10 research outputs found
Effects of artemisinin, with or without lumefantrine and amodiaquine on gastric ulcer healing in rat
No full textAbstract
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.
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Potassium bromate (KBrO3) Modulates Oxidative stress and inflammatory biomarkers in NaOH induced crohn’s colitis in Wistar rats
No full textPotassium bromate (KBrO3) present in consumed ozonised water was recently documented to exacerbate experimental gastric ulcer. Report is however vague as regards its effects in the colon; where water reabsorption occurs. In this study, we observed the possible effects of KBrO3 on oxidative stress and inflammatory biomarkers in NaOH induced crohn’s colitis. Wistar rats (180-200g) were divided into 6 groups (n=10); 1-control, 2-untreated crohn’s colitis (induced by 1.4% NaOH; intra-rectal administration) and 3-6: crohn’s colitis treated with vitamin E, KBrO3, vitamin E+KBrO3 and sulphazalazine respectively for seven days. Body weight and stool score were monitored daily. By 3 and 7, excised colon was evaluated for ulcer scores, biochemical and histological analysis. Collected blood samples on days 3 and 7 were assayed for haematological indices using standard methods. Data were subjected to ANOVA and p ≤0.05 considered significant. Platelet/lymphocyte ratio, colonic ulcer score, , malondialdehyde and mast cells were significantly decreased while colonic sulfhydryl, Ca2+ and Na+/K+ ATPase activities were increased following KBrO3 treatment compared with crohn’s colitis untreated. Findings suggest that KBrO3 may mitigate against NaOH induced crohn’s colitis via inhibiting mast cell population, oxidative and inflammatory content but stimulating colonic sulfhydryl, Ca2+ and Na+/K+ ATPase activities.The presentation of the authors' names and (or) special characters in the title of the pdf file of the accepted manuscript may differ slightly from what is displayed on the item page. The information in the pdf file of the accepted manuscript reflects the original submission by the author
KOLAVIRON ATTENUATES ISCHEMIA-REPERFUSION INJURY IN THE STOMACH OF RATS.
Get PDFKolaviron (KV), an active complex of at least three compounds in Garcinia kola seed known for its antioxidant and anti-inflammatory activity was investigated for its gastro-protective effect in the stomach of rats subjected to ischemia-reperfusion-induced gastric ulceration. Male adult Wistar rats (180 – 210 g) were used, randomized into six groups (n = 15) as follows; 1: control, 2: ulcerated untreated (UU), 3: KV alone (KVA), 4: KV + ulcer (KVU), 5: Ulcer + KV (UKV) and 6: Ulcer + omeprazole (20 mg/kg) (UOme). Ulcer was induced through ischemia-reperfusion method after two weeks of daily oral KV (100 mg/kg). Rats were weighed daily, gastric acid secretion, ulcer scores, hematological, biochemical and histological variables were assessed 1 h after induction, 3 and 7 days post ulceration. Body weight decreased in KVA (179.1 ± 1.6 g), and KVU (170.1 ± 2.2 g) compared with UU (199.0±1.4 g). Gastric acid secretion decreased significantly in KVU after 1 h and 3 day post ulceration (0.27 ± 0.03 mEq/L; 0.49 ± 0.02 mEq/L) compared with UU (0.60 ± 0.06 mEq/L; 0.85 ± 0.29 mEq/L), respectively. There was significant reduction in neutrophil/lymphocyte ratio of KVA (0.29 ± 0.06) and KVU (0.35 ± 0.02) compared with UU (0.54 ±0.04). Malondialdehyde level decreased significantly with concomitant increase in anti-oxidative activities and nitric oxide level in the KV treated groups (KVA, KVU, UKV) compared with UU. In conclusion, treatment with KV protects the stomach by reducing gastric acid secretion, promoting antioxidant activity and suppressing action of reactive oxygen speciesThe accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author
Trivalent Chromium Promotes Healing of Experimental Colitis in Mice by Suppression of Inflammation and Oxidative Stress
No full textCrohn’s Colitis–Induced Alterations in Colonic Morphology, Immunology, and Microbiota Are Modulated by Potassium Bromate in Experimental Rats
No full textThyroid hormones increase stomach goblet cell numbers and mucin expression during indomethacin induced ulcer healing in Wistar rats
No full textEffects of quinine on gastric ulcer healing in Wistar rats
