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Aim To study the protective effect of the compound flavones on chronic alcohol induced testicu-lar damage in mice. Methods One hundred SPF C57 BL/6 mice were randomly divided into 5 groups:normal control group, chronic alcohol group, alcohol+low-dose drug group, alcohol+high dose drug group, and drug control group. Chronic alcohol testicular inju-ry model in mice was established by intragastric admin-istration of increasing dose of alcohol every four weeks for 6 months, meanwhile compound flavone interven-tion was in process. The activity of super oxide dis-mutase( SOD) , the levels of malondialdehyde( MDA) and testosterone in testicular tissue were measured. HE staining was used to observe testicular histomorpholo-gy, and ultrastructure changes were detected by elec-tron microscope. Results In chronic alcohol group, MDA content was obviously increased, while SOD and testosterone levels were decreased compared with nor-mal control group ( P <0. 05 ) . In addition, germinal epithelium, support cells and sperm production at all levels showed degraded degeneration in chronic alcohol group. However, compound flavonoids could success-fully reverse alcohol-induced testicular damage in a dose-dependent way. Conclusion The compound of flavones may have therapeutic potential for alcohol-in-duced testicular injury through inhibiting lipid peroxi-dation and increasing the level of testosterone.
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Objective To investigate the protective effect of icariin against varicocele-induced damage on rat epididymis. Methods Forty adolescent male SD rats were randomly divided into control group (n=10), experimental varicocele (EV) group (n=15), icariin (ICA) therapy group (n=15). Experimental varicocele model in the EV group and ICA group was established. The EV was induced by partial ligation of the left renal vein. The rats in the control group underwent a sham operation that separated the spermatic vessels without ligation. Each rat in the control group and EV group was lavaged with 2 mL physiological saline every day for 6 weeks. Each rat in the ICA group was lavaged with icariin [100 mg/(kg·d)] for 6 weeks. Rats in all groups were executed after 6 weeks. The contents of sialic acid were measured by spectrophotometry. Carnitine concentrations were measured by DTNB. HE stain was used to observe the microstructure changes in the epididymal tissue. Electron microscopy was used for observing the ultrastructural changes of the epididymis. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) method was used to detect the apoptosis of the epididymal epithelium. Results Compared with the control group, the microstructure and ultrastructure of the epididymis in EV group showed pathological damage. Compared with the EV group, the damage of the epididymal microstructure and ultrastructure significantly alleviated. Apoptosis index (AI) of epididymal epithelium in the EV group was significantly higher than that in the control group (P<0.01). However, AI of epididymal epithelium in the ICA group was significantly lower than that in the EV group (P < 0.01). The sialic acid and carnitine concentrations of the epididymis in the EV group was significantly lower than that in the control group (P < 0.01), respectively. However, the sialic acid and carnitine concentrations of the epididymis in the ICA group was significantly higher than that in the EV group (P < 0.01), respectively. Conclusion This study indicates that varicocele could result in the apoptosis of epididymal epithelium and icariin decreased the varicocele-induced apoptosis , suggesting that varicocele could damage the structure and function of epididymis, which can be repaired by icariin.
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<p><b>OBJECTIVE</b>To study chemical constituents of aerial parts of Gueldenstaedtia stenophylla.</p><p><b>METHOD</b>Chemical constituents were extracted with 95% alcohol and separated by repeated silica gel column, MCI, Sephadex LH-20 and RP C18 column chromatographic separation from aerial parts of G. stenophylla. Their structures were identified on the basis of the physiochemical properties and spectral data.</p><p><b>RESULT</b>Twenty-two compounds were separated and identified as apigenin (1), chrysoeriol (2), farnisin (3), diosmetin (4), 4', 7-dihydroxyflavone (5), luteolin (6), 3', 4', 7-trihydroxyflavone (7), quercetin (8), m-hydroxy benzoic acid (9), trans-ferulic acid (10), isovanillic acid (11), E-beta-hydroxy-cinnamic acid (12), salicylic acid (13), trans-p-coumaric acid (14), protocatechuic acid (15), (S) -2-hydroxyphenylpropionic acid (16), esculetin (17), 7-methoxy coumarin (18), phaseic acid (19), blumenol A (20), (6S, 9R)-roseoside (21), kaempferol-7-O-alpha-L-rhamnopyranoside (22).</p><p><b>CONCLUSION</b>Except compounds 1, 5, 8 and 15, the rest compounds were separated from genus Gueldenstaedtia for the first time.</p>
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Fabaceae , ChemistryABSTRACT
The status of current clinical probation teaching is not satisfactory,so it is essential to establish and perfect clinical teaching mode based on laws and guide students to properly handle the relationship among the internship,employment and preparation for the examination for postgraduates,reform the clinical teaching system,strengthen the training and education of medical ethics and quality,integrate the clinical teaching resources and make full use of clinical cases,as well as strengthen the internship management so as to ensure the quality of teaching of clinical internship.
