glycogen and Stomach-Ulcer

The non-steroidal anti-inflammatory drug (NSAID), diclofenac causes hepato-renal toxicity and gastric ulcer. The aim of this study was to investigate the protective effect of Spirulina fusiformis on Diclofenac-induced toxicity in Wistar albino rats.. Rats were treated as follows: normal control (group I); diclofenac (50mg/kgb.w., i.p.) treated rats (group II); diclofenac-induced (50mg/kgb.w., i.p.) rats treated with Spirulina fusiformis (400mg/kgb.w., p.o.) (group III); diclofenac-induced (50mg/kgb.w., i.p.) rats treated with silymarin (25mg/kgb.w., p.o.) (group IV); Spirulina fusiformis (400mg/kgb.w., p.o.) alone treated rats (groupV). Biochemical (liver and kidney functional markers) and antioxidant parameters (enzymic and non-enzymic antioxidants) were measured in the blood and tissue homogenates of the rats. Evaluation of intestinal ulcer score and assessment of liver and kidney histology were also done.. Alterations in the levels of biochemical and antioxidant assays and histopathological changes in liver and kidney proved the toxic effect of diclofenac. The ulcer score was significantly increased in the diclofenac treated rats. Spirulina fusiformis showed to reduce such changes and was able to restore normal antioxidant status in the rats.. Our study proves the hepato-renal and gastroprotective activity of Spirulina fusiformis in diclofenac-treated rats.

Topics: Animals; Antioxidants; Biomarkers; Blood Proteins; Diclofenac; Female; Glycogen; Intestinal Mucosa; Kidney; Lipids; Liver; Protective Agents; Rats, Wistar; Spirulina; Stomach Ulcer

Chronic stress produces some morphological changes in rats, including thymus weight reduction, adrenal hypertrophy, and peptic ulcers in stomach. Repeated administration of phytoadaptogenic drugs (ginseng and bilobil) decreased these stress-induced disorders. The antistressor activity of drugs was attenuated upon by removal of the pineal gland. Histochemical and morphometric investigation of pineal tissues in stressed animals showed that that the pharmacological effect was accompanied by increasing functional activity of the pineal gland. It is suggested that pineal mobilization may participate in antistressor activity of phytoadaptogenic drugs.

Topics: Adrenal Glands; Animals; Anti-Anxiety Agents; Electroshock; Ginkgo biloba; Glycogen; Immobilization; Male; Melatonin; Organ Size; Panax; Phytotherapy; Pineal Gland; Plant Extracts; Rats; RNA; Stomach Ulcer; Stress, Physiological; Thymus Gland

The purpose of this study was to investigate the potential acute and 28-day repeated oral toxicities of besifloxacin (BAF) in Wistar albino rats. In oral acute and repeated dose study, BAF was administered to both sex of rats, at dose levels of 0, 300, 600, 900 mg/kg/day and 0, 100, 200, 500 mg/kg/day, respectively. In the acute study, total white blood cell (WBC) (male, 43.74%; female, 42.60%) and total bilirubin (T-BIL) (male, 80%; female, 60%) were significantly increase, total protein (TP) (male, 23.24%; 27.80%) was significantly decreased, and significant incidence of pericholangitis (male, 83.33%; female, 75%) was shown in males and females of high-dose groups. In repeated oral dose toxicity study, similar type effects were also observed after serum hematological and serum biochemical analysis, whereas additionally sever hepatic injury and focal ulceration in gastric mucosa also observed in high dose groups of both sexes after histopathological analysis. However these toxic effects of besifloxacin were transient and reversible and no-observed adverse effect level (NOAEL) were 300 mg/kg/day for acute and 100 mg/kg/day for repeated dose toxicity study, respectively.

Topics: Achilles Tendon; Animals; Anti-Bacterial Agents; Azepines; Bilirubin; Blood Platelets; Chemical and Drug Induced Liver Injury; Disease Models, Animal; Female; Fluoroquinolones; Glycogen; Joints; Leukocyte Count; Liver; Male; Photosensitivity Disorders; Rats; Rats, Wistar; Stomach Ulcer; Thrombocytosis; Toxicity Tests, Acute; Toxicity Tests, Subacute

In this study, the effects of fucoidan on aspirin-induced ulcers in rats were evaluated: both biochemical and immunological parameters were taken into consideration. The status of stomach tissue glycogen storage and histological changes were also examined. Examination of basic biochemical parameters showed significant (p<0.01) alterations in aspartate (AST) and alanine (ALT) transaminases in ulcer-induced rats. Also, moderate alterations (p<0.05) were observed in the levels of cholesterol and blood urea nitrogen (BUN). Histopathological examination showed neutrophil infiltration and inflammation in oxyntic cells with altered glycogen storage. Analysis of serum cytokines of aspirin-induced rats showed a moderate decrease in interleukin-10 (IL-10) with considerable increase of interleukin-6 (IL-6) and interferon-gamma (INF-gamma) when compared with control. Administration of fucoidan showed considerable (p<0.05) protection against ulceration by inhibiting the acute alterations of AST, ALT, cytokines and stomach glycogen. However, aggravated serum INF-gamma was observed in the fucoidan-pretreated group. These findings suggest that the anti-ulcer property of fucoidan might contribute in protecting the inflammatory cytokine-mediated oxidative damage to gastric mucosa.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Aspirin; Blood Urea Nitrogen; Gastric Mucosa; Glycogen; Interferon-gamma; Interleukin-10; Interleukin-6; Liver Function Tests; Male; Neutrophil Infiltration; Polysaccharides; Rats; Rats, Wistar; Stomach Ulcer

