OBJECTIVETo investigate the effect of Rhizoma Atractylodis extract (ERA) in protecting gastric mucosa and modulating gastrointestinal immune function of a rat model of spleen deficiency syndrome and elucidate the mechanism by which ERA improves spleen deficiency syndrome.

METHODSMale rats were fed with Xiaochengqi decoction and subjected to irregular feeding to induce spleen deficiency syndrome. The established models were randomized into model group, high-, moderate- and low-dose ERA groups, and domperidone group. After corresponding treatment for 30 days, the content of IgA in the intestinal lavage fluid, serum IgG, and the indices of the spleen and thymus were determined. The pathological changes in the gastric mucosa was observed with HE staining, gastric mucosal blood flow was evaluated with laser Doppler rheometry, and the expression of TFF1 in the gastric mucosa and TLR4 expression in the colon tissue were detected with immunohistochemistry.

RESULTSThe rat models of spleen deficiency syndrome showed obvious abnormalities in gastric mucosal morphology, blood flow and immunological indexes. Compared with the model rats, the rats receiving ERA treatment as different doses all showed significant improvements in gastric mucosal morphology, blood flow volume, gastric mucosa trefoil factor 1 (TFF1) expression, intestinal lavage fluid IgA content, serum IgG content, indices of the spleen and thymus, and TLR4 expression in the colon TLR4 (P<0.05 or P<0.01).

CONCLUSIONERA can inhibit gastric mucosal damage, protect and repair the damaged mucosal tissues, and improve the immune function of in rats with spleen deficiency.

Animals ; Atractylodes ; chemistry ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; Gastric Mucosa ; drug effects ; pathology ; Immunoglobulin A ; metabolism ; Immunoglobulin G ; blood ; Immunohistochemistry ; Male ; Peptides ; metabolism ; Rats ; Rhizome ; chemistry ; Spleen ; physiopathology ; Trefoil Factor-2

BACKGROUND/AIMS: The aims of this study were to investigate whether a broccoli sprout extract containing sulforaphane (BSES) inhibited the Helicobacter pylori infection density and exerted an antioxidative effect on gastric mucosal damage. METHODS: The enrolled subjects were randomized in a double-blinded manner into three groups. Finally, 33 H. pylori (+) BSES treatment subjects (group A), 28 H. pylori (+) placebo subjects (group B), and 28 H. pylori (-) BSES treatment subjects (group C) were studied. H. pylori infection density was indirectly quantified by a 13C-urea breath test (UBT), and the ammonia concentration in gastric juice aspirates was measured through gastroscopic examination. Malondialdehyde (MDA), an oxidative damage biomarker, and reduced glutathione (GSH), an antioxidant biomarker, were measured in the gastric mucosa by an enzyme-linked immunosorbent assay. RESULTS: BSES treatment did not significantly affect the UBT values or ammonia concentration in group A (p=0.634 and p=0.505, respectively). BSES treatment did significantly reduce mucosal MDA concentrations in group A (p<0.05) and group C (p<0.001), whereas the gastric mucosal GSH concentrations did not differ before and after treatment in any of the groups. CONCLUSIONS: BSES did not inhibit the H. pylori infection density. However, BSES prevented lipid peroxidation in the gastric mucosa and may play a cytoprotective role in H. pylori-induced gastritis.
Adult ; Ammonia/metabolism ; Antioxidants/*pharmacology ; Biomarkers/analysis ; Brassica/*chemistry ; Breath Tests ; Double-Blind Method ; Enzyme-Linked Immunosorbent Assay ; Female ; Gastric Juice/enzymology ; Gastric Mucosa/*drug effects/metabolism ; Glutathione/analysis ; Helicobacter Infections/*drug therapy ; *Helicobacter pylori ; Humans ; Isothiocyanates/*pharmacology ; Lipid Peroxidation/*drug effects ; Male ; Malondialdehyde/analysis ; Middle Aged ; Plant Extracts/chemistry/*pharmacology ; Urea

