巨型艾美耳球虫感染鸡空肠粘膜肥大细胞数量和组织胺含量的变化

通过用地塞米松处理鸡和用特异性抗原作刺激因子的微量全血淋巴细胞转化试验(LPA),研究了雏鸡抗 Eimeria maxima 再感染中细胞免疫现象。结果表明,地塞米松处理可损伤鸡抗 E.maxima 再感染的免疫力.这提示了 CD8+T 细胞、γIFN 及 IL-2等在抗 E.maxima 卵囊抗原刺激因子的微量全血 LPA结果表明,其刺激指数值与鸡抗 E.maxima 再感染抵抗力有关。此反应可用于体外监测鸡体抗 E.maxima再感染的抵抗力。     

Dexamethasone pretreatment attenuates reperfusion arrhythmia in rats

AIM: To investigate the effect of dexamethasone (DEX) preconditioning on reperfusion arrhythmia. METHODS: 46 Sprague-Dawley rats were divided randomly into DEX and control (CON) group, the rats were pretreated with DEX or sodium chloride before their hearts were separated for Langendorff perfusion and for ischemia/reperfusion. The reperfusion arrhythmias were observed dynamically after 60 min reperfusion following 30 min ischemia. The expression of HSP72 in myocardium was examined by Western blotting and immunohistochemistry at reperfusion 60 min. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and the activities of Na+-K+-ATP ase, Ca2+-Mg2+-ATPase on myocardial plasma membrane were detected. RESULTS: Compared with control group, the accumulated points and persistence time of ventricular arrhythmia were reduced significantly in DEX group (P<0.05), the expression of HSP72 was significant upregulated (P<0.05), the level of MDA was reduced significantly, the activities of SOD, CAT, GSH-Px and Na+-K+-ATPase were significantly higher (P<0.05). CONCLUSION: Dexamethasone pretreatment markedly reduces the reperfusion ventricular arrhythmias in rats, which may be attributed to upregulation of HSP72, SOD, CAT, GSH-Px , Na+-K+-ATPase and inhibition of lipid peroxidation.     

Protective effect of panaxadiols against brain injury induced by LPS through inhibiting NOS activity and p38 expression

AIM: To explore the protective effect of panaxadiols (PDS) on brain injury induced by endotoxin and its mechanism. METHODS: Rats were divided into control,LPS,LPS+dexamethasone (DEX) and LPS+PDS group, respectively. NOS activity, NO content and phosphorylated p38 expression in brain cortex were assayed 4 h after intravenous injection of LPS. RESULTS: NOS activity, NO content and phosphorylated p38 expression in brain cortex in LPS group were obviously higher than those in LPS group. NOS activity, NO content and phosphorylated p38 expression in brain cortex in LPS+DEX and LPS +PDS groups were obviously lower than those in LPS group. CONCLUSION: The protective effects of PDS against brain injury induced endotoxin may be related to decreasing NOS activity, NO content in the brain tissue, and this process is involved in p38MAPKs signal transduction.     

地塞米松与肝素对HL－60细胞增值和生物大分子合成的影响

用地塞米松（Ｄｅｘ）和肝素（Ｈｅｐ）Ｉｃ６０及Ｉｃ５０低一个剂量，对ＨＬ－６０细胞增殖、生长曲线和分裂指数均有明显的抑制作用，联合应用时抑制作用显著增强；对ＤＮＡ和蛋白质合成抑制作用大于ＲＮＡ，联合应用抑制作用均显著增强，提示两药抑制ＨＬ－６０细胞增殖、分裂和生长可能与它们抑制ＤＮＡ和蛋白质合成有关，亦与抑制ＲＮＡ合成有一定关系。     

Influence of Steroidal Anti-Inflammatory Drugs on Viability and Fertility of Equine Semen

Considering the efficiency of steroidal anti-inflammatory drugs (SAIDs) in the immunomodulation of breeding-induced endometritis and the possibility of using these drugs by intrauterine route instead of the parenteral application, the present study aimed at evaluating the effect of SAIDs added to the semen extender on equine sperm viability and fertility. In experiment 1, 15 SAIDs were individually added to a skim milk-based extender and, based on the results of sperm motility, dexamethasone was the drug of choice for the subsequent trials. The effect of dexamethasone on the viability of fresh and 24-hour cooled semen was investigated in experiment 2. In experiment 3, fertility rate was measured in both post-breeding endometritis-resistant and susceptible mares. Although dexamethasone supplementation caused a premature decrease in sperm total and progressive motility and in sperm velocities (P < .05), no difference was observed for sperm membrane integrities and fertility (P > .05). Based on these results, we can conclude that dexamethasone can be added to equine semen at the time of insemination or before cooling, although its use was not able to increase fertility.     

