OBJECTIVETo compare the effect of three preparations of xiaoyao formula (xiaoyao capsule, xiaoyao pill and Xiaoyao decoction) on soothing liver and strengthening spleen.

METHODThe liver depression and spleen deficiency rat model were established by forcing swimming, confining movement test and feeding on alternate days. The rats were randomly divided into eight groups, namely the blank group, the model group, the Cisapride group (2.7 mg x kg(-1)), the xiaoyao decoction group (1.62 g x kg(-1)), the xiaoyao pill group (1.62 g x kg(-1)) and the Xiaoyao capsule groups of high dose (3.24 g x kg(-1)), medium dose (1.62 g x kg(-1)) and low dose (0.81 g x kg(-1)), with intragastric administration for 3 weeks. The contents of NE, DA, 5-HT in serum were measured by HPLC-electrochemical detection method. The contents of motilin (MTL) and somatostation (SS) in plasma was determined by radioimmunassay. The expressions of MTL and SS in tissue were determined by immunohistochemical method.

RESULTThe contents of NE and MTL in the xiaoyao decoction group was significantly higher than that in the model group, while the content of 5-HT and SS was significantly lower than that in the model group (P < 0.01). The expression of MTL in the xiaoyao capsule group (1.62 g x kg(-1)) was significantly higher than that in the model group and the contents of 5-HT and SS was significantly lower than that in the model group (P < 0.05). The mean optical density of MTL in gastrointestinal tissue of rats in the xiaoyao decoction group and the xiaoyao capsule group (1.62 g x kg(-1)) was remarkably higher than that in the model group, while the expression of SS was notably lower than that in the model group (P < 0.05).

CONCLUSIONAll of the three preparations of Xiaoyao formula have the effect on soothing liver and strengthening spleen. Xiaoyao decoction shows better effect than xiaoyao capsule with same dosage, while xiaoyao capsule shows better effect than xiaoyao pill with same dosage.

Animals ; Body Weight ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Intestines ; drug effects ; metabolism ; Liver ; drug effects ; metabolism ; Male ; Motilin ; metabolism ; Rats ; Somatostatin ; metabolism ; Spleen ; drug effects ; metabolism ; Stomach ; drug effects ; metabolism

Acetylcholine ; pharmacology ; Adenocarcinoma ; metabolism ; Cell Line, Tumor ; Gastric Mucosa ; cytology ; drug effects ; metabolism ; Humans ; Receptors, Cholinergic ; metabolism ; Stomach Neoplasms ; metabolism

OBJECTIVETo preliminarily study the effective dosage range and mechanism of the abirritation of volatile oil of Evodia Fructus on the stomach cold syndrome model in mice, and discuss the correlation between its accompanying toxicity and oxidative damage mechanism, in order to provide the experimental basis for explaining the efficacy-syndrome-toxicity correlation.

METHODThe stomach cold-syndrome model in mice was induced by the classic hot plate test by orally administrating with different doses of volatile oil of Evodia Fructus, in order to observe its abirritation and companying toxic and side effects and detect serum ALT, AST, PGE2, NO, NOS, MDA, SOD, GSH, GSH-Px, BUN, CR and hepatic ALT, AST. The companying toxic symptoms in mice were recorded in toxic reaction integral table.

RESULTVolatile oil of Evodia Fructus had an obvious analgesic effect at 30 min after the oral administration and reached the peak effect at 60 min, with certain "dose-effect" and "time-effect" relations, rises in serum and hepatic ALT and AST levels, serum PGE2, MDA, NO and NOS and hepatic indexes, decreases in SOD, GSH and GSH-Px and no notable change in BUN, CR levels and kidney weight/body ratio. Conclusion: The abirritation mechanism of volatile oil of Evodia Fructus was related to the inhibition of pain transmitter release, peroxidative damage and NO damage, which is accompanied by certain hepatotoxicity, mainly mainly oxidative damage, with a concurrent "dose-time-toxicity" relationship.

Animals ; Drugs, Chinese Herbal ; administration & dosage ; toxicity ; Evodia ; chemistry ; toxicity ; Female ; Fruit ; chemistry ; toxicity ; Humans ; Liver ; drug effects ; metabolism ; Mice ; Oils, Volatile ; administration & dosage ; toxicity ; Oxidative Stress ; drug effects ; Stomach ; drug effects ; metabolism ; Stomach Diseases ; drug therapy ; metabolism

OBJECTIVETo investigate the effect of trichostatin A(TSA) on SGC- 7901 cells.