No full textAbstractBackgroundQuinine (QT) is an important anti-malarial drug; however, there is little information about its effects on the gut. Therefore, this study aimed to investigate the effects of a therapeutic dose of QT on the healing of gastric ulcer in rats.MethodsMale Wistar rats weighing 150–200 g were divided into three groups: control rats without ulcer (group 1), ulcerated rats treated with 1 mL/kg (p.o.) normal saline (NS) (group 2), and ulcerated rats treated with 10 mg/kg (p.o.) QT (group 3). Ulcers were induced by serosal application of 80 % acetic acid to the stomach of rats anaesthetized with 50 mg/kg thiopentone sodium and treatment was given three times daily. Healing was assessed on days 3, 7 and 10 after ulcer induction by macroscopic measurement of: ulcer area, histology, lipid peroxidation, superoxide dismutase activity and gastric mucus secretion.ResultsAt day 3, there was no significant difference (p>0.05) in ulcer areas between NS- and QT-treated rats. By day 10, however, the percentage area healed in NS treated (59.6±2.35 %) was significantly higher (p<0.05) than in QT rats (49.0±2.20 %) and clearing of inflammatory cells and re-epithelization was greater in NS-treated group. By days 7 and 10, lipid peroxidation was significantly higher in QT animals, when compared with NS-treated rats and controls (p<0.05). Superoxide dismutase activity and mucus secretion were significantly (p<0.05) higher in NS-treated than QT-treated rats.ConclusionsQT delayed ulcer healing by prolonging the inflammatory phase of healing, increasing oxidative stress, reducing antioxidant activity and gastric mucus secretion</jats:sec
Seeds of <i>Buchholzia coriacea</i> in Diet Mitigate Ischemic Reperfusion–Induced Gastric Ulceration in Experimental Rats
No full textThyroid hormones increase stomach goblet cell numbers and mucin expression during indomethacin induced ulcer healing in Wistar rats
No full textAbstract Background Gastric ulcers are mucosal discontinuities that may extend into the mucosa, submucosa or even deeper. They result from an imbalance between mucosal aggressors and protective mechanisms that include the mucus bicarbonate layer. Thyroid hormones have been shown to accelerate gastric ulcer healing in part by increasing the adherent mucus levels. However, the effects of thyroid hormones on goblet cell numbers and expression of neutral and acidic mucins during ulcer healing have not been investigated. Methods Thirty six adult male Wistar rats were randomly divided into six groups each with six animals. Group 1 (normal control) and group 2 (negative control) were given normal saline for eight weeks. Groups 3 and 4 were given 100 μg/kg per day per os of thyroxine so as to induce hyperthyroidism. Groups 5 and 6 received 0.01% (w/v) Propylthiouracil (PTU) for 8 weeks so as to induce hypothyroidism. After thyroid hormonal levels were confirmed using radioimmunoassay and immunoradiometric assays, ulcer induction was done using 40 mg/kg intragastric single dose of Indomethacin in groups 2, 3 and 5. Stomachs were extracted after day 3 and 7 of ulcer induction for histological examination. Histochemistry was carried out using Periodic Acid Shiff and Alcian Blue. The number of acidic and neutral goblet cells were determined by counting numbers per field. Mucin expression (%) was determined using Quick Photo Industrial software version 3.1. Results The numbers of neutral goblet cells (cells/field) increased significantly (P < 0.05) in the ulcer+thyroxine (14.67 ± 0.33), thyroxine (17.04 ± 1.71) and ulcer+PTU (12.89 ± 1.06) groups compared to the normal control (10.78 ± 1.07) at day 3. For the acidic goblet cells, differences between treatment groups were more pronounced at day 7 between the ulcer+thyroxine (22.56 ± 1.26) and thyroxine (22.89 ± 0.80). We further showed that percentage expression of both neutral and acidic mucins was significantly higher in the ulcer+thyroxine (9.23 ± 0.17 and 6.57 ± 0.35 respectively) and thyroxine groups (9.66 ± 0.21 and 6.33 ± 0.38 respectively) as compared to the normal control group (4.08 ± 0.20 and 4.38 ± 0.11 respectively) at day 3 after ulcer induction. Conclusion This study confirms the role played by thyroid hormones in healing of indomethacin induced gastric ulcers. The study further demonstrates increased numbers of both neutral and acidic goblet cells and the increase in expression of both neutral and acidic mucins during healing of indomethacin induced ulcers
