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2.
Mol Biol Rep ; 47(11): 8867-8879, 2020 Nov.
Article in English | MEDLINE | ID: mdl-33135128

ABSTRACT

The aim of the study was to investigate traditionally used Royal Jelly (RJ) for treating an ethanol-induced gastric ulcer model in rats. A total of 32 Wistar albino male rats were divided into 4 groups of 8: group I = Control, group II = Ethanol, group III = RJ + Ethanol, and group IV = Lansoprazole + Ethanol. In groups II, III, and IV, animals were administered 1 ml of absolute ethanol orally after a 24-h fast to induce ulcer formation. The histopathological changes in the gastric mucosa were determined using hematoxylin-eosin (H&E) staining. Immunohistochemically, inducible nitric oxide (iNOS) and nuclear factor kappa beta (Nf-κß) markings were evaluated in gastric tissue. Cell death in the gastric mucosa was determined by the TUNEL method. Oxidative status markers, superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT), and myeloperoxidase (MPO) levels were determined spectrophotometrically. Expression of the interleukin - 1 beta (IL-1ß) and tumor necrosis factor-α (TNF-α) genes in gastric tissues was determined by real-time PCR; and TNF-α, IL-10, and IL-1ß levels were determined. RJ was found to inhibit iNOS and Nf-κß activity in the gastric mucosa and prevent epithelial cell apoptosis. In particular, pro-inflammatory cytokines TNF-α and IL-1ß levels were significantly decreased in the RJ + Ethanol group compared to the Ethanol group. In addition, a decrease in the MPO level indicated that RJ prevented tissue damage, especially by preventing inflammatory cell infiltration. The study demonstrated a possible gastroprotective effect of RJ in a rat ethanol-induced gastric ulcer model.


Subject(s)
Disease Models, Animal , Ethanol/toxicity , Fatty Acids/pharmacology , Gastric Mucosa/drug effects , Stomach Ulcer/prevention & control , Animals , Apoptosis/drug effects , Catalase/metabolism , Central Nervous System Depressants/toxicity , Cytokines/genetics , Cytokines/metabolism , Gastric Mucosa/injuries , Gastric Mucosa/metabolism , Gene Expression/drug effects , Male , Malondialdehyde/metabolism , NF-kappa B/metabolism , Oxidative Stress/drug effects , Rats, Wistar , Stomach Ulcer/chemically induced , Stomach Ulcer/metabolism , Superoxide Dismutase/metabolism
3.
Biotech Histochem ; 95(4): 297-304, 2020 May.
Article in English | MEDLINE | ID: mdl-31850807

ABSTRACT

We investigated the protective effect of hesperetin on hepatic damage after blunt chest trauma in rats using histological and biochemical methods. We used 18 adult male rats in three groups of six: control, chest trauma and chest trauma + hesperetin. Chest trauma was caused by dropping a metal cylinder onto the right hemithorax. Hesperetin, 100 mg/kg, was administered orally for 7 days. At the end of the seventh day, liver tissue samples were obtained. Serum tumor necrosis factor-alpha (TNF-α), interleukin 1-beta (IL-1ß), alanine aminotransferase (AST), aspartate transferase (ALT) and lactate dehydrogenase (LDH) enzyme activities were measured in blood samples taken from the heart. The general structure of liver tissue was investigated using hematoxylin and eosin staining. Nuclear factor kappa beta (Nf-κß) expression in liver tissue was determined by the indirect immunohistochemical method. Apoptosis was determined using the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) method. Decreased TNF-α, AST and ALT enzyme activity, fewer histopathological changes and lower Nf-kB expression were observed in the hesperetin treated group compared to the chest trauma group. We also found reduced hepatic apoptosis in the chest trauma + hesperetin group compared to the chest trauma group. Hesperetine inhibits liver damage by reducing proinflammatory cytokines and by suppressing Nf-κß activity in a blunt chest trauma model in rats.


Subject(s)
Hesperidin/therapeutic use , Inflammation/drug therapy , Liver Diseases/drug therapy , Liver/injuries , Wounds and Injuries/pathology , Animals , Apoptosis , Liver/pathology , Liver Diseases/etiology , Liver Diseases/pathology , Rats
4.
Turk Gogus Kalp Damar Cerrahisi Derg ; 28(2): 359-368, 2019 Jun.
Article in English | MEDLINE | ID: mdl-32551168

ABSTRACT

BACKGROUND: In this experimental study, we aimed to investigate the effects of hesperetin, a natural flavonoid, on a lipopolysaccharideinduced acute lung injury model in rats. METHODS: Between March 2019 and May 2019, a total of 18 adult male Wistar albino rats, weighing approximately 250 to 300 g, were randomly divided into three groups as control, lipopolysaccharide, and lipopolysaccharide + hesperetin groups (n=6 in each group). The wet/dry weight ratio of lung tissue was determined. Histopathological changes were examined using light and scanning electron microscopy. Pulmonary nuclear factor-kappa beta, inducible nitric oxide synthase, and alpha-smooth muscle antigen activity were determined with indirect immunohistochemical methods. Pulmonary apoptosis was detected with the terminal deoxynucleotidyl transferase dUTP nick-end labeling method. Tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, and interleukin-10 concentrations were measured with enzyme-linked immunosorbent assay. RESULTS: Treatment with hesperetin significantly improved the architecture of lung tissue and reduced the wet/dry weight ratio, nuclear factor-kappa beta, inducible nitric oxide synthase, and alphasmooth muscle antigen expression, pulmonary apoptosis, and levels of proinflammatory cytokines. CONCLUSION: Our study results suggest that hesperetin has a potent protective effect against lipopolysaccharide-induced acute lung injury in rats via suppression of the proinflammatory cytokine cascade, nuclear factor-kappa beta, signaling pathway activation, and apoptosis.

5.
Obes Surg ; 15(8): 1137-43, 2005 Sep.
Article in English | MEDLINE | ID: mdl-16197786

ABSTRACT

BACKGROUND: We investigated the effects of Botox-A on weight loss and gastric emptying in an experimental obese rat model. Although there is evidence of weight loss in normal-weight rats after Botox-A injection, there are no studies indicating the effect of Botox-A injection on weight loss and gastric emptying time in obese rats. METHODS: 37 female Wistar Albino rats were given high calorie diet for 90 days. They were separated into 3 groups. The first group (Botox group) consisted of 15 obese rats whose gastric antrum was injected with 20 U of Botulinum Toxin Type A. The second group (Saline group) consisted of 15 obese rats whose gastric antrum was injected with 20 U of saline. The third group (Control group) had no surgical intervention. Gastric scintigraphy was performed in the 3 groups pre- and postoperatively. RESULTS: The saline group had a weight reduction in the early postoperative days but began to gain weight thereafter. The mean weight of the Botox group between the 16th and 28th days postoperatively was significantly lower than the mean weights of the control and the saline groups (P<0.05, P<0.001). The results of gastric emptying scintigraphy in all 3 groups at day 20 revealed significantly higher T1/2 values in the Botox-A group when compared to the results of the control and saline groups (P<0.001). CONCLUSION: Botox-A application to the gastric antrum in obese rats leads to weight loss by increasing the gastric emptying time.


Subject(s)
Botulinum Toxins, Type A/pharmacology , Gastric Emptying/drug effects , Neuromuscular Agents/pharmacology , Pyloric Antrum/drug effects , Weight Loss/drug effects , Animals , Botulinum Toxins, Type A/administration & dosage , Female , Injections , Models, Animal , Neuromuscular Agents/administration & dosage , Obesity/drug therapy , Rats
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