The myocardial calcium paradox model was made on isolated perfused guinea-pig heart. Sodium tanshinonc Ⅱ_A sulfonate (DS-201) was used as a protection agent. The protein release and the calcium uptake of the myocardium were measured to observe and evaluate the protection effect of DS-201 against myocardial calcium paradox. The effect was compared with that of verapamil, a known calcium antagonist, to study the calcium antagonism of DS-201. The results demonstrated that DS-201 acted as a calcium antagonist and contributed an outstanding protection to myocarcial calcium para- dox. DS-201 inhibited the calcium uptake and the protien (enzymes) release of the myocardium occured during the calcium paradox (P

Treated 36 cases of infantile enuresis by acupuncturing Zuyunganqu (Foot Motor Sensory Area),Guanyuan (CV 4), Qihai (CV 6), Zhongwan (CV 12),Zusanli (ST 36), Yinlingquan (SP 9), Pishu (BL 20),Weishu (BL 21) and Shenshu (BL 23). After two courses,29 cases were cured, 5 cases were improvement and 2cases were no effect.

Objective To investigate the antitumor effect of flavopiridol in ovarian cancer. Methods After the treatment with flavopiridol of AO cells,cell apoptotic rate and cell cycle distribution were detected by flow eytometer and the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling(TUNEL).Real time PCR was used to detect the expression of cyclin D and active caspase-3 in AO cells.Subcutaneous tumor models and abdominally spread tumor models of human ovarian carcinoma using AO ceils in BALB/c nude mice were established.The mouse survival rates were measured for abdominally spread tumor models and the volume of tumor nodules was determined for subcutaneous tumor models following the treatments of flavopiridol.TUNEL was used to detect cell apoptosis,and immunohistochemistry was used to measure microvessel density(MVD)in tumor tissues. Results AO cells showed apoptotic rates of 4.1%,10.7% and 7.6% following the treatments with flavopiridol at 150,300 and 500 nmol/L respectively,accompanied by an increase in G_1 progression and a decrease in S phase progression.The level of active caspase-3 increased(2.55 vs 2.49)and the level of cyclin D expression decreased significantly(0.25 vs 0.69,P

Polycystic ovary syndrome (PCOS) is one of the most popular diseases in obstetrics and gynecology research at internal and abroad at present, traditional Chinese medicine(TCM)in the clinical treatment of the disease have the advantage. Clinical epidemiological study of descriptive research method this research adopts investigation, observation of TCM syndromes and improper diet through 401 cases in Jiangsu Province confirmed PCOS patients, to explore the relationship between TCM syndrome type distribution and improper diet factors, and to provide the clinical basis for further etiology of this disease research. TCM syndrome type distribution of the disease is kidney deficiency, phlegm stagnation syndrome, qi stagnation and blood stasis syndrome, syndrome of dampness heat of liver channel and is composed of 4 basic syndromes and formed complex syndrome, and the composite and syndrome type (60.85%); combined with the analysis of traditional Chinese medicine dialectical, Pure empirical syndrome this disease (46.88%), followed by the actual card (45.39%), pure deficiency is rare. Improper diet factors associated with the disease, in which improper diet with different TCM syndrome type distribution significantly related. Stagnation of phlegm dampness syndrome is the main syndrome of the disease type, improper diet factors and every syndrome PCOS type distribution is as follows: the partial eclipse fatness greasy with basic syndromes of phlegm dampness stagnation of kidney deficiency syndrome, the nephrasthenia syndrome is less; eating spicy stimulation by basic syndromes of stagnation of Qi and blood stasis; eating cold people the basic certificate type of qi stagnation and blood stasis; The diet of patients are more prone to stagnation of phlegm dampness syndrome.
Adolescent ; Adult ; China ; Diagnosis, Differential ; Diet ; Eating ; Female ; Humans ; Medicine, Chinese Traditional ; Polycystic Ovary Syndrome ; diagnosis ; metabolism ; physiopathology ; Young Adult

OBJECTIVETo observe the effect of Pi transportation, dampness resolving and phlegm expelling herbs (PTDRPEH) on the obesity degree, fat hormones, and leptin resistance in diet-induced obesity (DIO) rats.

METHODSAmong the 120 Wister rats, 10 were recruited as the blank control group (fed with basal forage), and the remaining 110 were administered with high-fat high-nutrition forage for 17 weeks. According to weight, we obtained 40 DIO rats and 10 diet-induced obesity resistance (DIO-R) rats. DIO rats were further divided into four groups, i.e., the DIO model group (normal saline, at the daily dose of 2 mL), the sibutramine group (at the daily dose of 1.6 mg/kg), the dampness resolving and phlegm expelling group (DRPE, at the daily dose of 3.2 g/kg), and the Pi transportation group (PT, at the daily dose of 3.2 g/kg). All were given by gastrogavage. Normal saline (2 mL) was given by gastrogavage to rats in the blank control group and the DIO-R group. The basal forage was administered to rats in the blank control group, while high fat forage was continually given to rats in the remaining five groups. Their body weights and body lengths were measured after 16 weeks of gastrogavage. All intra-abdominal fat was taken out to measure the degree of obesity and fat contents. Insulin resistance index (IRI), blood glucose, triglycerides, cholesterol, leptin, neuropeptide Y (NPY), tumor necrosis factor alpha (TNF-alpha), and adiponectin were detected after blood withdrawing. Leptin, TNF-alpha, adiponectin, suppressors of cytokine signaling-3 (SOCS-3), and other relevant adipose hormones and inflammatory cytokines were examined in the fat homogenate.

