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OBJECTIVE This study aimed to investigate the role and mechanism of Astragaloside IV (AS-IV)in rats with myocardial infarction.METHODS The myocardial infarction model was established by ligation of the left anterior descending artery. The rats were randomly divided into sham, DMSO, model group, AS-IV and CID755673 groups. The rats were sacrificed 4 weeks later, and segmental heart samples were used for hematoxylin and eosin staining and masson staining. The expression of PKD1, HDAC5 and VEGF were analyzed using immunohistochemistry, reverse transcription poly-merase chain reaction and western blot. RESULTS Compared with the sham operation and DMSO groups,morphology of myocardium in model group was disordered,accompanied with necrotic myocar-dial cells and obvious collagen tissues. After treatment with AS-IV, the morphology of myocardium was obviously improved, and the number of new blood vessels increased significantly. However, after treatment with CID755673, the myocardial tissue of rats became disordered again, the necrotic cells increased, and some vessels closed. The expression levels of PKD1, HDAC5 and VEGF mRNA and protein in myocardial tissue of model group were significantly lower than the other four groups(P<0.05), whereas these levels in the AS-IV group were significantly higher than those in the other four groups (P<0.01). Additionally, the CID755673 group had significantly higher levels of PKD1, HDAC5 and VEGF mRNA and protein than the sham group, DMSO group and model group (P<0.05). CONCLUSION AS-IV may partly promote the angiogenesis of myocardial tissue in rats with myocardial infarction via the PKD1-HDAC5-VEGF pathway.
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AIM:To investigate the angiogenic effect and mechanisms of astragaloside IV(AS-IV)in rats with myocardial infarction via protein kinase D 1(PKD1)-histone deacetylase 5(HDAC5)-vascular endothelial growth factor (VEGF)signaling pathway.METHODS:The classic model of myocardial infarction by ligation of the left anterior de-scending coronary artery was replicated,and the rats were randomly divided into model group,AS-IV group,and AS-IV+CID755673(PKD1 inhibitor)group.The sham operation control group and DMSO control group were also set up.All the rats were given intravenous injection via caudal vein.The rats were sacrificed 4 weeks later,and segmental heart samples were used for HE staining and Masson staining.The expression of PKD1,HDAC5 and VEGF was analyzed by immunohis-tochemistry,RT-PCR and and Western blot.RESULTS:Compared with sham operation group and DMSO group,the myo-cardium in model group showed disordered arrangement, accompanied with necrotic myocardial cells and obvious fibrosis tissue.After treatment with AS-IV,the morphological changes of myocardium were obviously improved,and the number of new blood vessels increased significantly.However,after treatment with AS-IV+CID755673,the myocardial tissues of the rats became disordered again,with increased necrotic cells and some closed vessels.The mRNA and protein expression of PKD1,HDAC5 and VEGF in myocardial tissue in model group was significantly lower than that in sham operation and DMSO groups(P<0.05).The expression in AS-IV group was significantly higher than that in model group(P<0.01), while that in AS-IV+CID755673 group was significantly lower than that in AS-IV group(P<0.05).CONCLUSION:AS-IV promotes the angiogenesis of myocardial tissues in the rats after myocardial infarction partly by regulating the PKD 1-HDAC5-VEGF signaling pathway.