Non-steroidal anti-inflammatory drugs (NSAIDs) induce tissue damage and oxidative stress in animal models of stomach damage. In the present study, the protective effects of wheat peptides were evaluated in a NSAID-induced stomach damage model in rats. Different doses of wheat peptides or distilled water were administered daily by gavage for 30 days before the rat stomach damage model was established by administration of NSAIDs (aspirin and indomethacin) into the digestive tract twice. The treatment of wheat peptides decreased the NSAID-induced gastric epithelial cell degeneration and oxidative stress and NO levels in the rats. Wheat peptides significantly increased the superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and decreased iNOS activity in stomach. The mRNA expression level of μ-opioid receptor was significantly decreased in wheat peptides-treated rats than that in in the control rats. The results suggest that NSAID drugs induced stomach damage in rats, wchih can be prevented by wheat peptides. The mechanisms for the protective effects were most likely through reducing NSAID-induced oxidative stress.
Animals ; Anti-Inflammatory Agents, Non-Steroidal ; adverse effects ; Antioxidants ; pharmacology ; Aspirin ; adverse effects ; Gastric Mucosa ; drug effects ; Gene Expression ; Glutathione Peroxidase ; drug effects ; Indomethacin ; adverse effects ; Male ; Nitric Oxide ; biosynthesis ; Nitric Oxide Synthase ; chemical synthesis ; Oxidation-Reduction ; Oxidative Stress ; drug effects ; Plant Proteins ; pharmacology ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid, mu ; drug effects ; Stomach ; drug effects ; Superoxide Dismutase ; drug effects ; Triticum ; chemistry

BACKGROUND/AIMS: The major compounds of Cochinchina momordica seed extract (SK-MS10) include momordica saponins. We report that the gastroprotective effect of SK-MS10 in an ethanol-induced gastric damage rat model is mediated by suppressing proinflammatory cytokines and downregulating cytosolic phospholipase A2 (cPLA2), 5-lipoxygenase (5-LOX), and the activation of calcitonin gene-related peptide. In this study, we evaluated the gastroprotective effects of SK-MS10 in the nonsteroidal anti-inflammatory drug (NSAID)-induced gastric damage rat model. METHODS: The pretreatment effect of SK-MS10 was evaluated in the NSAID-induced gastric damage rat model using aspirin, indomethacin, and diclofenac in 7-week-old rats. Gastric damage was evaluated based on the gross ulcer index by gastroenterologists, and the damage area (%) was measured using the MetaMorph 7.0 video image analysis system. Myeloperoxidase (MPO) was measured by enzyme-linked immunosorbent assay, and Western blotting was used to analyze the levels of cyclooxygenase (COX)-1, COX-2, cPLA2, and 5-LOX. RESULTS: All NSAIDs induced gastric damage based on the gross ulcer index and damage area (p<0.05). Gastric damage was significantly attenuated by SK-MS10 pretreatment compared with NSAID treatment alone (p<0.05). The SK-MS10 pretreatment group exhibited lower MPO levels than the diclofenac group. The expression of cPLA2 and 5-LOX was decreased by SK-MS10 pretreatment in each of the three NSAID treatment groups. CONCLUSIONS: SK-MS10 exhibited a gastroprotective effect against NSAID-induced acute gastric damage in rats. However, its protective mechanism may be different across the three types of NSAID-induced gastric damage models in rats.
Animals ; Anti-Inflammatory Agents, Non-Steroidal/adverse effects ; Arachidonate 5-Lipoxygenase/drug effects ; Calcitonin Gene-Related Peptide/drug effects ; Cyclooxygenase 1/drug effects ; Cyclooxygenase 2/drug effects ; Disease Models, Animal ; Gastric Mucosa/chemistry/drug effects ; Group IV Phospholipases A2/drug effects ; Male ; Momordica/*chemistry ; Peroxidase/drug effects ; Plant Extracts/*pharmacology ; Rats ; Rats, Sprague-Dawley ; Seeds/*chemistry ; Stomach Ulcer/chemically induced/*prevention & control ; Treatment Outcome

OBJECTIVETo study the changes of mucosa irritation of crude and processed Radix Phytolaccae.

