Effects of artemisinin, with or without lumefantrine and amodiaquine on gastric ulcer healing in rat

2018 ◽  
Vol 29 (5) ◽  
pp. 515-524 ◽  
Author(s):  
Kazeem O. Ajeigbe ◽  
Benjamin O. Emikpe ◽  
Samuel Babafemi Olaleye
Keyword(s):  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Neutrophil Infiltration ◽  
Mucosal Injury ◽  
Total Leukocyte Count ◽  
Control Group ◽  
Albino Rats ◽  
Gastric Ulcer Healing ◽  
Neutrophil Lymphocyte Ratio ◽  
Reactive Protein

Abstract Background Antimalarial drugs have been shown to predispose the stomach to ulceration in rats. However, their role in the modulation of gastric ulcer healing is not known. The aim of the present study is to investigate the effect of artemisinin-based combination therapies on ulcer healing. Methods Gastric kissing ulcers were induced in 40 male albino rats (150–180 g) using 0.2 mL 50% acetic acid. One day after the ulcer induction, experimental rats were divided into four groups and treated once daily orally for 3 days as follows: (1) normal saline, (2) artemether-lumefantrine (2/12 mg/kg), (3) artesunate-amodiaquine (4/10 mg/kg), and (4) artesunate (2 mg/kg) only. A fifth group of 10 rats served as overall control with no ulcer induced and no treatment given. Ulcer healing was determined on days 4 and 7 post induction using ulcer score and planimetry. Results Artesunate decreased ulcer severity by 12.5% and 52.0% on days 4 and 7, respectively. Significant increases in severity were observed in rats treated with artemether-lumefantrine (25.0% and 40.0%) and artesunate-amodiaquine (50.0% and 95.0%). Lipid peroxidation was decreased by artesunate by day 7 (27%; p<0.05) but increased in artemether-lumefantrine and artesunate-amodiaquine administered rats (63.6% and 55%; p<0.05). The activity of superoxide dismutase was reduced by artesunate-amodiaquine on day 7 (22%; p<0.05) but no effect in the artemether-lumefantrine treatment. Neutrophil infiltration, total leukocyte count, neutrophil-lymphocyte ratio, and C-reactive protein values were significantly increased in the artemether-lumefantrine and artesunate-amodiaquine treated groups when compared with the untreated ulcer control group (p<0.05). These variables were all reduced by artesunate (p<0.05). Conclusions This study revealed that although artesunate may be beneficial in gastric ulcer healing, its combination with either lumefantrine or amodiaquine may delay healing of gastric mucosal injury.

scholarly journals ANTIOXIDANT AND GASTRIC ULCER HEALING EFFECT OF ORTHOSIPHONSTAMINEUS (BENTH.) LEAVES EXTRACT IN ASPIRIN-INDUCED RATS

2017 ◽  
Vol 10 (2) ◽  
pp. 397 ◽  
Author(s):  
Ari - Yuniarto
Keyword(s):  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Control Group ◽  
Histopathological Analysis ◽  
Antiulcer Activity ◽  
Gastric Ulcer Healing ◽  
Orthosiphon Stamineus ◽  
Mucosal Integrity ◽  
Healing Effect ◽  
Dpph Method

Objective: In the gastrointestinal system, gastric ulcer is one of the common serious problems in human life and gives contribution against morbidity and mortality incidence. The pathophysiology of gastric ulcer is an imbalance between aggressive factor and mucosal integrity factor. Increase of aggressive factors and decrease of mucosal integrity factors have potential against developed of gastric ulcer disease. The objective of the research was to evaluate antioxidant and gastric ulcer healing effect of Orthosiphon stamineus (Benth.) leaves extract in aspirin-induced rats.Methods: In vivo antiulcer activity of Orthosiphon leaves extract was evaluated through several parameters involves gastric acidity, number of ulcers, diameters of ulcers, ulcer index (UI), and healing ratio. Dose level of Orthosiphon leaves extract which used in this study such as 250 and500 mg/kg, respectively. Antioxidant activity of Orthosiphon leaves extract was evaluated by 1,1-diphenyl-2-picrylhydrazyl hydrate (DPPH) method. Histopathological of the stomach was performed using hematoxylin-eosin stained.Results: The results of the study showed that groups which given Orthosiphon leaves extract have significantly different for gastric ulcer healing compared to the control group and were supported by histopathological analysis. The Orthosiphon leaves extract also showed maximum scavengingactivity at a concentration of 100 µg/ml (58.86% inhibition) and minimum at 50 μg/ml (29.60% inhibition) with inhibitory concentration 50% (IC  )50 84.54 µg/ml when compared to ascorbic acid as the standard with IC5.08 µg/ml by DPPH method.Conclusion: It can be concluded that from the experimental study of O. stamineus (Benth.) leaves extract has potential antiulcer activity in aspirin- induced rats model and antioxidant effect using DPPH method. Stomach tissues regeneration in gastric ulcer model might be affected by the improvement of antioxidant status.Keywords: Orthosiphon stamineus (Benth.), Extract, Ulcer, Aspirin, 1,1-diphenyl-2-picrylhydrazyl hydrate.

