硝酸甘油对大鼠重症急性胰腺炎ET／NO、TXA2／PGI2的影响

目的探讨硝酸甘油对大鼠重症急性胰腺炎（SAP）ET／NO、TXA2／PGI2和胰腺病理形态学的影响。方法SD大鼠60只分为5组：A正常胰腺组,B、C、D和E组为实验组,胰胆管逆行注射5％牛磺胆酸钠制作SAP模型。C、D和E组分别静脉注射硝酸甘油0．5、1．0、2．0μg/（kg·min）,A、B纽注射生理盐水。6h及12h后分别检测各组ET、NO、TXB2及6-keto—PGFIa值并进行胰腺病理标本评分。结果6h及12h时的标本数据分别显示,与B组比较,C、D和E组的胰腺病理评分、ET、ET／NO、TXB2、TXB2／6-keto—PGFIa比值都降低（P〈0．05）。结论硝酸甘油具有降低大鼠血液ET、ET／NO、TXA2、TXA2／PGI2值的作用,改善胰腺血液微循环,延缓大鼠重症急性胰腺炎的炎性病理变化的作用。     

脑血流灌注显像对难治性发作性癫痫诊断的研究

Objective To explore the effect of injection salvia miltiorrhiza plus magnesium sulfate on plasma concentrations of nitric oxide(NO), endothelin-1 (ET-1), thromboxan A2 (TXA2), prostaglandin I2 (PGI2)and renal function in women with pregnancy-induced hypertension syndrome (PIH). Methods Fifty-four women with PIH were randomly divided into magnesium sulfate treated group (27 cases, control group)and injection salvia miltiorrhiza plus magnesium sulfate treated group (27 cases, observe group). The levels of NO, ET-1, TXA2, PGI2 and renal function parameters such as α1-microglobulin (α1-MG), blood urea nitrogen (BUN)and creatinine (Cr)were measured. Results The NO, ET-1, TXA2, PGI2 were (985.43±224.17) nmol/L, (53.52±3.88) ng/L, (426.33±26.52) pg/L, (277.34±14.06) pg/L and (832.35±192.43) nmol/L,(61.43±3.56) ng/L,(472.24±22.28) pg/L, (202.12±11.56) pg/L in two groups respectively. There was significant difference on the levels of NO, ET-1, TXA2 between before and after treatment in two groups(P<0.05), and the observe group was better than the control group (P<0.05). There were significant difference on the levels of α1-MG, BUN and Cr between before and after treatment in two groups (P<0.05). The renal function in the observe group was improved greater than that in the control group (P<0.05). Conclusions Injection salvia mihiorrhiza plus magnesium sulfate treatment can well balance the plasma concentration levels of NO, ET-1, TXA2 and PGI2 in women with PIH. It has protective effect on renal function.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

哮喘大鼠肺组织Ca^2＋/CaN-NFATc活性及其与TH1/TH2失衡的关系

目的 探究哮喘大鼠肺组织Ca^2＋/CON-NFATc的活性及其与TH1/TH2失衡的关系.方法 24只Wistar大鼠随机分为哮喘组和对照组,12只/组.用鸡卵白蛋白（OVA）溶液致敏和激发复制大鼠哮喘模型.Maclab系统记录分析大鼠肺功能;HE染色观察气道炎症并测量气道管壁厚度;检测肺组织钙含量、CaN活性、去磷酸化NFATc蛋白的表达及IL-4、IL-2的含量.结果 与对照组相比,哮喘组大鼠支气管管壁厚度明显增加（t=-7.99,P〈0.01）;气道阻力和呼吸频率增加（t=2.59,P〈0.05;t=7.94,P〈0.01）,每分通气量减少（t=6.87,P〈0.01）;与对照组相比,哮喘组大鼠肺组织中IL-4含量和IL-4/IL-2比值增高（t=-8.69,11.40,P〈0.01）,而IL-2含量降低（t=8.29,P〈0.01）;与对照组相比,哮喘组大鼠肺组织中CaN活性和去磷酸化NFATc蛋白的相对表达量均增加（t=-2.91,-22.45,P〈0.01）,而肺组织钙含量降低（t=4.75,P〈0.01）;肺组织中CaN活性与去磷酸化NFATc蛋白的相对表达量呈正相关（r=0.39,P〈0.05）;去磷酸化NFATc蛋白的相对表达量与IL-4/IL-2比值呈正相关（r=0.83,P〈0.01）;而肺组织中IL-4/.IL-2比值与大鼠支气管管壁厚度成正相关（r=0.84,P〈0.01）.结论 哮喘大鼠肺组织中CaN-NFATc的活性增加,其活性的增加可促进IL-4/IL-2比值增加,推测CaN-NFATc信号通路可能参与了哮喘大鼠肺组织TH1/TH2失衡的形成.     