RESULTSCompared with the blank control group, DIO model rats' body weight, body mass index (BMI), fat factor, IRI, serum leptin, TNF-alpha, and SOCS-3 significantly increased (P < 0.05, P < 0.01); serum NPY, serum leptin, and adiponectin decreased (P < 0.05). Leptin increased and NPY decreased in DIO-R model rats. Compared with the DIO group, DIO-R model rats' body weight, BMI, fat factor, IRI, serum NPY, TNF-alpha, and SOCS-3 all decreased (P < 0.05, P < 0.01); leptin and adiponectin in serum and the fat homogenate all increased (P < 0.05, P < 0.01). After intervention with Sibutramine, rats' body weight, BMI, fat factor, and TNF-alpha in the fat homogenate obviously decreased (P < 0.05, P < 0.01). Serum TNF-alpha decreased, leptin and adiponectin increased in rats of the DRPE group (P < 0.05, P < 0.01). BMI, fat factor, IRI, leptin, and SOCS-3 showed a decreasing tendency, but with no statistical difference (P > 0.05). The body weight, BMI, fat factor, IRI, TNF-alpha, and SOCS-3 all decreased in the PT group (P < 0.05, P < 0.01); leptin and adiponectin in the serum and the fat homogenate increased (P < 0.05, P < 0.01).

CONCLUSIONSSibutramine could reduce body weight and TNF-alpha in the adipose tissue. Herbs of PT could inhibit fat diet-induced obesity and insulin resistance (IR), with superior effect to herbs of DRPE. Its mechanism might be closely related to promoting leptin and adiponectin secreted by fat, reducing leptin resistance, and elevating serum levels of leptin and adiponectin.

Adiponectin ; blood ; Animals ; Diet, High-Fat ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; Insulin Resistance ; Leptin ; blood ; Male ; Obesity ; blood ; drug therapy ; Rats ; Rats, Wistar ; Tumor Necrosis Factor-alpha ; metabolism

Adolescent ; Carcinoma, Squamous Cell ; pathology ; surgery ; Cell Transformation, Neoplastic ; Craniopharyngioma ; pathology ; surgery ; Humans ; Male ; Pituitary Neoplasms ; pathology ; surgery

Objective To determine if aquaporin1 ( AQP1) and aquaporin5 ( AQP5) are expressed in the alveolar-capillary membrane in rats, and to investigate the changes of AQP1 and AQP5 expression in the rat with acute lung injury.Methods The distribution of AQP1 and AQP5 in alveolar capillary membrane was investigated by immunohistochemistry and immunoelectron microscopy with affinity-purified antibodies to human AQP1 and AQP5.The possibility that alveolar capillary membrane AQP1 and AQP5 undergo altered regulation was studied by a rat model established using intra-tracheal instillation of lipopolysaccharide (LPS).Results Immunolabelling showed that AQP1 was stained primarily in the microvascular endothelium of normal lungs, while AQP5 was expressed in type I pneumocytes. Immunohistochemical analysis showed a significant decrease in the expression of AQP1 and AQP5 in injured lungs at 4 -48 h after LPS instillation.AQP1 protein was resumed partly at 24 h after LPS instillation and steroid administration, whereas AQP5 was unchanged.Conclusions The decreased expressions of AQP1 and AQP5 in injured lungs suggest that both of them may play a role in abnormal fluid transportation.

This study examined the effect of resveratrol on the secretion of vascular endothelial growth factor (VEGF) and subsequent proliferation of human leukemia U937 cells, and explored the mechanisms involved. Human leukemia U937 cells were treated with resveratrol of different concentrations (12.5-200 micromol/L) for different time lengths (12-48 h). The proliferation of the U937 leukemic cells was determined by MTT assay. Apoptosis was observed by Annexin-V-FIFC/PI double staining and flow cytometry (FCM). Cells cycle was analyzed by PI staining and FCM. The content of VEGF was determined by ELISA. Human umbilical vein endothelial cells were examined for vasoformation in vitro after exposures to resveratrol of various concentrations. The results showed that resveratrol inhibited the proliferation of U937 leukemia cells in a dose-and time-dependent manner. Resveratrol induced apoptosis and S-phase cell cycle arrest in human leukemic U937 cells. Resveratrol inhibited the secretion of VEGF in U937 cells. Resveratrol inhibited the vasoformation of human vein endothelial cells in a dose-dependent manner. It was concluded that resveratrol could down-regulate the secretion of VEGF, induce apoptosis and suppress the proliferation of U937 cells.
Angiogenesis Inhibitors/*pharmacology ; Antineoplastic Agents, Phytogenic/pharmacology ; Apoptosis/*drug effects ; Cell Proliferation/drug effects ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Stilbenes/*pharmacology ; U937 Cells ; Vascular Endothelial Growth Factor A/*secretion

Urid acid is one of the terminal metabolites of human body.More and more attention was paid to its metabolic mechanisms in intestinal tract;however, few studies were seen so far.This study aims to illuminate the metabolic mechanism of uric acid in intestinal tract by two ways:one is the transporters associated with intestinal epithelium, including ABCG2 and SLC2A9, the other is decomposition of uric acid by intestinal flora.We hope this review can provide new insights to decrease blood uric acid and treat urate-related diseases, and also provide a new way to alleviate drug-induced kidney damage.

Glycosaminoglycan(GAG) has recently become an important landscape of discovering new mechanisms of apoptosis stressed by oxidative stress.In this review,we focused the signal transduction passways of GAG in lysosome which can inhibit apoptosis induced by oxidative stress.