Currently, about 300 million people worldwide are affected by asthma. Most of these sufferers inhale immunosuppressants (ie corticosteroids) and beta-adrenergic receptor agonists for their asthma treatment. However, about 5%-10% of patients of asthma have poor response to such treatment. Investigation of kinase signaling pathway and nuclear transcription factor as a target molecule in the treatment of allergic asthma has been the concern of scholars home and abroad. This paper reviewed inhibitors of kinase signaling pathway and nuclear transcription factors for the treatment of asthma.

Objective To study the effect of Xinji Huoliyin on the apoptosis of myocardial cell and apoptosis-related gene expression of experimental dilated cardiomyopathy rats, and explore its mechanism. Methods Sixty animals were randomly divided into 6 groups. Dilated cardiomyopathy model was made by injecting adriamycin. Experimental rats were given Xinji Huoliyin and Huangqi Shengmaiyin respectively. The genic expression of p53 and Fas was tested by S-P immunohistochemistry technique after 4 weeks. Results The apoptosis rate of myocardial cell of model group was higher than that of normal group (P

Proliferation and differentiation of neural stem cells is regulated by autologous or external, adjacent or remote cell signaling pathways. This paper reviewed the studies about the Notch, BMP, Wnt, Shh signaling pathways related to brain neurogenesis.

This article was aimed to study the protective effects and mechanism of resveratrol (Res) on endothelial injury induced by atherosclerosis ( AS ) . Lysophosphatidylcholine ( LPC ) was applied to induce the model of injured endothelial cells. Flow cytometer was used to detect the rate of cell apoptosis. TUNEL staining was used to detect the cell apoptosis. MTT colorimetric test was used to detect the cell viability. Automatic biochemistry analyzer was used to measure the LDH level . ELISA was used to detect TNF-α level . RT-PCR was used to determine the mRNA levels of calcitonin gene-related peptide (CGRP). The results showed that Res with the concentration of 20 μmol/L can effectively slow down the degree of endothelial cell injury induced by LPC which caused the cell disability, high LDH level and high TNF-α level (P < 0.01). Res showed effects on mRNA expression of CGRP. It was concluded that Res can protect against endothelial injury induced by AS, the mechanism of which may be associated with accelerating CGRP synthesis and release by activating VR1.

AIM: To investigate the functions of GR in the course of hepatic secondary injury after severe multiple injury. METHODS: Rat model was produced by adopting severe thoracic impact injury accompanied with mono-side femur fracture, and glucocorticoid receptor was blocked before severe multiple injury. Hepatic macropathology and alterations under light microscope were examined. Maximal binding volume of glucocorticoid receptor (GR) in hepatic tissue was assayed by radio-ligand binding assay and protein content was assayed by Western blot. RESULTS: Maximal binding volume and protein content of GR were gradually decreased in hepatic tissue after severe multiple injury, obviously lower than that in normal control at 4 h after trauma ( P

Electronics ; organization & administration ; Health Promotion ; Humans ; Occupational Health Services

