The effect of miR-129-5p in pancreatic cancer cells on apoptosis through targeted of HMGB1

Objective:To investigate the role of miR-129-5p in regulating HMGB1 expression in pancreatic cancer cell apoptosis.Methods:The untreated pancreatic cancer SW1990 cells were used as the control group.Mimics-NC(empty vector),miR-129-5p mimics,inhibitor-NC(empty vector)and miR-129-5p inhibitor were transfected into SW1990 cells by liposome transfection method as the mimics-NC group,miR-129-5p overexpression group(miR-129-5p mimics group),inhibitor-NC group and miR-129-5p low expression group(miR-129-5p inhibitor group).The binding site of miR-129-5p and HMGB1 was predicted by online target gene prediction website Target genes,and the targeting relationship between miR-129-5p and HMGB1 was verified by dual luciferase gene report experiment.The expression of miR-129-5p in each group was detected by qRT-PCR,and the expression of HMGB1 protein and apoptosis-related proteins Caspase 3 and Bcl-2 by Western blot.Hoechst staining was used to observe the changes of apoptosis.Results:Compared with the mimics-NC group and control group,miR-129-5p mimics transfection significantly up-regulated miR-129-5p level(P<0.01),inhibited HMGB1(P<0.01)and Bcl-2(P<0.05)protein expression,pro-moted Caspase 3 protein expression(P<0.05),and promoted apoptosis;compared with the inhibitor-NC group and control group,miR-129-5p inhibitor transfection significantly down-regulated miR-129-5p level(P<0.05),promoted HMGB1 and Bcl-2 protein expression(all P<0.05),inhibited Caspase 3protein expression(P<0.01),and inhibited apoptosis.The results of dual luciferase reporter gene assay showed that miR-129-5p could inhibit the fluorescence activity of wildtype HMGB1 cells and target the expression of HMGB1.Conclusion:miR-129-5p promotes the apoptosis of pancreatic cancer SW1990 cells by targeting inhibition of HMGB1 expression.

血小板蛋白酶活化受体-1水平对稳定型心绞痛患者长期预后的影响

目的探讨血小板蛋白酶活化受体-1(PAR-1)水平对稳定型心绞痛(SAP)患者长期预后的影响。方法纳入125例SAP患者,收集患者的一般临床资料并检测入院时富血小板血浆中PAR-1的水平,记录随访18个月期间心血管事件的发生情况。采用受试者工作特征曲线分析PAR-1对SAP患者发生心血管事件的预测效能,分析SAP患者发生心血管事件的影响因素。结果 125例SAP患者PAR-1水平为(2. 79±0. 34) pg/ml。TC、LDL、心绞痛加拿大心血管协会分级、PAR-1水平均为SAP患者心血管事件发生的影响因素(均P <0. 05)。当PAR-1为2. 854 ng/ml时,其预测SAP患者发生心血管事件的敏感度、特异度分别为76. 1%、91. 4%。结论 PAR-1水平升高是SAP患者发生心血管事件的重要危险因素,其可作为评估SAP长期预后的指标。

急性胰腺炎患者外周血淋巴细胞亚群的改变及其与自噬、凋亡的关系

目的:探讨急性胰腺炎(AP)患者外周血淋巴细胞亚群的改变及其与自噬、凋亡的关系。方法:收集AP患者73例,其中轻症AP(MAP)患者25例,中度重症AP(MSAP)患者25例,重症AP(SAP)患者23例,并选择25位健康志愿者作为对照组。流式细胞术检测AP患者外周血淋巴细胞亚群、CD4+/CD8+比值及淋巴细胞自噬率、凋亡率;ELISA检测外周血自噬基因LC3及凋亡基因Caspase-3水平。结果:SAP及MSAP组CD3+、CD4+、CD19+淋巴细胞比率均较对照组、MAP组下降(P<0.05);SAP组与MSAP组下降(P<0.05);MAP组与对照组差异无统计学意义(P>0.05);AP各组CD4+/CD8+比值均较对照组下降(P<0.05),SAP组较MSAP、MAP组下降(P<0.05),MSAP组较MAP组下降(P<0.05)。SAP组血清LC3、Caspase-3水平及淋巴细胞自噬率、凋亡率较对照组、MAP组及MSAP组升高(P<0.05),MSAP组较MAP及对照组升高(P<0.05),MAP组与对照组差异无统计学意义(P>0.05)。MSAP、SAP组血清LC3、Caspase-3水平分别与淋巴细胞自噬率及凋亡率呈正相关(P<0.05),与CD4+、CD19+淋巴细胞比率及CD4+/CD8+比值呈负相关(P<0.05)。结论:AP尤其是SAP患者外周血CD3+、CD4+、CD19+淋巴细胞比率、CD4+/CD8+比值降低,机体免疫功能受损。LC3、Caspase-3水平升高、淋巴细胞自噬、凋亡增加可能是AP患者淋巴细胞亚群改变的重要原因。

CX3CL1-CX3CR1与脓毒症发病机制的研究进展

脓毒症预后不良,发病机制尚未明确。趋化因子CX3CL1(Fractalkine,FNK)具有趋化、黏附和介导免疫损伤等多种功能。CX3CR1是CX3CL1的唯一受体,共同参与了脓毒症的发生发展过程。本文就CX3CL1及CX3CR1的结构、生物学功能及参与脓毒症发病的可能机制作一综述。