AIMTo investigate the effects of puerarin on pulmonary vascular structure in pulmonary hypertension rats induced by chronic hypoxia. METHODSThirty male spragu-dawley rats were randomly divided int o three groups:control group(NC), hypoxia group(HH), hypoxia+puerarin group(HP). Collagen Ⅰ, Ⅲ and collagen I mRNA were observed in pulmonary arterioles by th e technique of immunohistochemistry and in situ hybridization. RESULTS①mPAP was much higher in rats of HH group than that of NC group(P0 05). ②The contents of lung homoge nates SOD and MDA of HP group were obviously higher than those of HH group(P 0 05). CONCLUSIONPuerarin can improve pulmonary vessel remodeling.

Objective To explore the effects of family and telephone follow-up on quality of life of the patients with tota1 hip arthroplasty(THA).Methods One hundred and twelve patients with THA were randomly divided into experiment group and control group with 56 cases in each group.The experiment group was treated with rehabilitative instruction by family and telephone follow-up.The control group was treated with outpatient follow-up after leaving the hospital.The living quality in both groups were compared by the medical outcomes study 36-item short-form health survey(SF-36 QOL)one year after leaving the hospital.Results One-year after leaving the hospital,the total score and demension score of experiment group were better than those of the control group.There was significant difference between the control group and in experiment group(P<0.05).Conclusion Family and telephone follow-up is an effective implementation for THA patients to accomplish physiological functional recovery and promote the quality of life.

Objective:To compare the therapeutic and toxic profile of topotecan given intraperitoneally with intravenously in human ovarian cancer xenografted into athymic nude mice.Methods: Eighty female Balb-c/nu-nu mice were randomized assigned into eight groups (n=10). Xeneografts resulted from intramesentery injection of cultured human ovarian cancer cells SKOV3 in athymic mice. Onset of intraperitoneal treatment with either topotecan or cisplatin (7.5 mg/kg) was on day 7. Animals scheduled for topotecan i.p. received intraperitoneal application of topotecan (1.5 mg/kg×2, 3.0 mg/kg×2, 6.0 mg/kg×2 or 10.0 mg/kg×1). Animals scheduled for topotecan i.v. received intravenous administration of topotecan (6.0 mg/kg×2 or 10.0 mg/kg×1). Two weeks after drug application animals were killed. Tumor growth inhibition were assessed and compared with untreated mice and cisplatin intraperitoneally administered mice. Acute toxicity was determined by loss of body weight. Cell cycle division and apoptosis after drug administration was determined by flow cytometric analysis.Results: In a panel of ten tumour xenografts, intraperitoneal topotecan was significantly more effective than intravenous administration. The toxicity profile suggested a better tolerability in terms of weight loss after intraperitoneal administration than cisplatin control. Topotecan 10.0 mg/kg i.p. per day (1 day) schedule was an optimal treatment for ovarian cancer and well tolerated by mice with no signs of acute toxicity. Topotecan and cisplatin induce cells G0-G1 arrest and apparent apoptosis. No significant difference among mice treated with topotecan intraperitoneally or intravenously or cisplatin was observed in term of apoptosis and cell cycle perturbation.Conclusion:The results may have implications for the future design of clinical studies on intraperitoneal application of topotecan. It suggests that apoptosis and cell cycle perturbation play an limited role in the mechanism of topotecan administration.