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Objective To investigate the differences of hand and foot morphology and genetic phenotypic characteristics in adults of Hui and Han nationality in Southwestern Henan.Methods The indicators of height,weight,hand and foot were measured by the morphological measurements,the hand and foot genetic phenotype classification was observed and performed the statistical analysis.Results The hand width,foot length and foot width of the Hui adult men and women in Southwestern Henan were(8.27±0.55,23.10±1.20,9.34±0.83)cm and(7.41±0.44,20.50±1.23,8.79±0.69) cm,respectively,while which of the Han adult men and women were(8.56±0.09,24.57±1.33,9.47±0.70)cm and(7.74±0.36,22.46±1.21,8.91±0.85) cm,respectively.The total number of both hands fingerprint ridge line in Hui adult men and women were(135.06 ± 19.87) and (125.50 ±20.44)respectively,and which in Han adult men and women were (144.46 ±14.08) and (129.20 ± 20.34)respectively,the difference was statistically significant(P＜0.05).The tPD,atd angle and a-b crest line number among the Hui and Han nationalities were 16.07± 6.46,(44.61±8.66)°,34.04±5.47 and 16.53±6.27,(43.19±9.52)°,36.73±4.22 respectively.And the handedness,fingernail form,thumb type,footedness,right type ratio of foot and toe length of the Hui and Han nationalities were 90.01％,38.52％,85.59％,70.47％,56.92％ and 89.33％,45.26％,70.91％,96.98％,74.89％,respectively,the difference between the Hui and Han nationalities was statistically significant(P＜0.05).Conclusion The national differences and gender differences exist in the multiple indicators of hand and foot morphology,finger and palm prints,and genetic phenotype among the Hui and Han adults in Southwestern Henan.
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Aim To explore the effect of protein kinase D1 (PKD1 )on adherence,migration,proliferation, microvascular formation,and eNOS expression in bone marrow-derived endothelial progenitor cells(EPCs)of rats.Method The EPCs were isolated from bone marrow of rats,cultured and detected,the effects of PKD1 and its specific blocking agent CID755673 on adhesion,migration,proliferation,or microvascular formation were observed,as well as mRNA and protein expression of endothelial nitric oxide synthase (eNOS ) in EPCs.Results PKD1 significantly promoted adhe-sion,migration,proliferation and microvascular forma-tion of EPCs,and upregulated the mRNA and protein expression of eNOS in EPCs,according to the cell cul-ture experiments of EPCs in vitro.Conclusion PKD1 has the role of angiogenesis through regulation of EPCs,which might be dependent on eNOS.
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AIM:Todeterminetheeffectofsalviaextractonangiogenesisofthemyocardiumintheratswith myocardial infarction (MI) and to analyze its possible mechanism .METHODS: Left coronary artery of Sprague-Dawley rats was ligated to establish a MI model .The rats were randomly divided into MI model group , 3 different dose groups of salvia (10, 20 and 40 mg? kg-1? d-1), and sham operation group.Each group consisted of 8 rats.The rats in all treat-ment groups were orally administered with the salvia extract , and the rats in MI group and sham operation group were fed with the same volume of saline .The rats were sacrificed 4 weeks later .The hemodynamic changes of the rats were deter-mined , and the segmental heart samples were used for morphological observation by hematoxylin and eosin staining , Masson staining, or electron microscopic analysis.The expression of vascular endothelial growth factor (VEGF) and cluster of dif-ferentiation 34 ( CD34 ) was analyzed according to immunohistochemistry .RESULTS: Compared with sham operation group, the morphological changes of the myocardium in MI group were disordered , part of myocardial cell outline disap-peared , and obvious fibrosis in the necrosis myocardial tissue and fuzzy or disappearing microvascular ultrastructure were al -so observed .Compared with MI group , the number of new microvessels in all the treatment groups increased obviously , and the morphological changes of the endothelial cells were relatively complete according to electron microscopy .Compared with sham operation group , the protein expression of VEGF and CD 34 in the cytoplasm of the myocardial tissues in MI group in-creased only a little .Compared with MI group , the protein expression of VEGF and CD 34 in the cytoplasm of the myocardi-al tissues in all treatment groups increased significantly ( P<0.01 ) .CONCLUSION: Salvia extract obviously promotes angiogenesis of the myocardial tissues in the rats after myocardial infarction .
