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Objective To study the mechanism of the signaling pathway-related LncHOTAIR on the invasion and metastasis of hepatocellular carcinoma(HCC) and provide experimental basis for the treatment of liver cancer with target gene level.Methods Thirty specimens of liver cancer and tissue adjacent to carcinoma on liver and gallbladder surgery surgical resection were collected in the People′s Liberation Army General Hospital from September 2012 to June 2013.Expression of LncHOTAIR,vascular endothelial growth factor(VEGF) and endothelial growth factor receptor(VEGFR) in Hepatocellular Carcinoma and Paracancerous Tissues were detected by Real-time Quantitative Real-time PCR,the relationship between the pathological features and the pathological features of the patients with HCC was analyzed.Results The expression of LncRNA HOTAIR,VEGF and VEGFR were higher in HCC tissues than that in adjacent tissues,which was closely related to tumor size(P=0.512,0.003,0.008),TNM staging(P=0.094,0.001,0.014),portal vein thrombosis(P=0.065,0.046,0.031),invasion and metastasis (P=0.002,0.046,0.031) and 2-year recurrence((P=0.001,0.003,0.021).Conclusion Lnc HOTAIR-related VEGF signal pathways are closely related to the development of liver cancer,si-HOTAIR is expected to become a new focus in the clinical treatment of liver cancer in the future.
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Objective To evaluate the role of adiponectin (ADP) and adiponectin receptor-1(ADPR1) in limb ischemic precondi-tioning(LIPC) against apoptosis after myocardial ischemia-reperfusion injury(MIRI) .Methods SD rats were divided into 3 groups (n=10 ,4 rats of every group were prepared for detecting apoptosis ) .Group sham (group in sham operated) were processed identi-cally except the left coronary artery was not be ligated ;group MIRI (group in ischemia reperfusion) were subjected to occlusion of the left coronary artery anterior descending (LAD) followed by reperfusion ,occlusion for 30 min and reperfusion for 120 min;group LIPC (group in limb ischemic preconditioning) were subjected to ischemia and reperfusion on the left hind limb for 5 min in turn for 3 d .LAD were performed ischemia for 30 min and reperfusion for 120 min at the 4th day .The expression of the level of myocardial ADP and ADPR1 mRNA of group sham ,group MIRI and group LIPC were determined by reverse transcriptase polymerase chain reaction(RT-PCR) .The apoptosis index of every group were determined by mothod of terminal-deoxynucleoitidyl transferase medi-ated nick end labeling(TUNEL)respectively .Results Compared with group sham ,the expression of ADP and ADPR1 mRNA in group MIRI lessened apparently (P<0 .05);compared with group MIRI ,the expression of ADP and ADPR1 mRNA in group LIPC increased statistically significant(P<0 .05);compared with group sham ,the apoptosis index(AI) of myocardial cells in group MIRI increased apparently(P<0 .05);compared with group MIRI ,the AI of myocardial cells in group LIPC decreased significantly (P<0 .05) .Conclusion Limb ischemic preconditioning ;decreased apoptosis after myocardial ischemia-reperfusion injury via activating ADP signaling pathways ,which played a protective role in myocardial tissue .
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Objective To investigate the myocardial protection of adiponectin (ADP) /adiponectin receptor 1 (ADPR1) related-signal pathway in rats with limb ischemic preconditioning.Methods Thirty SD male rats were randomly divided into sham-operation group,myocardial ischemia reperfusion injury (MIRI) group,limb ischemic preconditioning (LIPC) group,LY294002 (the PI3-specific inhibitor) pretreatment group and LY294002+LIPC group (n=10 each).The mRNA level of myocardial ADP and ADPR1,the protein expressions of phosphatidylinositol 3-kinase (PI3k)phosphorylated Akt (p-Akt) were determined by RT-PCR and Western blot,respectively. Results As compared with sham-operation group,the mRNA levels of ADP and ADPR1 in MIRI group were significantly decreased (0.53 ± 0.07 vs.0.74 ± 0.08 and 0.52 ± 0.02 vs.0.72 ± 0.04,P＜0.05).Compared with MIRI group,the mRNA levels of ADP (0.72±0.21) and ADPRI (0.80±0.023) in LIPC group were increased,ADP(0.49±0.07) and ADPR1 (0.52± 0.02) mRNA were decreased in LY294002 group (both P＜0.05),but there were no difference in ADP(0.70±0.16) and ADPR1(0.78±0.05) mRNA between LY294002+LIPC group and MIRI group.The protein levels of Pl3k and p-Akt were lower in MIRI group than in sham-operation group (3.85±0.23 vs.2.83±0.22and 3.77±0.32 vs.2.66±0.29,P＜0.05).In contrast to MIRI group,the yield of PI3k (2.65±0.32)and p-Akt(2.26±0.27) protein (P＜0.05) were increased in LIPC group,but there were unproductive protein of PI3k (3.75 ± 0.65) and p-Akt (4.01 ± 0.71) in LY294002 group with no differences versus the levels of PI3k (3.23 ± 0.48) and p-Akt (3.17 ± 0.54) in LY294002 + LIPC group. Conclusions Limb ischemic preconditioning may protect myocardium by promoting serum adiponectin levels,improving myocardial mRNA expressions of ADP and ADPR1,activating the ADP/PI3k/Akt signaling pathway in reperfusion injury.
