Acupuncture Therapy ; Adult ; Female ; Hip ; innervation ; Humans ; Male ; Middle Aged ; Nerve Compression Syndromes ; therapy ; Young Adult

Expression of the GST-? in 51 cases of lung cancer was researched by quantitative RT-PCR. The results suggested that the expression of GST-? was significantly higher in lung cancer than in normal tissues adjacent to cancer, and tumoral native resistance might be dominant in tumoral resistance to chemotherapeutic drugs. No relationship was found between GST-? expression and clinicopathological parameters including tumor class, stage and differentiation. The study of GST-? expression is of importance in the evaluation of tumoral resistance to anticancer drugs.

Aim To investigate the effects of sesamin on inflammation response of asthma and to explore its possible mechanism of action. Methods Forty male BALB/c mice were randomly divided into five groups with 8 mice in each group: normal group, ovalbumin ( OVA) group, sesamin low dose group, sesamin high dose group and dexamethasone( DXM) group. Asthma model mice were induced by OVA in vivo. The left lung was isolated for pathological examination. Experi-ment of ELISA and Western blot were used to deter-mine the effect of sesamin on IL-4 , IL-5 , IL-13 and IFN-γ expression. Hematoxylin and eosin stain was used to investigate pathological examination in lung tis-sue. Western blot was performed to detect the IκBαphosphorylation and NF-κB nuclear translocation. Re-sults The mice developed the following pathophysio-logical features of asthma: increased numbers of in-flammatory cells, increased levels of IL-4, IL-5 and IL-13 , decreased level of IFN-γ in bronchoalveolar lavage fluids ( BALF ) and lung tissues ( P <0. 05 ) , and increased IκBα phosphorylation and NF-κB nucle-ar translocation in lung tissues ( P <0. 05 ) . Adminis-tration of sesamin markedly reduced airway inflammato-ry cell recruitment, reduced the production of IL-4, IL-5 , IL-13 and increased IFN-γ in BALF and lung tissues( P <0. 05 ) . The increased IκBα phosphoryla-tion and NF-κB nuclear translocation after OVA inhala-tion were inhibited by the administration of sesamin. Conclusion Sesamin attenuates inflammation re-sponse of asthma through suppression of NF-κB activa-tion.

Objective To investigate the relationship between nuclear factor(NF)-κB activity and lactacystin induced prostate cancer cell apoptosis.Methods Two prostate cancer cell were divided into two groups:blank control group treated with culture solution,lactacystin group treated with different concentration of lactacystin(0.5,1.0,2.0,4.0 μ mol/L),the action time were 8,16 and 24 hours.The cell survival rate was measured by MTT assay.NF-κB DNA binding activity was measured by enzyme-linked immunosorbent assay,the expression of NF-κB P65 nuclear protein was detected by Western blot assay,and caspase-3 activity was analyzed by enzyme analysis assay.Results On basal condition,the NF-κ B DNA binding activity was much higher in DU145 cell than that in LNCaP cell(t=4.728,P=0.001).Compared with blank control group,different concentration of lactacystin groups'NF-κ B DNA binding activity in both the LNCaP and DU145 cell were reduced.The expression of NF-κB p65 nuclear protein decreased along with raising of lactacystin concentration in LNCaP cell,but it did not change in DU145 cell.On basal condition,caspase-3activity in DU145 cell was higher than that in LNCaP cell(t=4.519,P=0.001).After lactacystin acting of 24 hours,caspase-3 activity increased along with raising of lactacystin concentration in both the LNCaP and DU145 cell(2.0 μmol/L lactacystin group compared with 1.0 μmol/L lactacystin group,DU145 cell P=0.000,LNCaP cell P=0.000).Conclusions Lactacystin has different killing effects on prostate cancer cell.The mechanism may be related to inducing the apoptosis by down-regulation of NF-κB activity.There may be additional cell survival/death pathway in androgen-independent prostate cancer cell.

AIM:To investigate the effects and mechanisms of sphingosine-1-phosphate receptor-2 (S1P2R) on lipopolysaccharide (LPS)-induced acute lung injury (ALI).METHODS:ALI model was induced by intratracheal ad-ministration of LPS in both wild-type mice and S1P2R-deficient mice.The pathological changes in the lung tissues were ob-served, and the protein concentration , total cell number, neutrophil ratio, TNF-αlevel and IL-6 level were determined in the bronchoalveolar lavage fluid (BALF) 24 h after LPS injection.In order to investigate the mechanisms of S1P2R in LPS-induced ALI, 10 min before LPS injection, both wild-type mice and S1P2R-deficient mice were injected with nitric oxide synthase inhibitor by tail vein injection , the pathological changes of the lung tissues were observed , and the protein concen-tration and total cell number in BALF were determined 12 h after LPS injection .RESULTS: Compared with wild-type mice, S1P2R-deficient mice showed more severe LPS-induced ALI, and the protein concentration , neutrophils and inflam-matory cytokines in BALF were significantly increased in S1P2R-deficient mice.Administration of nitric oxide synthase in-hibitor Nω-L-nitro-arginine methyl ester protected S1P2R-deficient mice from aggravation of ALI .CONCLUSION:S1P2R mediates the protection from LPS-induced ALI possibly through inhibiting nitric oxide synthase .

