 2 (3) ◽  
pp. 59
Author(s):  
Prasanta Kumar Mitra
1987 ◽  
Vol 2 (4) ◽  
pp. 309-316 ◽  
Author(s):  
WAI-MO HUI ◽  
SHIU-KUM LAM ◽  
PAT-YIM CHAU ◽  
JOANA HO ◽  
WAN-YEE LAU ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-3
Author(s):  
Nitin Vashistha ◽  
Dinesh Singhal ◽  
Gurpreet Makkar ◽  
Suneel Chakravarty ◽  
Vivek Raj

Giant gastric ulcer (GGU) is defined as an ulcer more than 3 cm in diameter. Now infrequent in clinical practice, in the pre-H2 receptor antagonist (H2RA) era, the incidence of GGU varied between 12 and 24% of all gastric ulcers. Proton pump inhibitors reportedly achieve better healing rates and symptom relief in comparison to H2RA. The GGU is associated with high incidence of serious complications such as hemorrhage. A perforated GGU though rare (<2%) offers serious challenges in management. We report one such case wherein the role of multidetector CT scan (MDCT) for diagnosis and treatment planning, surgical options for GGU perforations, and factors affecting outcome are discussed.


2010 ◽  
Vol 31 (S29) ◽  
pp. 24-29 ◽  
Author(s):  
HELEN M. BERSCHNEIDER ◽  
A. T. BLIKSLAGER ◽  
M. C. ROBERTS

2001 ◽  
Vol 280 (6) ◽  
pp. G1296-G1304 ◽  
Author(s):  
Satoru Takahashi ◽  
Takuya Fujita ◽  
Akira Yamamoto

We investigated the role of nuclear factor-κB (NF-κB) in gastric ulcer healing in rats. NF-κB was activated in ulcerated tissue but not in normal mucosa, and the level of the activation was decreased with ulcer healing. NF-κB activation was observed in fibroblasts, monocytes/macrophages, and neutrophils. Treatment of gastric fibroblasts, isolated from the ulcer base, with interleukin-1β activated NF-κB and the subsequently induced cyclooxygenase-2 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) mRNA expression. Inhibition of activated NF-κB action resulted in suppression of both their mRNA expression and increases in PGE2 and CINC-1 levels induced by interleukin-1β. Persistent prevention of NF-κB activation caused an impairment of ulcer healing in rats. Gene expression of interleukin-1β, CINC-1, cyclooxygenase-2, and inducible nitric oxide synthase in ulcerated tissue had been inhibited before the delay in ulcer healing became manifest. The increased levels of cyclooxygenase-2 protein and PGE2 production were also reduced. These results demonstrate that NF-κB, activated in ulcerated tissue, might upregulate the expression of healing-promoting factors responsible for gastric ulcer healing in rats.


2018 ◽  
Author(s):  
Jing‑Jing Wan ◽  
Su‑Juan Fei ◽  
Sheng‑Xiang Lv ◽  
Shu‑Tang Han ◽  
Xing‑Gang Ma ◽  
...  

2020 ◽  
Vol 11 (19) ◽  
pp. 3077-3088
Author(s):  
Rehab E. Abo El Gheit ◽  
Marwa M. Atef ◽  
Omnia S. El Deeb ◽  
Ghada A. Badawi ◽  
Hanan A. Alshenawy ◽  
...  

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