METHODGastrointestinal experiments on rats and mice and the rabbits' eyes irritation experiments were applied to investigate the changes of mucosa irritation of crude and processed Radix Phytolaccae.

RESULTThe mucosa irritation of processed Radix Phytolaccae decreased obviously compared to crude one.

CONCLUSIONAfter being processed with vinegar, the mucosa irritation on Radix Phytolaccae decreased obviously.

Acetic Acid ; chemistry ; Animals ; Dinoprostone ; metabolism ; Drug Compounding ; Drugs, Chinese Herbal ; adverse effects ; chemistry ; Eye ; drug effects ; Gastric Mucosa ; drug effects ; metabolism ; Male ; Mice ; Phytolacca ; chemistry ; Plant Roots ; chemistry ; Rats

OBJECTIVETo explore the effects of Zuojin Pills and its similar formulas on the stomach cold syndrome in a Wei cold model in rats.

METHODSThe rat Wei cold model was established by intragastric administration of glacial NaOH, and the gastric mucosa injury indices, together with the levels of motilin and gastrin in the stomach, were determined. The preventive and curative effects of Zuojin Pills and its similar formulas on gastric mucosa injury were investigated.

RESULTSZuojin Pills and its similar formulas could protect the gastric mucosa in the gastric cold model in rats at different levels. Fanzuojin Pills had the best effect in inhibiting gastric mucosa injury.

CONCLUSIONThe different pharmacological effects of Zuojin Pills and its similar formulas in the rat gastric cold model were partially correlated with the degrees in cold and heat properties of the formulas.

Animals ; Chemistry, Pharmaceutical ; Cold Temperature ; Disease Models, Animal ; Drug Evaluation, Preclinical ; Drugs, Chinese Herbal ; administration & dosage ; chemistry ; pharmacokinetics ; pharmacology ; Gastric Mucosa ; drug effects ; pathology ; Malondialdehyde ; blood ; Rats ; Rats, Sprague-Dawley ; Stomach Diseases ; blood ; drug therapy ; pathology ; Superoxide Dismutase ; blood ; Tablets ; Therapeutic Equivalency

OBJECTIVETo observe the effect of volatile oil of amomum (VOA) on the expressions of mastocarcinoma-related peptide (PS2) and platelet activating factor (PAF) in helicobacter pyloriassociated gastritis (HPG) and to analyze its potential mechanism.

METHODSEighty patients with HPG were randomly assigned to two groups, 42 patients in the treated group treated with 0.5 mL VOA, thrice per day; and the 38 patients in the control group receiving Western tertiary medicinal treatment. Gastroscopic picture and helicobacter pylori (HP) infection (by quick urease and Warthin-Starry stain) of the gastro-membrane, expressions of PS2 and PAF (by immunohistochemical assay and Western blotting) as well as the contents of aminohexose and phospholipid (by Neuhaus method) in the gastric membrane of all patients were detected before treatment and 4 weeks after treatment. The clinical efficacy in the two groups was compared.

RESULTSThe total effective rate in the treated group was 88.1%, which was significantly higher than that in the control group (78.9%, P<0.05). After treatment, in the treated group, gastric membranous contents of aminohexose and phospholipid was increased, expression of PS2 elevated but that of PAF lowered, all showing significant difference as compared with those in the control group (P<0.01). In the control group, the expressions of PS2 and PAF changed insignificantly. The radical eliminating rate of HP in the treated group and the control group was insignificantly different between them (76.1% vs. 65.8%, P>0.05).

CONCLUSIONThe mechanism of VOA for anti-gastritis might be related with its action in increasing the expression of PS2 and decreasing the expression of PAF, and thus regulating the hydrophobicity of the gastric membrane.