Annexin-1 modulates repair of gastric mucosal injury

2008 ◽  
Vol 294 (3) ◽  
pp. G764-G769 ◽  
Author(s):  
Gary R. Martin ◽  
Mauro Perretti ◽  
Roderick J. Flower ◽  
John L. Wallace
Keyword(s):  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Mucosal Injury ◽  
Formyl Peptide Receptor ◽  
Gastric Mucosal Damage ◽  
Gastric Ulcers ◽  
Wild Type ◽  
Gastric Ulcer Healing ◽  
Annexin 1 ◽  
Deficient Mice

Annexin-1 is a glucocorticoid-inducible protein that plays an important effector role in the resolution of inflammation and has recently been shown to contribute to the resistance of the stomach to injury. Using an integrated genetic and pharmacological approach, we have tested the hypothesis that annexin-1 contributes to the healing of mucosal injury, given that such injury is accompanied by an inflammatory response, which is often associated with an overexpression of annexin-1 expression. Gastric ulcers were induced in mice through serosal application of acetic acid. Annexin-1 expression during the healing of the ulcers was examined. The effects on gastric ulcer healing of treatment with an annexin-1 mimetic (Ac2-26), an antagonist of the annexin-1 receptor (Boc2), or a glucocorticoid (dexamethasone) were examined. Finally, susceptibility to and healing of indomethacin-induced gastric lesions were compared in wild-type and annexin-1-deficient mice. Expression of annexin-1 was significantly increased in the gastric ulcer margin throughout the healing process. Treatment with an annexin-1 mimetic (Ac2-26) significantly enhanced gastric ulcer healing. In contrast, both dexamethasone and an formyl peptide receptor-like-1 (FPRL-1) antagonist impaired the early phase of ulcer healing. Annexin-1-deficient mice exhibited the same susceptibility as wild-type mice to indomethacin-induced gastric damage, but the healing of that damage was impaired in the former. These data support the hypothesis that annexin-1 contributes significantly to the process of healing of gastric mucosal damage.

Bacterial colonization and healing of gastric ulcers: the effects of epidermal growth factor

2000 ◽  
Vol 278 (1) ◽  
pp. G105-G112 ◽  
Author(s):  
Susan N. Elliott ◽  
J. L. Wallace ◽  
W. McKnight ◽  
D. G. Gall ◽  
J. A. Hardin ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Ulcer Healing ◽  
Bacterial Colonization ◽  
Neutrophil Infiltration ◽  
Gastric Ulcers ◽  
Gastric Ulcer Healing ◽  
Epidermal Growth

.—Experimental gastric ulcers are rapidly colonized by various bacteria, resulting in significantly impaired healing. Epidermal growth factor (EGF) is capable of preventing bacterial colonization of the healthy intestinal mucosa. In this study, we examined the possibility that EGF accelerates gastric ulcer healing by reducing bacterial colonization of the ulcer. Gastric ulcers were induced by serosal application of acetic acid. The effect of daily administration of EGF on ulcer healing and bacterial colonization was assessed and compared with the effect of daily treatment with broad-spectrum antibiotics. EGF administration reduced colonization levels and accelerated ulcer healing as effectively as the antibiotic treatment. EGF was without effect on acid secretion or neutrophil infiltration into the ulcer. Bacterial growth was not inhibited in the presence of EGF in vitro. These results demonstrate that EGF reduces bacterial colonization during an established infection of a compromised mucosal surface. This effect may contribute to the ability of EGF to accelerate gastric ulcer healing. This effect is acid independent and not due to an anti-inflammatory effect or to direct bactericidal actions.