METHODSCytotoxicity and cell viability of gastric cancer cell line SGC- 7901 were assayed by MTT method. Morphologic assessment of apoptosis was performed with fluorescence microscope. Cell cycle and apoptosis rate were analyzed by flow cytometry. Histone H3 acetylation was detected by Western blot.

RESULTSTSA showed apparently cytotoxicity in SGC- 7901 cells. The growth curve showed the growth ratio decreased with the increase of TSA concentration. Apoptosis rate were significantly different between TSA treated group(75 ng/ml for 72 h)and control group (P < 0.05). Morphologic changes of apoptosis including nuclear chromatin condensation and fluorescence strength were observed with fluorescence microscope.TSA treatment (75 ng/ml for 72 h) sensitively induced apoptosis in the cell,which was demonstrated by the migration of many cells to the sub- G1 phase,the reduction of G1- phase cells and the increment of apoptosis rate (29.54%) in flow cytometric analysis. The expression of acetylated histone H3 was increased in TSA group(75 ng/ml) for 48 h compared with control group by Western blot.

CONCLUSIONSTSA can induce SGC- 7901 cell apoptosis. The expression of acetylated histone H3 may contribute to the apoptosis.

Acetylation ; drug effects ; Apoptosis ; drug effects ; Cell Line, Tumor ; Histones ; metabolism ; Humans ; Hydroxamic Acids ; pharmacology ; Stomach Neoplasms

OBJECTIVETo study the effect of valproate acid sodium(VPA) on apoptosis of human gastric cancer cell BGC-823 and to explore its possible mechanism.

METHODSCell growth inhibition was examined by MTT assay. Apoptosis rate was detected by FCM with Annexin V/PI staining. The activities and protein expression levels of caspase 3, caspase 8 and caspase 9 were examined by spectrophotometry and indirect immunofluorescence technique respectively.

RESULTSThe growth inhibition rate and apoptosis rate of human gastric cancer cells, treated with 0.75-4.00 mmol/L VPA for 24 h and 48 h, elevated in time- and dose-dependent manner. Apoptosis rates of VPA 0.75 mmol/L 24 h and 48 h were (7.2 +/- 0.5)% and (9.2 +/- 1.0)%, of VPA 4.00 mmol/L 24 h and 48 h were (16.7 +/- 2.2)% and (20.4 +/- 1.6)% respectively, which were significantly different as compared to the control [24 h, (4.9 +/- 0.2)%, 48 h, (5.1 +/- 0.8)%] (P< 0.001). The activities and protein expression levels of caspase 3 and caspase 9 were up-regulated compared with the control group (P< 0.001), meanwhile the activity and protein expression of caspase 8 enhanced slightly after VPA treatment for 48 h.

CONCLUSIONVPA can inhibit the growth and induce the apoptosis of BGC-823 cells mainly through the activation of caspase 9 pathway.

Apoptosis ; drug effects ; Caspases ; metabolism ; Cell Line, Tumor ; Humans ; Stomach Neoplasms ; pathology ; Valproic Acid ; pharmacology

Acetylcholine ; pharmacology ; Cell Line, Tumor ; Cell Membrane ; Epithelial Cells ; cytology ; Gastric Mucosa ; cytology ; drug effects ; metabolism ; Humans ; Receptors, Nicotinic ; drug effects ; metabolism ; Stomach Neoplasms ; metabolism

Peroxiredoxin II (Prx II) is known not only to protect cells from oxidative damage caused by hydrogen peroxide (H2O2), but also to endow cancer cells with resistance to both H2O2 and cisplatin and to grant them radioresistance. In this study, we examined whether Prx II antisense could enhance cisplatin-induced cell death. When gastric cancer cells were transfected with various concentrations of Prx II antisense plasmid, pPrxII/AS, and then treated with the same concentrations of cisplatin, Prx II antisense enhanced cisplatin-induced cell death. The combination index (CI) at all doses of the combination was below 1, indicating that Prx II antisense sensitized cisplatin-induced cell death. This synergism was also observed in the cells transfected with a Prx II antisense oligomer. Our present results, therefore, suggest that Prx II antisense would be a very good sensitizer for cisplatin, and that Prx II as a target for chemosensitizers constitutes a promising avenue for future research.
Antineoplastic Agents/*pharmacology ; Antioxidants/metabolism ; Apoptosis/drug effects ; Cell Death/*drug effects ; Cisplatin/*pharmacology ; Dose-Response Relationship, Drug ; Drug Synergism ; Genetic Vectors ; Human ; Oligonucleotides, Antisense/*metabolism ; Peroxidases/*metabolism ; Plasmids/genetics/metabolism ; Stomach Neoplasms/*metabolism ; Tumor Cells, Cultured