Adult ; Aged ; Amomum ; Blotting, Western ; Chronic Disease ; Female ; Gastric Mucosa ; chemistry ; Gastritis ; drug therapy ; metabolism ; Helicobacter Infections ; drug therapy ; metabolism ; Helicobacter pylori ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Oils, Volatile ; adverse effects ; therapeutic use ; Peptides ; analysis ; Phospholipids ; analysis ; Platelet Activating Factor ; analysis

OBJECTIVETo study the accumulated toxic action to bandicoot of aqueous extract of crude and processed Radix Aristolochice and the pharmacodynamic action of aqueous and alcoholic extract of crude and processed Radix Aristolochice.

METHODThe LD50 of acute toxicity to mice and chronic accumulated toxicity to bandicoots of crude and processed Radix Aristolochice were observated. Intestinal and myokinetic influence of normal and revulsive hyperactive gastrointestinal motility of mice induced by neostigmine were observated by giving aqueous extract and alcoholic extract of crude and processed Radix Aristolochice. Relieving pain and eliminating inflammation to mice also were observated.

RESULTThe LD50 of aqueous extract of crude and processed Radix Aristolochice were 146. 45, 846.06 g X kg(-1) (equivalently to crude drug) respectively by intragastric administration. Bandicoot' general condition, peripheral blood, serum, organic coefficient, histopathologic examination weren't obvious changes after 1 month administrating aqueous extract of crude and processed drug in three dose. Serum indicators-urea nitrogen, cholesterol total, alkaline phosphatase manifestly were heightened and some animals'hepatic cells, nephric tubules and mucosa emerged differently damage at histomorphology by giving crude high dose after 2 months. Above organs emerged different damage in crude middle and high dose and processed high dose after 3 months and serum indicators- creatinine, urea nitrogen manifestly were increased, the coefficients of liver, kidney and gaster manifestly were heightened. However, the toxicity of identical dose processed product was lower than that of crude one. Aqueous extract and alcoholic extract of crude and processed Radix Aristolochice could obviously inhibite normal and revulsive hyperactive gastrointestinal motility by neostigmine of mice, relieve pain in mouse, stretching and heat stimulation models and inhibite dimethyl benzene-induc mouse, auricle inflammation. Pharmacodynamic action wasnt obvious difference in same dose of crude product and processed one.

CONCLUSIONAcute toxicity and chronic accumulated toxicity are stepped down after giving processed Radix Aristolochice, but pharmacodynamic effect wasn t lower. In pharmacodynamic effect, aqueous extract can't compare with alcoholic extract in same dose.

Analgesics ; administration & dosage ; pharmacology ; toxicity ; Animals ; Anti-Inflammatory Agents ; administration & dosage ; pharmacology ; toxicity ; Aristolochia ; chemistry ; Dose-Response Relationship, Drug ; Drug Compounding ; methods ; Drugs, Chinese Herbal ; administration & dosage ; isolation & purification ; pharmacology ; toxicity ; Ear Diseases ; pathology ; prevention & control ; Female ; Gastric Mucosa ; drug effects ; Gastrointestinal Motility ; drug effects ; Hot Temperature ; Inflammation ; pathology ; prevention & control ; Lethal Dose 50 ; Male ; Mice ; Mice, Inbred ICR ; Pain ; physiopathology ; prevention & control ; Pain Measurement ; Plant Roots ; chemistry ; Plants, Medicinal ; chemistry ; Random Allocation ; Rats ; Rats, Wistar

OBJECTIVETo study the effect and mechanism of mexican tea herb and pilular adina herb (abbreviated to MP) on concrescence of gastric mucosa in experimental gastric ulcer rats by observing the changes of epidermal growth factor (EGF), nitrogen monoxidum (NO) and expression of epidermal growth factor receptor (EGFR).