Objective:To evaluate the effects of stellate ganglion block (SGB) on the activation of M1 microglia during cerebral ischemia-reperfusion (I/R) in rats.Methods:Fifty-four SPF healthy male Sprague-Dawley rats, aged 8-10 weeks, weighing 240-270 g, were divided into 3 groups ( n=18 each) using a random number table method: sham operation group (group Sham), cerebral I/R group (group IR) and SGB group.Blood vessels were only exposed, without occlusion in group Sham.Cerebral I/R was induced by occlusion of the middle cerebral artery for 90 min followed by reperfusion in group IR.Cervical sympathetic trunk transaction was performed to induce left SGB immediately after onset of reperfusion in group SGB.Blood samples were collected from the apex of the heart at 6, 12 and 24 h of reperfusion for determination of the concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β in the serum (using enzyme-linked immunosorbent assay). The animals were sacrificed after the neurological function was evaluated at 24 of reperfusion, and brain tissues were removed for microscopic examination of the pathological changes in cortex, for determination of percentage of cerebral infarct size (by TTC staining), for assessment of cell apoptosis and apoptosis rate in cortex (by TUNEL), and for determination of the expression of microglial biomarker Iba-1 and activated M1 microglia biomarker CD68 (by Western blot). Results:Compared with group Sham, the neurological function score, percentage cerebral infarct size, apoptosis rate in cortex, concentrations of TNF-α, IL-6 and IL-1β in the serum, and the expression of Iba-1 and CD68 were significantly increased in IR and SGB groups ( P<0.05). Compared with group IR, the neurological function score, percentage cerebral infarct size, apoptosis rate in cortex, concentrations of TNF-α, IL-6 and IL-1β in the serum, and the expression of Iba-1 and CD68 were significantly decreased in group SGB ( P<0.05), and the pathological changes of brain tissues were significantly attenuated in group SGB. Conclusion:The mechanism by which SGB reduces cerebral I/R injury is related to inhibiting activation of M1 microglia in rats.

BACKGROUND:Phytohemagglutinin (PHA) can stimulate the peripheral blood mononuclear cells (PBMCs) into cellcycle, and cause their immune activation, which is a common immune proliferation model. However, the role of non-PBMC ingredient of peripheral blood is unclear, as wel as the expression of endothelial cells related cytokines. OBJECTIVE:To study the effect of whole blood culture and PBMCs alone culture with PHA on the PBMC proliferation and apoptosis, expression of inflammatory cytokine and endothelial cellsecreted cytokine markers. METHODS:Morphological changes of PBMCs separated from normal karyotype human peripheral blood individual y cultured with or without PHA were observed. The PBMCs were col ected by whole blood culture or PBMC separated culture. mRNA was extracted for the fluorescence quantitative RT-PCR, which was applied to detect the cellproliferation, apoptosis, and expression of inflammatory cytokine and endothelial cellsecreted cytokines. The statistic analysis was used for the significance explication. RESULTS AND CONCLUSION:PBMCs alone cultured ere different from those undergoing whole blood culture. The PHA could up-regulate the gene expression of Ki67, proliferating cellnuclear antigen, Caspase 3, interferon-γ, tumor necrosis factor-βand interleukin-6, but down-regulate Protein C. This indicted that PHA could promote the proliferation and apoptosis of PBMCs and up-regulate the expression of inflammatory cytokines, but down-regulate the expression of endothelial cells secreted coagulation cytokines.

AIM: To explore the roles of vascular endothelial growth factor (VEGF) in hypoxia pulmonary hypertension and effects of SHENYI Capsule. METHODS: Thirty SD rats were randomly divided into normal control group (N), hypoxia hypercapnia group (F), and hypoxia hypercapnia+SHENYI Capsule group (S). The levels of VEGF in serum and lung tissue are measured by ELISA, the ultrastructure of pulmonary arterioles was observed by electron microscopy, and the expression of VEGFmRNA was observed by in situ hybirdization. RESULTS: Mean pulmonary arterial pressure (mPAP), weight ratio of RV to LV+S, the levels of VEGF in serum, and lung tissue of group F were significantly higher than those of group N and group S (P