Rapid effects of dexamethasone on activation of ERK and p38 in HO-8910cells

AIM: To investigate the effects of synthetical glucocorticoid dexamethasone(Dex) on the activation of two members of mitogen-activated protein kinase (MAPK) family, extracellular signal-regulated protein kinase1/2(ERK1/2) and p38 MAPK (p38) in human ovarian cancer cell line HO-8910. METHODS: The activation of ERK1/2 and p38 was determined by Western blot. RESULTS: Inhibition of activation of ERK1and ERK2 by10^-7 mol/L Dex occurred at 5 min, with maximum up to 41% and 54% respectively at 30min (P<0.01), and sustained until 4 h. On the contrary, p38 activity was rapidly stimulated by 10^-7 mol/L Dex, with maximum to 84% at15 min (P<0.01), and sustained till1h. Furthermore, these effects increased with the concentration of Dex(10^-10-10^-6 mol/L). RU486, an antagonist of glucocorticoid receptor (GR), did not affect these effects. CONCLUSION: Dex can rapidly inhibit ERK1/2 and stimulate p38 activation in a GR-independent manner in HO-8910cells, which might play a role in Dex-mediated growth inhibition in these cells.     

Dioscorea opposita reverses dexamethasone induced insulin resistance

The effects of Dioscorea opposita (huai shan yao, HSY) on dexamethasone-induced insulin resistance were investigated in vitro and in vivo. D. opposita extract reduced significantly the blood insulin and glucose levels in dexamethasone-induced diabetic rats. In vitro, HSY significantly enhanced insulin-stimulated glucose uptake in 3T3-L1 adipocytes. Moreover, HSY increase the mRNA expression of GLUT4 glucose transporter in 3T3-L1 adipocytes. These data suggest that D. opposita has insulin sensitivity that is associated with the regulation of GLUT4 expression.     

Adrenal response to adrenocorticotropic hormone in dogs before and after surgical attenuation of a single congenital portosystemic shunt

BACKGROUND: Dogs with single congenital portosystemic shunts (CPSS) often develop postoperative hypoglycemia and prolonged anesthetic recovery. These abnormalities could be attributable to inadequate adrenal response. However, adequacy of adrenal response after CPSS surgery is unexplored. HYPOTHESIS: Dogs with CPSS have inadequate postoperative adrenal response. ANIMALS: Eight nonoperated, 8 ovariohysterectomy (OHE), and 16 CPSS dogs. METHODS: Consecutive day ACTH stimulation tests were performed on nonoperated healthy dogs, healthy dogs before and after OHE, and CPSS dogs before and after surgery. Adequate response was defined as >50% or >30 ng/mL increase in cortisol after ACTH administration. Blood glucose (BG) was monitored before and after surgery. Prolonged anesthetic recovery and refractory hypoglycemia episodes were recorded. RESULTS: Results of consecutive day ACTH stimulation tests did not vary in normal dogs. Results of preoperative ACTH stimulation tests of CPSS and OHE dogs were not significantly different. Dogs with CPSS had higher postoperative baseline cortisol concentrations (median, 329 ng/mL) than OHE dogs (median, 153 ng/mL). Postoperative cortisol increase after ACTH in CPSS was < or =50% in 10/16 and < or =30 ng/mL in 6/16. After surgery, BG was < or =60 mg/dL in 7/16 CPSS dogs. Cortisol concentrations were not correlated with BG. Two CPSS dogs had refractory hypoglycemia and 4 had delayed recovery; all improved with dexamethasone administration (0.1-0.2 mg/kg/IV). CONCLUSIONS AND CLINICAL IMPORTANCE: Contrary to previous reports, baseline cortisol concentrations in CPSS and healthy dogs are similar. Many CPSS dogs have postoperative hypercortisolemia. Response to ACTH does not correlate with postoperative hypoglycemia or prolonged anesthetic recovery.     

Significant anti-proliferation of human acute lymphoblastic leukemia cells by combined treatment with chloroquine and dexamethasone

AIM：To explore the promoting action of chloroquine on the anti-proliferation effect of dexamethasone on acute lymphoblastic leukemia cells. METHODS：CCK-8 assay was used to assess the viability of the dexamethasone-resistant human acute lymphoblastic leukemia CEM-C1 cell line treated with the combination of chloroquine and dexamethasone. Western blotting, quantitative real-time PCR and LysoTracker Red staining were utilized to examine the mechanism. RESULTS：Combination of chloroquine and dexamethasone significantly inhibited the proliferation of CEM-C1 cells compared with control group (P<0.01). The combination of chloroquine and dexamethasone increased the abundance of glucocorticoid receptor and inhibited lysosomal function, while lysosomal inhibitor bafilomycin A1 also increased glucocorticoid signaling. CONCLUSION：Dexamethasone combined with chloroquine triggers an anti-proliferation effect on CEM-C1 cells via a lysosome-mediated pathway.