METHODSThe rat ulcer model was established by 100% glacial acetic injection into the subserosa. The ulcer index (UI) was measured by sliding caliper. The levels of NO and EGF in tissue and serum were measured by the nitrate reductase method and enzyme-linked immunosorbent assay, respectively. The expression of EGFR in the mucosa around the ulcer was detected by the immunohistochemical assay and microimage analysis system.

RESULTS(1) Compared with the model group, UI of MP groups (10, 15 and 20 mg.kg(-1).d(-1)) and ranitidine group was lower (P<0.05 or P<0.01), the levels of NO and EGF in the tissue and serum were higher (P<0.05), the thickness of regenerated mucous membrane increased, and the width loss of lamina muscularis mucosa decreased (all P<0.05). (2) The expression of EGFR is weakly positive in gastric mucosa cells in the normal group, mainly in the cytoplasm and cytomembrane. In the model group, the expression of EGFR was mainly in epithelial cells in cervical part and basilar part of gastric gland around the ulcer margin, and the number of cells with EGFR weakly positive expression was more than that in the normal group. Compared with that in the normal and model groups, the number of cells with EGFR positive in MP groups and ranitidine group increased (all P<0.05), with weakly positive expression.

CONCLUSIONMP can protect gastric mucosa, cure gastric ulcer, restrain the secretion of gastric acid, and boost multiplication, differentiation, migration and repair of the endothelial cell by promoting the secretion of NO and EGF, and increasing the expression of EGFR of gastric mucosa epithelial cells.

Animals ; Drugs, Chinese Herbal ; therapeutic use ; Epidermal Growth Factor ; analysis ; Female ; Gastric Mucosa ; chemistry ; drug effects ; pathology ; Immunohistochemistry ; Male ; Nitric Oxide ; analysis ; Rats ; Rats, Sprague-Dawley ; Receptor, Epidermal Growth Factor ; analysis ; Regeneration ; Stomach Ulcer ; drug therapy ; pathology ; Tea

OBJECTIVETo study the effects and its possible mechanisms of total alkaloids (TA) from rhizoma Coptis chinensis on H. pylori LPS induced gastric lesion in rats.

METHODH. pylori lipopolysaccharide was applied to rat intragastrically for 4 days to induce a pattern of mucosal responses resembling that of acute gastritis. After treatment with 50, 100, 200 mg x kg(-1) TA, we identified the changes on gastric histopathology, the effects on the activities of cNOS and NOS-2, the contents of TNF-alpha and the gastric mucus epithelial cell apoptosis.

RESULTH. pylori LPS could significantly induce the epithelial cell apoptosis of gastric mucus, increase the expression of NOS-2 and decline the expression of cNOS, and enhance the content of TNF-alpha in serum. Treatment with 50, 100, 200 mg x kg(-1) TA led to reduction in the extent of mucosal inflammatory changes elicited by H. pylori LPS and decrease in epithelial cell apoptosis. Furthermore, this effect of TA was associated with decrease in content of TNF-alpha in serum, decline in NOS-2, and increase in cNOS.

CONCLUSIONThe findings suggest that TA is a potent protective agent against H. pylori LPS induced gastric mucosal inflammation. The concerned mechanisms may be related to its inhibition on epithelial cell apoptosis, and the suppression of the inflammatory responses by upregulating cNOS and interfering with the events propagated by NOS-2, and reducing the content of TNF-alpha.

Acute Disease ; Alkaloids ; isolation & purification ; pharmacology ; Animals ; Apoptosis ; drug effects ; Coptis ; chemistry ; Epithelial Cells ; drug effects ; enzymology ; pathology ; Gastric Mucosa ; drug effects ; enzymology ; pathology ; Gastritis ; blood ; chemically induced ; prevention & control ; Lipopolysaccharides ; Male ; Nitric Oxide Synthase Type II ; metabolism ; Nitric Oxide Synthase Type III ; metabolism ; Plants, Medicinal ; chemistry ; Protective Agents ; isolation & purification ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Rhizome ; chemistry ; Tumor Necrosis Factor-alpha ; blood