scholarly journals Accelerated gastric ulcer healing in thyroxine-treated rats: roles of gastric acid, mucus, and inflammatory response

2018 ◽  
Vol 96 (6) ◽  
pp. 597-602 ◽  
Author(s):  
Olasupo S. Adeniyi ◽  
Benjamin O. Emikpe ◽  
Samuel B. Olaleye
Keyword(s):  
Gastric Ulcer ◽  
Acid Secretion ◽  
Gastric Acid ◽  
Ulcer Healing ◽  
Gastric Mucus ◽  
Gastric Ulcer Healing ◽  
Neutrophil Lymphocyte Ratio ◽  
Ulcer Area ◽  
Thyroxine Treatment ◽  
Male Wistar Rats

The roles of gastric acid, mucus, and inflammation on the pro-ulcer-healing effect of thyroid hormone were investigated. Male Wistar rats were randomly divided into four groups: control, thyroidectomised, thyroidectomised with thyroxine treatment (100 μg·kg–1·day–1), and sham-operated animals treated with thyroxine. Thirty-five days after thyroidectomy, sham surgery, or thyroxine treatment, an ulcer was experimentally induced. Healing was assessed 3, 7, and 10 days post-ulceration by measurement of the ulcer area, gastric mucus and acid secretion, and neutrophil lymphocyte ratio (NLR) as an index of inflammation. By day 10, the ulcer area had decreased in all groups. Recovery was significantly greater (P < 0.05) in thyroxine-treated rats (78.5% ± 1.6% reduction in ulcer area) than in controls (72.3% ± 1.2% reduction) or thyroidectomised rats (63.3% ± 1.9% reduction). Thyroxine-treated animals also had the highest reduction in NLR (65.0% ± 2.5%). Mucus secretion was significantly lower (P < 0.05) in thyroidectomised rats by days 3 and 7. Furthermore, by day 10, the concentration of basal acid decreased by 77.4% ± 2.6% in thyroxine-treated, 65.0% ± 0.0% in control, and 51.5% ± 3.3% in thyroidectomised rats. We conclude that thyroxine accelerates gastric ulcer healing by altering mucus and acid secretion and reducing NLR.

Gastric ulcer healing is regulated by platelets through endostatin release: Modulation by ticlopidine, aspirin and celecoxib

2001 ◽  
Vol 120 (5) ◽  
pp. A143-A143
Author(s):  
L MA ◽  
S ELLIOTT ◽  
G CIRINO ◽  
A BURET ◽  
J WALLACE
Keyword(s):  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Gastric Ulcer Healing

Gastric ulcer healing is regulated by platelets through endostatin release: Modulation by ticlopidine, aspirin and celecoxib

2001 ◽  
Vol 120 (5) ◽  
pp. A143
Author(s):  
Li Ma ◽  
Susan N. Elliott ◽  
Giuseppe Cirino ◽  
Andre Buret ◽  
John L. Wallace
Keyword(s):  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Gastric Ulcer Healing

Chronic gastric ulcer healing in rats subjected to selective and non-selective cyclooxygenase-2 inhibitors

2002 ◽  
Vol 442 (1-2) ◽  
pp. 125-135 ◽  
Author(s):  
Bettina Berenguer ◽  
Catalina Alarcón de la Lastra ◽  
Francisco Javier Moreno ◽  
Maria José Martı́n
Keyword(s):  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Cyclooxygenase 2 ◽  
Chronic Gastric Ulcer ◽  
Gastric Ulcer Healing ◽  
Cyclooxygenase 2 Inhibitors

Role of nuclear factor-κB in gastric ulcer healing in rats

2001 ◽  
Vol 280 (6) ◽  
pp. G1296-G1304 ◽  
Author(s):  
Satoru Takahashi ◽  
Takuya Fujita ◽  
Akira Yamamoto
Keyword(s):  
Gastric Ulcer ◽  
Mrna Expression ◽  
Ulcer Healing ◽  
Nuclear Factor Κb ◽  
Normal Mucosa ◽  
Cyclooxygenase 2 ◽  
Interleukin 1Β ◽  
Nuclear Factor ◽  
Gastric Ulcer Healing

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.

Sign in / Sign up

Export Citation Format

Share Document