We focused on over-dose insulin (250 IU/kg i.p.) induced gastric ulcers and then on other disturbances that were concomitantly induced in rats, seizures (eventually fatal), severely damaged neurons in cerebral cortex and hippocampus, hepatomegaly, fatty liver, increased AST, ALT and amylase serum values, breakdown of liver glycogen with profound hypoglycemia and calcification development. Calcium deposits were present in the blood vessel walls, hepatocytes surrounding blood vessels and sometimes even in parenchyma of the liver mainly as linear and only occasionally as granular accumulation. As an antidote after insulin, we applied the stable gastric pentadecapeptide BPC 157 (10 microg/kg) given (i) intraperitoneally or (ii) intragastrically immediately after insulin. Controls received simultaneously an equivolume of saline (5 ml/kg). Those rats that survived till the 180 minutes after over-dose application were further assessed. Interestingly, pentadecapeptide BPC 157, as an antiulcer peptide, may besides stomach ulcer consistently counteract all insulin disturbances and fatal outcome. BPC 157 rats showed no fatal outcome, they were mostly without hypoglycemic seizures with apparently higher blood glucose levels (glycogen was still present in hepatocytes), less liver pathology (i.e., normal liver weight, less fatty liver), decreased ALT, AST and amylase serum values, markedly less damaged neurons in brain and they only occasionally had small gastric lesions. BPC 157 rats exhibited mostly only dot-like calcium presentation. In conclusion, the success of BPC 157 therapy may indicate a likely role of BPC 157 in insulin controlling and BPC 157 may influence one or more causative process(es) after excessive insulin application.

Topics: Animals; Anti-Ulcer Agents; Antidotes; Brain; Calcinosis; Drug Overdose; Endothelium, Vascular; Glycogen; Hepatomegaly; Hypoglycemia; Hypoglycemic Agents; Insulin; Liver; Male; Neurons; Peptide Fragments; Proteins; Rats; Rats, Wistar; Seizures; Stomach Ulcer

The healing activity of malabaricone B and malabaricone C, the major antioxidant constituents of the spice Myristica malabarica against the indomethacin-induced gastric ulceration in mice has been studied. The histological indices revealed maximum ulceration on the 3rd day after indomethacin administration, which was effectively healed by malabaricone B, malabaricone C (each 10 mg/kg body weight/day) and omeprazole (3 mg/kg body weight/day) for 3 days. Compared to the untreated ulcerated mice, treatment with malabaricone B, malabaricone C and omeprazole reduced the ulcer indices by 60.3% (P<0.01), 88.4% and 86.1% respectively (P<0.001). All the test samples accelerated ulcer healing than observed in natural recovery even after 7 days. Stomach ulceration reduced the total antioxidant status of plasma by 41% (P<0.05), which was significantly increased by malabaricone B (36%, P<0.01), malabaricone C (61%, P<0.001) and omeprazole (53%, P<0.001). Compared to the ulcerated untreated mice, those treated with malabaricone B reduced the levels of thiobarbituric acid reactive substances and protein carbonyls by 17% and approximately 34% respectively (P<0.05), while malabaricone C and omeprazole reduced the parameters almost equally (approximately 30%, P<0.01, and approximately 40%, P<0.01 respectively). Likewise, all the test samples reduced the oxidation of protein and non-protein thiols significantly (P<0.05). The antioxidant activity of the test samples could partly account their healing capacities. However, the differential potency of them was explainable by considering their relative abilities to modulate mucin secretion, PGE(2) synthesis and expression of EGF receptor and COX isoforms, malabaricone C being most effective in controlling all these factors.

Topics: Animals; Anti-Ulcer Agents; Antioxidants; Cyclooxygenase 1; Cyclooxygenase 2; Dinoprostone; Disease Models, Animal; Dose-Response Relationship, Drug; ErbB Receptors; Fruit; Gastric Mucins; Gastric Mucosa; Glycogen; Indomethacin; Lipid Peroxidation; Male; Membrane Proteins; Mice; Myristicaceae; Omeprazole; Oxidative Stress; Periodic Acid-Schiff Reaction; Plant Extracts; Protein Carbonylation; Resorcinols; Stomach; Stomach Ulcer; Time Factors; Wound Healing

Topics: Adrenal Glands; Animals; Corticosterone; Epinephrine; Glycogen; Liver Glycogen; Male; Myocardium; Organosilicon Compounds; Rats; Silicon; Stomach Ulcer; Stress, Psychological

The significance of mucous change in the human duodenum in a series of patients with peptic ulcer disease has been appraised. No specific correlation was demonstrated with the acid output of the stomach if the extent of the change is considered, but it was shown to be more common in the higher acid states. Electron microscopic studies confirmed the specific structure of the mucous cells of the duodenum and suggest that they arise either by transformation of Brunner's gland cells or as a distinctive population in the crypts. It is suggested that the mucous change is a protective mechanism involved in some way as yet unknown with the healing of ulcers.

Topics: Biopsy; Cell Membrane; Cell Nucleus; Cytoplasm; Cytoplasmic Granules; Desmosomes; Duodenum; Endoplasmic Reticulum; Epithelial Cells; Epithelium; Extracellular Space; Gastric Juice; Glycogen; Golgi Apparatus; Humans; Intestinal Mucosa; Microscopy, Electron; Mitochondria; Peptic Ulcer; Pyloric Stenosis; Ribosomes; Stomach Neoplasms; Stomach Ulcer

Topics: Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Anaerobiosis; Animals; Energy Metabolism; Gastric Mucosa; Glucosephosphates; Glycogen; Glycolysis; Ischemia; Lactates; Liver; Male; Muscles; Necrosis; Pyruvates; Rats; Shock, Hemorrhagic; Stomach Ulcer; Stress, Physiological

Topics: Biopsy; Cell Division; Cholelithiasis; Chromosomes; Glycogen; Humans; Liver; Stomach Ulcer