Objective To study the effects of the inhibition of nuclear factor kappa-B ( NF-κB) , on the hepatic heat shock protein 70 (HSP70) expression as well as on the changes of hepatic function and ultrastructure in a rodent model of hemonhageic shock. Method Hemorrhagic shock was produced by inducing bilateral femoral fractures in male Wistar rats. Intraperitoneal injection of pyrrolidine dithiocarbamate(PDTC)was used to inhibit NF-κB activation 1 hour before induction of shock. A total of 66 adult male Wistar rats were randomly divided into 3 groups: control group (Control, n = 6), trauma shock (TS, n = 30), and NF-κB inhibition followed by trauma shock (NF-κB inhibition, n =30). Measurements of hepatic NF-KB and HSP70, hepatic function bio-markers, TNF-α and IL-6 were obtained 0.5, 2, 4, 6, 8 hours after trauma. Histopathological changes in liver tissues were also noted. Hepatic expression of NF-κB was determined by using electrophoretic mobility shift assay, while HSP70 was assayed by western blot and analyzed with computer imaging. Results In rats with trauma shock, both hepatic NF-κB activity and HSP70 expression increased significantly compared to the control group, reaching peaks at 6 hour post injury. Serum alanine transferase (ALT) and total bilirubin (TB) also rose significantly,reaching peaks at 8 hours post trauma. Light microscopy revealed hepatic congestion with infiltration of inflammatory cells into hepatic sinusoid in the TS group at 8 hours. Inhibiting the activity of NF-κB one hour before trauma significantly decreased expression of HSP70 at 6 hours post trauma [16.9±4.4 (NF-κB inhibition) vs. 23.0±1.7 (TS), P ＜ 0.05]. In addition,levels TNF-α and IL-6 in the liver tissue also decreased, and hepatic congestion as well as hepatic cell degeneration were ameliorated, showing minimal inflammatory infiltrates in the hepatic sinusoids. NF-κB inhibition also significantly lowered the levels of ALT and TB at 4 hours post trauma [ALT, 540.8 ±66.2 nmol/L (NF-KB inhibition) vs. 640.6±80.2 nmol/L (TS), P ＜ 0.05; TB,2.3±0.3 mol/L (NF-κB inhibition) vs. 4.7 ±1.1 mol/L (TS), P ＜ 0.05]. Conclusions NF-κB and HSP70 are involved in the pathogenesis of hepatic injury during hemorrhagic shock, and the degree of NF-κB activity and HSP70 expression may be consistent with the extent of hepatocellular damage. Inhibition of NF-κB helps ameliorate liver injury due to trauma shock.

Objective To investigate the protecting mechanism of heat stress pretreatment on acute lung injury(ALI). Methods The oleic acid ALI mouse model was built to dynamically observe the binding capacity and the binding affinity of glucocorticoid receptor(GR),the levels of GR,heat shock protein 90(Hsp90)and Hsp70 before and after hyperthermic stress pretreatment. Results Heat stress pretreatment had significant protective effect on ALI.Western blotting showed insignificant changes of GR levels but progressive increase of level of Hsp70 and Hsp90.Heat stress pretreatment exerted insignificant effect on Bmax and Kd of GR,shown by radio ligand binding assay after ALI. Conclusion The protective effects of heat stress pretreatment on ALI of mouse may relate to its ability of keeping stable GR level and increasing levels of Hsp70 and Hsp90.

ObjectiveTo investigate the mechanism of dexamethasone (Dex) in inhibiting monocyte adhesion and phagocytose function.Methods Under the stimulation of phorbo1-12-myristate-13-acetate (PMA),U937 monocytes cultured in vitro were treated with Dex and Fasudil respectively.The adhesion rate of U937 monocles to human umbilical vein endothelial cells (HUVECs) and their phagocytic ability of India ink were studied.The protein content and activity of rho-associated coiled-coil protein kinase 1 ( ROCK1 ) as well as the effects of mifepristone and cycloheximide on Dex were determined.ResultsBoth DEX and Fasudil could significantly inhibit the adhesion tate and phagocytosis of U937 cells stimulated by PMA and suppressed the activity of ROCK1.While mifepristone and cycloheximide could not alter these effects of DEX.ConclusionDEX interferes with the adhesion and phagocytosis function of U937 cells by inhibiting ROCKI activity.

Objective To investigate the effects of morroniside on the expression of vascular endothelial growth factor (VEGF) and fi-broblast growth factor-2 (FGF-2) in rat cortex after focal cerebral ischemia-reperfusion. Methods 30 male Sprague-Dawley rats were ran-domly divided into sham group, model group, morroniside-low group (30 mg/kg), morroniside-middle group (90 mg/kg) and morroni-side-high group (270 mg/kg). Middle cerebral arteries of rats were occluded for 30 minutes with Longa's method and re-perfused. The ex-pression of VEGF and FGF-2 in the ischemic ipsilateral cortex was detected with Western blotting 7 days after reperfusion. Results The ex-pression of both VEGF and FGF-2 increased in the ischemic ipsilateral cortexin in all the ischemic groups compared with the sham group (P<0.05). The expression of VEGF further increased in a dose-dependent manner in all the morroniside groups compared with that of model group (P<0.05), and the expression of FGF-2 increased in the morroniside-high group (P<0.001). Conclusion Morroniside could increase the expression of VEGF and FGF-2 after ischemia-reperfusion, which might promote angiogenesis.