This study is to investigate the anti-allergic effect of anthocyanidin and to explore its possible mechanism. The experiments of passive cutaneous anaphylaxis reaction (PCA) and colorimetry were used to determine the effect of anthocyanidin on degranulation of mast cells in vivo. For in vitro study, various concentrations of anthocyanidin (100, 50 and 25 micromol x L(-1)) were added to the culture medium of mast cells cultured with 100 microg x L(-1) of dinitrophenyl (DNP) specific IgE overnight. The azelastine (100 micromol x L(-1)) was selected as the positive control. The antigen (DNP-human serum albumin, DNP-HAS)-induced release of degranulation was measured by enzymatic assay, histamine was determined by EIA, and interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were measured by Western blotting, separately. In addition, the effects of anthocyanidin on phosphorylation of NF-kappaB, p38MAPK and Akt were observed by Western blotting. The results showed that treatments with anthocyanidin (100 and 50 mg x kg(-1)) were followed by a decrease in PCA of rats. Anthocyanidin (100 and 50 micromol x L(-1)) obviously suppressed the degranulation from mast cells, whereas results from anthocyanidin (100 and 50 micromol x L(-1)) group indicated significant inhibitory effect on histamine, the calcium uptake, TNF-alpha, IL-6, phosphorylation of NF-kappaB, p38MAPK and Akt of mast cells induced by antigen. Anthocyanidin may suppress the anaphylactic reaction by inhibiting the action of mast cells. NF-kappaB, p38MAPK and Akt at least in part contribute to this event.

In order to provide us new clues to induce some endogenous protective molecular mechanisms, the changes in gene expression profile induced by ischemia-reperfusion in pulmonary tissues of rats were investigated and the dynamic mechanism of pulmonary ischemia-reperfusion injury was elucidated. Thirty male Wistar rats were randomly divided into 6 groups: 5 ischemia-reperfusion (I/R) groups (I/R 0-h, I/R 1-h, I/R 3-h, I/R 6-h, I/R 24-h) and control group (n=5 in each). An in situ ischemia-reperfusion lung injury rat model was established by occluded hilus of lung. The RatRef-12 Expression Beadchip (22 226 gene probes per array) was used to analyze the pattern of gene expression in all groups. The results showed that 648, 340, 711, 1279 and 641 genes were differentially expressed in I/R 0-, 1-, 3-, 6-and 24-h groups respectively. The differentially expressed genes were classified as following 7 functional categories: cytokine, adhesion molecule, growth factor and apoptosis-related factor, oxidation and antioxidation molecule, metabolic enzyme, ion channel and aquaporin, signal transduction molecule. It was suggested that gene chip technology was an effective and quick method for screening differentially expressed genes. Many differentially expressed genes with different functions interacted each other to result in pulmonary ischemia-reperfusion injury.
Gene Expression Profiling ; Lung/*blood supply ; Random Allocation ; Rats, Wistar ; Reperfusion Injury/*genetics

Objective To assess the influence of community intervention on blood pressure and quality of life in aged patients with hypertension.Methods A total of 378 elderly hypertensive patients received community intervention with anti-high blood pressure agents for one year.Before and after intervention,blood pressure was recorded and genetic quality of life inventory(GQOLI-74),symptom checklist(SCL-90),self-rating anxiety scale(SAS),and self-rating depression scale(SDS)were carried out on the basis of giving unite guiding words.Results In addition to blood pressure degraded,the blood pressure control rate was improved after intervention(67.7% vs.40.1% before intervention,x2=57.59, P<0.05).Observation items of body health dimension,psychological health dimension,social function dimension were better than those recorded before intervention(P<0.05).But difference of the material life dimension was not statistically significant(P>0.05).With 41 scores as a SDS rude mark to judge the depression incidence.the incidence was decreased from 22.7% before intervention to 12.5%after intervention(x2=12.565,P<0.05).Conclusions Community intervention is a practical and valuable strategy for controlling high blood pressure and improving quality of life in aged patients.

Aim To study the effects of pyrin recombi-nant protein ( PRP ) on VEGF/VEGFR2/ MMP-9 sig-naling pathway in bleomycin-induced pulmonary fibro-sis of rats. Methods Sixty male Wistar rats were ran-domly divided into groups of control ( n=10 ) , model ( n=20 ) , PRP ( n=20 ) , and SU5416 ( n=10 ) . All the rats, except for those in control group, were estab-lished as the model of interstitial pulmonary fibrosis by perfusion of bleomycin (5 mg·kg-1 ) through tracheal intubation. From the second day after modeling, all rats were intragastrically administered with drugs or sa-line, according to different groups designed. The rats were sacrificed on the 14th and 28th day, and lung samples were taken out. The pathological changes of interstitial pulmonary fibrosis were observed by HE staining and Masson staining to evaluate the degree of alveolitis and pulmonary fibrosis. Expressions of VEGF, VEGFR2, MMP-9 protein and mRNA were de-tected by immunohistochemistry and RT-PCR. Results On the 14th and 28th day, the alveolitis, pulmonary fibrosis, expression of VEGF, VEGFR2, MMP-9 and mRNA increased significantly in the model group com-pared with in the control group ( P <0. 05 ) , and de-creased significantly in PRP group than those in the model group ( P <0. 05 ) . Conclusion PRP plays a role of anti-pulmonary fibrosis via the down-regulation of VEGF/VEGFR2/MMP-9 signaling pathway.