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Objective To explore the expression and clinical significance of peroxisome proliferator-activated receptor gamma (PPAR γ) in breast tissue in obese patients with breast cancer.Methods Breast tissue samples were collected from 60 obese patients with breast cancer (obese group),60 normal weight patients with breast cancer (normal weight group),the expression of PPAR γmRNA and protein of breast tissue were detected by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry in all patients,and the data was analyzed between PPARγ mRNA and protein.Results Compared with normal weight group,the expression of PPAR γ mRNA and protein of breast tissue in obese group were increased obviously(0.79 ± 0.06 vs 0.42 ± 0.04,0.55 ± 0.07 vs 0.23 ± 0.03 )(P＜ 0.05 ),while the expression of PPAR 3 mRNA and protein were positively correlated (r =0.81,P＜ 0.05 ).In obese group,the positive expression of PPAR γ was 47 cases with 10 cases (21.3％) recurrence and metastasis,the negative expression of PPAR 3 was 13 cases with 11 cases (84.6％) recurrence and metastaais,there was significant difference(P ＜ 0.05 ).In normal weight group,the positive expression of PPAR γwas 19 cases with 4 cases ( 21.1％ ) recurrence and metastasis,the negative expression of PPAR 3 was 41 cases with 10 cases (24.4％) recurrence and metastasis,there was no significant difference (P ＞ 0.05 ).Conclusions Obese patients with breast cancer own a high expression trend of expression of PPAR γ mRNA and protein of breast tissue,which indicates that PPARγ may be play an important role in occurrence,evolvement and prognosis of obesity-related breast cancer.
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ObjectiveTo investigate the role of peroxisome proliferator-activated receptor gamma (PPARγ)/Caspase-8/Caspase-3 signaling pathway in the development of hyperlipidemia in rats.Methods 60 healthy male SD rats 〔4-week old,weight (110 ± 10) g〕 were randomly divided into control group,high-fat diet group,folic acid group,vitamin B12 group,folic acid and vitamin B12 group.After one week's feeding for adaptability,the groups of foloc acid,vitamine B12 and foloc acid + vitamineB12 were dealt with intraperitoneal injection of folic acid (0.5 mg/d),vitamin B12 (0.05mg/d),and folic acid (0.5 mg/d) plus vitamin B12 (0.05 mg/d),respectively,and fed with high fat diet simultaneously.Control group was dealt with intraperitoneal injection of normal saline (0.5 ml/d)and fed with normal diet.High-fat diet group was only fed with high fat diet.Reverse transcription polymerase chain reaction (RT-PCR) was used to measure the mRNA level of PPARy,Caspase-8 and Caspase-3 in aorta abdominalis dissected at 17 weekends.Results Folic acid alone or jointed with vitamin B12 could effectively increase the level of PPARγ,while decrease the mRNA levels of Caspase8 and Caspase-3 as compared with high-fat diet group (P＜0.05),and folic acid plus vitamin B12 was more effective than folic acid alone (P＜0.05).Conclusions Folic acid alone or joined with vitamin B12 can improve the mRNA levels of PPARγ,Caspase-8 and Caspase-3 in vascular wall to protect endothelial injury from hyperlipidemia.
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Aim To study the effect of Peptide fragments that originate from the same proadrenomedullin on cAMP in rat aorta.Methods Isolated aortic tissues were exposed to ADM,PAMP and ADT for 2 h.The content of cAMP in the incubated media was assayed by radioimmunoassay.Results ① The content of cAMP in the aortic tissues that were exposed to ADM (10~(-7) and 10~(-8) mol·L~(-1)) was significantly increased. The content of cAMP in the aortic tissues stimulated by PAMP (10~(-8) mol·L~(-1))or ADT (10~(-8) mol·L~(-1))alone was significantly increased, compared with the control.② The content of cAMP was not in-creased when the tissues were treated with ADM (10~(-8) mol·L~(-1)) and PAMP (10~(-8) mol·L~(-1)) or ADT (10~(-8) mol·L~(-1)) in combination, compared with that after the treatment with ADM(10~(-8) mol·L~(-1))alone, but was significantly decreased than that in PAMP(10~(-8) mol·L~(-1)) or ADT(10~(-8)mol·L~(-1)) groups. After incubation with ADM,PAMP and ADT at the same dose (10~(-8) mol·L~(-1)), the content of cAMP did not change as compared with that of the ADM group (10~(-8) mol·L~(-1),P>0.05), but was greatly reduced, compared with that of the PAMP or ADT groups(10~(-8) mol·L~(-1),P<0.01).Conclusion ADM, PAMP and ADT which originate from the proadrenomedullin have an antagonism on cAMP production in rat aorta.
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0.05),but was greatly reduced,compared with that of the PAMP or ADT groups(10-8 mol?L-1,P