Aim To explore the effects of Puerarin on the Apelin and its receptor APJ of lung tissue in rats with hypoxia pulmonary hypertension.Methods Thirty SD rats were randomly divided into normal control group(N),and hypoxia hypercapnia group(F),and hypoxia hypercapnia+Puerarin group(P).The levels of Apelin-36 in serum and in lung tissue were measured by radioimmunity,the expressions of Apelin and APJ in pulmonary tissuse were observed by RT-PCR.Results ①Mean pulmonary arterial pressure(mPAP),weight ratio of RV to LV+S,the levels of Apelin in serum and in lung tissue of group F were significantly higher than those of group N(P

AIM: To investigate the changes of vascular endothelial growth factor (VEGF) in the pulmonary circulation of rats with different hypoxia and hypercapnia duration. METHODS: Forty SD rats were randomly divided into normol control group (N), exposed to hypoxia hypercapnia for 2 weeks group (T), for 4 weeks group (F), for 8 weeks group (E). The levels of VEGF were measured and the ultrastructure of pulmonary arterioles was observed by electron microscopy. RESULTS: Mean pulmonary arterial pressure (mPAP), weight ratio of RV to LV+S, the levels of VEGF in serum and lung tissue, the expression of VEGF and VEGF mRNA in group T, F, E were significantly higher than that in group N. With the prolong duration, base of endothelial cell was narrowed, proliferation of smooth muscle cells and collagenous fibers of pulmonary arterioles in rats were increased gradually. CONCLUSIONS: Hypoxia and hypercapnia increase the expression of VEGF mRNA and synthesis of VEGF. VEGF may play an important role in the pathogenesis of hypoxia pulmonary hypertension and reconstruction of pulmonary artery.

AIM: To study the role and the mechani sm of heme oxygenas/endogenous carbon monoxide on nitric oxide synthase/nitric oxide system in rats with pulmo nary hypertension induced by hypoxic hypercapnia. METHODS: Spr ague-Dawley rats w ere randomly divided into three groups: control group (A group),hypoxic hypercap n ic group (B group), hypoxic hypercapnia+hemin group (C group). Blood CO concentr at ion (COHb%),NO concentration,HO-1 activity, iNOS, cNOS in blood serum and lung h omogenate were measured, respectively. RESULTS: ① mPAP and RV /(LV+S) of B g roup were significantly higher than those of A and C group( P

Objective To investigate the effect of 17-β-estradiol (17-β-E2) on the expression of glucose transporter 4 (GLUT4) in rat primary culture skeletal muscle cells with insulin resistance (IR) induced by palmitinic acid (PA).Methods Rat skeletal muscle was primarily cultivated.The cells were identified by the technology of immunofluorescence.Cells were inclubated with 0.6 mmol/L palmitinic acid for 24 h to induce IR.The concentration of glucose in the medium was measured.The mRNA and protein expressions of protein kinase B (PKB/Akt) and GLUT4 were measured by real time polymerase chain reaction (PCR) and Western blot respectively.Results Compared the control with PA treated rats,the concentration of glucose in the medium was increased [(3.86±0.64)mmol/L vs.(5.43±0.55) mmol/L,q＝4.13,P＜0.05],uptake of glucose stimulated by insulin was decreased (P＜0.01),the expressions of GLUT4 and phosphorylation PKB/Akt were reduced in the PA group (all P＜0.05).In the 17-β-E2 (100 nmol/L) versus control,the concentration of glucose in the medium was higher [(3.86±0.64) vs.(3.77±0.35)mmol/L,q＝ 4.76,P＜0.05],uptake of glucose stimulated by insulin was increased (P＜0.01) and the expressions of GLUT4 and p-Akt were also increased (all P＜0.05).17-β-E2 (10 nmol/L and 100 nmol/L) reversed the decrease of basal and insulin-stimulated uptake of glucose induced by PA,reversed the decrease of GLUT4 and p-Akt expression induced by PA compared with the PA group (all P＜ 0.05).Conclusions 17-β-E2 inhibits insulin resistance induced by PA in rat primary culture skeletal muscle cells,the mechanism may be correlated with the up-regulation of expression of phospho-Akt and GLUT 4 induced by 17-β-E2.