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Objective To explore the effect of astragalus extracts on adherence, migration, cell viability, microvascular formation, and eNOS expression in bone marrow-derived endothelial progenitor cells (EPCs) of rats. Methods EPCs were cultured, isolated and identified in vitro and divided into four groups: low titer group (10-4 g/L of astragalus extracts), middle titer group (10-3 g/L of astragalus extracts), high titer group (10-2 g/L of astragalus extracts) and control group. The effects of astragalus extract on adhesion, migration or microvascular formation were observed under the inverted microscope and com?pared between all groups;Cell viability was detected by MTT assay;mRNA transcription and protein expression levels of en?dothelial nitric oxide synthase (eNOS) in EPCs were detected by reverse transcription PCR (RT-PCR) and Western blot re?spectively. Results Compared with the control group, cell adhesion, migration and microvascular formation of EPCs all en?hanced with addition of astragalus extracts in a dose dependent manner (F=15.256, 13.633, 97.549 respectively, and P <0.05 in all cases); Cell vitality of EPCs increased with administration of astragalus extracts in a time and dose dependant manner. (F=9.755 for time and F=10.18 for dose). mRNA transcription and protein expression of eNOS in EPCs were up-reg?ulated with addition of astragalus extracts in a dose dependent manner (F=56.356 and 77.125 respectively, and P<0.05 in both cases). Conclusion Astragalus extracts play important role in angiogenesis in EPCs probably through up-regulating expressions of eNOS.
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Objective To investigate the significance of serum CD25 / serum ferritin in the diagnosis of lymphoma-associated hemophagocytic syndrome (LAHS),so as to provide the clinical basis for improving its recognition and giving effective therapy. Methods The serums were collected from 70 patients with hemophagocytic syndrom in Beijing Friendship Hospital, Capital Medical University during the period from October 2008 to June 2011, including 31 LAHS cases and 39 other disease-associated HPS cases. The serum CD25 level in HPS patients was measured with enzyme-linked immunosorbent assay (ELISA), and the serum ferritin was measured on the same day. Then the serum CD25/ferritin ratio was calculated and the differences of the serum CD25, serum ferritin and serum CD25/ferritin ratio between two groups were compared. Results The variance of serum CD25 [(15760.52±7851.74) pg/ml vs (12727.41±11285.28) pg/ml,t=-1.78,P=0.075] and serum ferritin levels (1750.00 ng/ml vs 2947.00 ng/ml,Z=-1.490,P=0.136)were not statistically significant between two groups,while the serum CD25/serum ferritin ratio in LAHS patients was significantly higher than the other group(8.57×10-3 vs 2.84×10-3,Z=-2.106,P=0.035).Conclusion The serum CD25/ serum ferritin ratio is statistically higher in LAHS patients, which might be a novel useful marker for predicting underlying malignant lymphoma in HPS patients.
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In order to investigate the expression of serum sHLA-G in hemophagocytic syndrome (HPS) patients and to evaluate its clinical significance, the clinical data of HPS patients in Capital Medical University Beijing Friendship Hospital during the period from September 2008 to July 2010 were collected. They were divided into infection-associated HPS, tumor-associated HPS and rheumatological disease-associated HPS according to cause of diseases. The serum concentration of sHLA-G in HPS patients and 25 healthy controls was measured by enzyme-linked immunosorbent assay (ELISA), the correlations between sHLA-G level and laboratory indicators were analyzed. The results showed that the level of serum sHLA-G in HPS patients was significantly higher than that in healthy controls (p = 0.003), but the difference was not statistically significant between HPS groups of different causes (p = 0.233). The positive correlation of sHLA-G level in HPS patients with platelet count was found, but there was no positive correlation of their sHLA-G levels with WBC, Hb, Plt, ALT, AST, LDH, Alb, TBil, DBil, IBil, Cr, BUN, TG, fibrinogen and ferritin levels detected on same day. It is concluded that the the increase of serum sHLA-G levels in HPS patients may be caused by different factors such as infection, tumor, T cell activation and over-stimulation of several cytokines. sHLA-G can inhibit NK cell activity, resulting in formation of abnormal immune storm, and may be play a role in the pathogenesis of HPS.