Catecholamines ; blood ; Heart Rate ; Humans ; Water Sports ; physiology

Blood Chemical Analysis ; Humans ; Water Sports ; physiology

Animals ; Hippocampus ; metabolism ; Long-Term Potentiation ; Male ; Neurogranin ; biosynthesis ; Rats ; Rats, Wistar ; Sleep Deprivation ; metabolism

Objective To investigate the effect of propofol on LPS-induced TLR4 expression in rat alveolar type Ⅱ epithelial cells. Methods The primarily cultured alveolar type Ⅱ epithelial cells isolated from male rats were randomly assigned to one of 5 groups: group Ⅰ cells were incubated for 3 h without any additive (control) ; group Ⅱ cells were incubated with LPS 1 μg/ml for 3 h (LPS) ; group Ⅲ , Ⅳ , Ⅴ cells were incubated with LPS 1 μg/ml + propofol 25, 50 and 100 μmol/L respectively for 3 b (P1-3). TLR4 mRNA and TLR4 protein expression was detected by real time PCR and Western blot. TNF-α release amount was measured using ELISA. Results LPS significantly' increased TLR4 mRNA and protein expression in alveolar type Ⅱ epithelial cells as well as TNF-α release amount. Propefol at 50 and 100 μmol/L significantly inhibited LPS-imluced increase in TLR4 mRNA and protein expression and TNF-α release amount. Conclusion Propofol can dose-dependently inhibit LPS-induced inflammation in alveolar type Ⅱ epithelial ceils, through down-regnlation of TLR4 gene and protein expression.

The paper aims to explore the studying method for the pharmacokinetics of drugs in target organs, the pharmacokinetic process of tramadol hydrochloride in the extracellular fluid of frontal cortex (FrCx) of mice was investigated. Six male mice (Kunming strain) were anaesthetized (urethane, 1.8 g x kg(-1), ip) and secured on a stereotaxic frame. A microdialysis probe was implanted into the FrCx and perfused with artificial cerebrospinal fluid at a flow rate of 2 microL x min(-1). One hour later, mice were administrated (ip) with tramadol hydrochloride (50 mg x kg(-1)) and dialysates were collected continuously at 12-min intervals (24 microL each) for 6 h. The tramadol concentration in dialysates was determined by HPLC-Ultraviolet detection method, and the concentration-time curve and pharmacokinetic parameters of tramadol were calculated with DAS software. The results showed that the pharmacokinetic process of tramadol in the FrCx extracellular fluid of mice was fitted to a two-compartment open model, and the main pharmacokinetic parameters t1/2alpha, t1/2beta, t(max), C(max) and AUC(0-infinity) were (0.27 +/- 0.05) h, (2.72 +/- 0.24) h, (0.50 +/- 0.10) h, (2 110.37 +/- 291.22) microg x L(-1) and (4 474.51 +/- 441.79) microg x L(-1) x h, respectively. In conclusion, a studying method for pharmacokinetics of drugs in the target organ is established, which is simple and feasible. Tramadol hydrochloride shows a two-compartment model in the extracellular fluid of the mouse FrCx, and the distribution- and elimination half-life are 0.5 h and 2.7 h, respectively.

To guide the reasonable clinical application of modafinil (MOD), pharmacokinetics and pharmacodynamics of MOD in mice and the correlation between them were investigated. Male mice (Kunming strain) were given a single oral dose of MOD (120 mg x kg(-1)). The plasma concentration of MOD was measured by HPLC and the pharmacokinetic parameters were calculated with DAS 3.0 software. For another batch of male Kunming strain mice, their locomotor activities were recorded by an infrared ray passive sensor after a same oral dose of MOD, and the synchronization and correlation between the changes of MOD plasma concentration and the locomotor activity induced by MOD were compared and analyzed. The results showed that the plasma concentration-time curve of MOD was fitted to two-compartment open model with a first order absorption. The main pharmacokinetic parameters t1/2alpha, t1/2beta, t(max), C(max) and AUC(0-inifinity) were 0.42 h, 3.10 h, 1.00 h, 41.34 mg x L(-1) and 142.22 mg x L(-1) x h, respectively. MOD significantly increased locomotor activity and the effect lasted for about 4 h. The changes of MOD plasma concentration and the locomotor activity induced by MOD were synchronous. In conclusion, there is a significant correlation between the effect of MOD and its plasma concentration after administration of 120 mg x kg(-1) in mice.

Objective To explore the effects of chronic fluorosis on neurons in the cerebral cortex of rats,and to provide some morphological evidence of damage in the central nervous system induced by chronic fluorosis.Methods Male Wistar rats 40 days after birth were fed with high fluoride contented water(100 mg/L)for inducing chronic fluorosis.Immunocytochemistry and in situ hybridization were used to detect c-fos and Caspase 8 at cerebral cortical neurons respectively.Results c-fos positive cells rate and gray scale in the cerebral cortex of chronic fluorosis were 35.8%and 0.2756±0.0241,respectively,and that of control group were 32.1%and 0.2774±0.0331with statistical difference(χ2=0.305,t=0.826,P＞0.05).Caspase 8 positive cells rates of fluorosis group and control group were 18.7%and 14.1%,respectively,the difference being statistically significant(χ2=0.419,P＞0.05).The gray scale of fluorosis group and control group were 0.3874±0.0329 and 0.3884±0.0323,respectively,the difference being statistically significant(t=0.641,P＞0.05).Conclusion Chronic fluorosis had no significant influence on apoptosis of cerebral cortical neurons.