Peroxiredoxin II (Prx II) is known not only to protect cells from oxidative damage caused by hydrogen peroxide (H2O2), but also to endow cancer cells with resistance to both H2O2 and cisplatin and to grant them radioresistance. In this study, we examined whether Prx II antisense could enhance cisplatin-induced cell death. When gastric cancer cells were transfected with various concentrations of Prx II antisense plasmid, pPrxII/AS, and then treated with the same concentrations of cisplatin, Prx II antisense enhanced cisplatin-induced cell death. The combination index (CI) at all doses of the combination was below 1, indicating that Prx II antisense sensitized cisplatin-induced cell death. This synergism was also observed in the cells transfected with a Prx II antisense oligomer. Our present results, therefore, suggest that Prx II antisense would be a very good sensitizer for cisplatin, and that Prx II as a target for chemosensitizers constitutes a promising avenue for future research.
Antineoplastic Agents/*pharmacology ; Antioxidants/metabolism ; Apoptosis/drug effects ; Cell Death/*drug effects ; Cisplatin/*pharmacology ; Dose-Response Relationship, Drug ; Drug Synergism ; Genetic Vectors ; Human ; Oligonucleotides, Antisense/*metabolism ; Peroxidases/*metabolism ; Plasmids/genetics/metabolism ; Stomach Neoplasms/*metabolism ; Tumor Cells, Cultured

OBJECTIVETo investigate the effect of 1,25 (OH)(2)D(3) on cell proliferation and the expression of tumor necrosis factor-α (TNF-α ) in human gastric carcinoma SGC-7901 cells.

METHODSSGC-7901 cells were treated with 1×10(-6), 1×10(-7), 1×10(-8), and 1×10(-9) mol/L 1,25 (OH)(2)D(3) for 24, 48, 72 and 96 h. The cell proliferation was measured by MTT assay, and the cell cycle changes were analyzed using flow cytometry. RT-PCR and Western blotting were used to determine the expression of TNF-α mRNA and protein, respectively.

RESULTS1,25 (OH)(2)D(3) significantly inhibited SGC-7901 cell proliferation (P<0.05) in a time- and dose-dependent fashion. Treatment with 1,25 (OH)(2)D(3) for 72 h caused significant cell cycle arrest at G(0)/G(1) phase (F=9.81, P<0.05) and dose-dependently inhibited the expression of TNF-α at both mRNA and protein levels in SGC-7901 cells (P<0.05).

CONCLUSIONThe inhibitory effect of 1,25 (OH)(2)D(3) on SGC-7901 cell proliferation is probably associated with the down- regulation of TNF-α expression.

Calcitriol ; pharmacology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Stomach Neoplasms ; metabolism ; pathology ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo evaluate the toxicity of Radix Aristolochiae supplied experimental evidence of rational use of drug in clinic.

METHODAfter treatment with small dose Radix Aristolochiae, Guanxin Suhe Wan (with Radix Aristolochiae) and Guanxin Suhe Wan (without Radix Aristolochiae) in different group for a long- term, respectively, the biochemical indicator of PT, ALT, AST, ALB, ALP, Crea and BUN were detected, and the kidney, liver, stomach and urinary bladder were examined by pathologic assaying.

RESULTIn Radix Aristolochiae group and Guanxin Suhe Wan (with Radix Aristolochiae) group, all of biochemical indicator were changed significantly, and hepatonecrosis, renal tubular necrosis, gastric carcinoma and bladder carcinoma were discovered.

CONCLUSIONRadix Aristolochiae and Guanxin Suhe Wan (with Radix Aristolochiae) can damage kidney and liver, and cause gastric carcinoma and bladder carcinoma by intensive toxicity.

Animals ; Aristolochia ; chemistry ; toxicity ; Drugs, Chinese Herbal ; toxicity ; Kidney ; drug effects ; metabolism ; pathology ; Liver ; drug effects ; metabolism ; pathology ; Male ; Rats ; Rats, Sprague-Dawley ; Stomach Neoplasms ; chemically induced ; Urinary Bladder ; drug effects ; metabolism ; pathology ; Urinary Bladder Neoplasms ; chemically induced