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BACKGROUND: Calcitonin gene-related peptide(CGRP) can relieve myocardial ischemia-reperfusion injury. Because adrenomedulin(Adm) and CGRP share certain structural homology, it is assumed that Adm might have protective effect on myocardium.OBJECTIVE: To investigate Adm' s inhibitory effect on vascular cell adhesion molecule-1 (VCAM-1) expression in ischemia-reperfusion rats and its protective effect on myocardial ischemia.DESIGN: A randomized paired design using ischemia-reperfusion model of SD rats.MATERIALS: The experiment was conducted in the Experimental Animal Center of Xianning Medical College from December 2003 to May 2004. Twenty-four healthy male SD rats were selected.METHODS: The hearts of the rats were removed to make into ischemia-reperfusion model and then randomized to control group, Adm1-50(1× 10-9) mol/L group, Adm1-50(1 × 10-8) mol/L group and Adm1-50(1 × 10-7) mol/L group. After the hearts underwent ischemia for 60 minutes, the hearts in control group were reperfused with oxygenation Kerbs-Henseleit bicarbonate(KHB) for 60 minutes while those in the other three groups had reperfusion with oxygenation KHB and Adm1-50( 1 × 10-9),(1 × 10-8), and(1 × 10-7) mol/L, respectively, for 15 minutes and KHB perfusion for another 45 minutes. The liquid flowing from the coronary artery was collected, and the content of creatine kinase isoenzyme was detected. Myocardium in the left ventricle was collected for RNA extraction, and the expression of VCAM-1m RNA was determined with reverse transcription-polymerase chain reaction method.MAIN OUTCOME MEASURES: The expression of myocardial VCAM-1mRNA in control group and groups of different concentrations of Adm1-50.RESULTS: After electrophoresis, each group was found to have an obvious amplified band at 194bp, which was GADPH mRNA amplified segment, and the expression of GADPH mRNA in each group was the same. VCAM-1 mRNA amplified segment with strong brightness and clear border was found at 334bp in control group and Adml-50 (1 × 10-9) mol/L group. The brightness of VCAM-1 mRNA amplified band decreased significantly in Adm1-50(1 × 10-8) mol/L group whereas slight brightness and obscure amplified band was found in Adm1-50(1 × 10-7) mol/L group. The gray value of amplified VCAM-1mRNA and GAPDH mRNA in Adm1-50(1 × 10-8)group and(1 × 10-7) mol/L group was 0.6 ±0.31 and 0.5 ±0.36, respectively, which was obviously lower than that in control group( 1.2 ± 0. 52) ( P＜ 0. 05).CONCLUSION: Adm1-50 may inhibit the expression of myocardial VCAM-1mRNA in myocardial ischemia-reperfusion in a dose-dependent manner.
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Objective: To investigate the effects of adrenomedullin1-50 (Adm1-50) on vascular cell adhesion molecule-1 (VCAM-1) expression in isolated rat heart. Methods: Twenty-four male Sprague-Dawley rat, weighting 300 to 350g, were randomly divided into A, B, C, D group (n=6 for each group). The isolated rat hearts were perfused in a Langendorff mode for 20 min and followed by 60 min of global ischemia. Then, all groups were reperfused with Kerbs-Henseleit bicarbonate for 60 min, but group B, C, D were perfused with buffer in the presence of Adm1-50 10-9mol/L, 10-8mol/L, and 10-7mol/L respectively for 15 min after the onset of reperfusion. The post-ischemic change of creatine kinase-isoenzyme (CK-MB) in coronary effluent and the expression of myocardial VCAM-1 mRNA were measured. Results: After I/R, Adm1-50 dose-dependently decreased the expression of VCAM-1 and the CK-MB activity, The ratio of VCAM-1/GAPDH mRNA were 1 20?0 52, 1 10?0 45, 0 60?0 31, 0 50?0 36 for group A, B, C, D, respectively (P
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Aim To investigate the effects of Ginkgo biloba extract(EGB)on tumor necrosis factor-alpha(TNF-?)in TNBS-induced colitis in rats and its mechanisms.Methods Colitis in rats was induced by colonic administration with 2,4,6-trinitrobenzene sulfonic acid(TNBS).Wistar rats were randomly divided into four groups,10 in each:normal group,model group,5-aminosalicylic acid(5-ASA group)and Ginkgo biloba extract group(EGB group).The levels of nitric oxide(NO),and glutathion peroxide(GSH-Px)were measured by biochemical methods.The expressions of TNF-? and nuclear factor kappaBp65(NF-?Bp65)in the colon tissues of colitis rats were detected by means of immunohistochemistry.The expressions of induce nitric oxide synthase(iNOS)in the colon tissues of colitis rats were detected by reverse transcription polymerase chain reaction(RT-PCR).The effects of EGB on colonic inflammation and macroscopic and histological damage were evaluated as well.Results Compared with the model group,treatment with EGB for 4 weeks significantly reduced colon macroscopic and histological damage,elevated the activities of GSH-Px and reduced the contents of NO,inhibited the protein expressions of TNF-? andNF-?Bp65,and decreased the mRNA levels of iNOS in the colon tissues of experimental colitis.Conclusions The probable mechanisms of EGB was that it ameliorated inflammatory injury in TNBS-induced colitis in rats by its reduction of TNF-?,NF-?Bp65 and iNOS levels.Then EGB could curb the inflammatory cascade effects of inflammatory mediators to protect ulcerative colitis.