Objective To explore the relationship between the expression of basic fibroblast growth factor (bFGF) and microvessel density(MVD)in non-small cell lung cancer.Methods The expression of bFGF and MVD were observed in 54 eases of NSCLC were detected with in situ hybrldization and immunohistochemical detection.Resuits The expression of bFGF and MVD was greater in adenecarcinomas than in squamous cell carcinomas of NSCLC (P＜0.05).The expression of bFGF was significantly different among the three groups of both squamous cell carcinomas and adenocarecnomas with varying differentiation (P＜0.05).There was hisher bFGF expression and greater MVD in NSCLC patients with regional lymplmode involvement and those with laterdistant metastasis(P＜0.05).Condusion bFGF may play an important role in tumor angiogenesis and lymphatic metastasis of human NSCLC,and detection of bFGF may be a good metastasis and prognostic predictors for human NSCLC.

Objective To investigate the effects of Dihuang-Yinzi on cognition and energy metabolism of AD (Alzheimer’s disease) mice. Methods 60 Male APPsw/PS1ΔE9 mice were divided into 5 groups model, positive drug (Aricept), high, medium and low dosage of Dihuang-Yinzi. C57BL/6J mice with same age were served as normal control. All groups were orally administrated for 150 days. The spatial memory and passive avoidance were measured. The energy charge, activity of complex I, II and IV of respiratory chain, enzymatic activity of ATPase and mitochondrial membrane potential were assayed. Results APPsw/PS1ΔE9 mice showed significant impairments in cognition and energy production [(0.39±0.02),(3.28± 0.37)μOD/(min?μg),(0.19±0.04)mOD/(min?μg),(0.26±0.03)mOD/(min?μg),(0.19±0.02),(0.30±0.03)、(3.49±0.73)]with compaired to normal control[(0.57±0.06),(8.74±1.57)μOD/(min?μg),(0.43± 0.02)mOD/(min?μg),(0.69±0.02)mOD/(min?μg),(0.65±0.02),(0.51±0.01),(7.41±1.28)]. Dihuang-Yinzi ameliorates cognition decline, promotes acitivity of energy production related enyzmes, and restores mitochondrial membrane potential in AD mice[(0.57 ± 0.07),(8.42 ± 1.74)μOD/(min ?μg),(0.64 ± 0.03)mOD/(min?μg),(0.68±0.04),(0.55±0.01),(6.69±1.03), P<0.01 or 0.05]. Conclusion Dihuang-Yinzi could improve cognition and energy metabolism of APPsw/PS1ΔE9 mice by protecting mitochondria from pathologic injury.

Objective To evaluate the role of delta and kappa opioid receptors in sufentanil preconditioning (SPC)-induced attenuation of myocardial ischemia-reperfusion (I/R) injury in rats.Methods Forty adult male Sprague-Dawley rats,aged 2-3 months,weighing 250-330 g,were randomly divided into 5 groups (n =8 each) using a random number table:sham operation group (group S),group I/R,group SPC,δ receptor antagonist naltrindole + SPC group (NTD + SPC group),and κ receptor antagonist nor-binaltorphimine (nor-BNI) + SPC group (BNI + SPC group).Myocardial I/R was induced by 30 min occlusion of left anterior descending branch of coronary artery followed by 120 min reperfusion.In group SPC,5 min infusion of sufentanil 3μg/kg was repeated 3 times at 5 min interval before myocardial ischemia.In NTD + SPC group,naltrindole 5 mg/kg was intravenously injected,at 10 before SPC.In BNI + SPC group,nor-BNI 5 mg/kg was injected intravenously at 15 min before SPC.Arterial blood samples were collected at 120 min of reperfusion for measurement of the serum cardiac troponin I (cTnI) and creatine kinase isoenzyme-MB (CK-MB) concentrations.The rats were then sacrificed and hearts removed for determination of myocardial infarct size (IS) and area at risk (AAR).IS/AAR ratio was calculated.Results Compared with S group,the serum cTnI and CK-MB concentrations were significantly increased in I/R,NTD + SPC and BNI + SPC groups,and the serum CK-MB concentrations were increased in SPC group,and IS/AAR ratio was increased in I/R group (P ＜ 0.05 or 0.01).The serum cTnI and CK-MB concentrations were significantly lower in SPC,NTD + SPC and BNI + SPC groups and IS/AAR ratio was lower in SPC and BNI + SPC groups than in I/R group,and higher in NTD + SPC and BNI + SPC groups than in SPC group (P ＜ 0.05 or 0.01).Conclusion Both κ and δ opioid receptors mediate SPC-induced attenuation of myocardial I/R injury in rats.