辅助性T细胞亚群失衡与结核病的关系

目的通过检测结核病患者外周血和局部病灶的辅助性T细胞亚群细胞因子的表达,探讨结核病患者的免疫失衡.方法收集活动性结核病患者20例,其中肺结核15例,淋巴结结核5例;同时选取正常对照组15例.应用流式细胞仪在单个核细胞水平检测结核病患者外周血和局部病灶Th细胞内的细胞因子.结果结核病组20例外周血中Th1细胞较正常对照组普遍偏低(P=0.000),而Th2细胞较正常对照组无显著性差异(P＞0.05).其中5例淋巴结结核患者淋巴结活检标本中的Th1、Th2细胞和正常对照组相比均无显著性差异(P＞0.05),和其外周血相比均有显著性差异(P＜0.05).结论结核病的发生、发展与Th细胞亚群的失衡有密切关系,主要表现为Th1细胞数量低下.结核患者的Th1细胞低下主要表现在外周血,而局部病灶中的Th1细胞并未减少.在外周血Th1细胞低下的同时有Th2细胞的增加.     

青石棉诱导BEAS-2B细胞ERK1/2磷酸化表达的研究

目的 了解青石棉在致癌过程中引起信号转导蛋白变化的特点.方法 使用人呼吸道上皮细胞株（human bronchial epithelial cell line,BEAS-2B）体外培养,以终浓度100 μg/ml的青石棉和100nmoL/L表皮生长因子（epidermal growth factor,EGF）分别刺激BEAS-2B细胞30和120min,使用特异性抗磷酸化细胞外调节蛋白激酶（extracellular regulated protein kinase,ERK1/2）、ERK激酶（ERK kinase,MEK1/2）和抗总ERK1/2、MEK1/2抗体进行Western免疫印迹,检测相应的蛋白表达水平.结果 青石棉刺激BEAS-2B细胞30 min后,可诱导磷酸化ERK1/2的快速高表达,且此高表达可持续至120 min,与对照组比较,差异有统计学意义（P＜0.05）;EGF作为诱导磷酸化ERK1/2的阳性刺激物,在30和120 min两时段内均可诱导ERK1/2的激活,与对照组比较,差异有统计学意义（P＜0.05）;任何时间段刺激BEAS-2B,在对照、青石棉和EGF组间,总ERK1/2表达差异无统计学意义（P＞0.05）.青石棉刺激BEAS-2B细胞30、120 min后,可诱导磷酸化MEK1/2的快速高表达,与对照组比较,差异有统计学意义（P＜0.05）.结论 青石棉可快速诱导BEAS细胞产生磷酸化ERK1/2、MEK1/2蛋白的高表达,提示MAPKs参与了青石棉所致疾病的过程.     

DHA诱导3T3-L1前脂肪细胞G2/M期阻滞及ERK1/2通路的作用

目的探讨ERK1/2丝裂素活化蛋白激酶信号转导途径在DHA抑制3T3-L1前脂肪细胞增殖中的作用。方法四唑盐比色法(MTT法)检测DHA处理24h对体外培养的3T3-L1前脂肪细胞活力的影响,流式细胞术检测细胞周期,蛋白免疫印迹法检测ERK1/2、p-ERK1/2、p21水平。结果 MTT结果显示DHA干预24h可剂量依赖性降低3T3-L1前脂肪细胞的活力,抑制增殖,IC50为100μmol/L;流式细胞术结果表明,DHA可将3T3-L1前脂肪细胞阻滞在G2/M期;蛋白免疫印迹发现,DHA可明显升高3T3-L1前脂肪细胞ERK1/2磷酸化水平、增强p21蛋白表达。结论 DHA可能通过活化ERK1/2通路诱导G2/M期阻滞,进而抑制3T3-L1前脂肪细胞增殖。     

青春双歧杆菌和嗜酸乳酸杆菌对急性期和恢复期结肠炎小鼠Th1/Th2亚群的影响

Objective To observe and analyze the effect of B. Adolescentis and L. Acidophilus on the proportion of Th cell Th1/Th2 in peripheral blood of UC-mice in acute stage and recovery stage. Method 40 BABL/c mice were induced by 3% DSS water for 7 clays free drinking and then with distilled water for 10 days. They were randomly allocated in 4 groups: NS group, SASP group, BF0624 group and LT0637 group, also the fifth group-10 normal animals. The blood of mice were collected by removing their eyes at day 8 and day 18, and then the mononuclear cells were iso]atecl. The proportion of Th1/Th2 was analyze through flow eytometry,hy labeling the specific antibody ot Th cellular membrane with the CD4 antibody, and the cytoplastie antigen of Thl or Th2 with IIA antibody or IF'N-γ antibody. Result The proportion of Th1/Th2 in normal mouse was 0. 84 -0. 94,and it raised up in DSS-mice at both acute stage and recovery stage. It decreased unequally after 7 or 17 days'B, adoleseentis, L. Acidophilus and SASP treatment, but that of all three groups were lower than NS group (2.21±0. 83). Even the proportion got close to the normal animals after 17 days'L. Acidophilus -treated. Conclusion The proportion of Thl/Th2 increased at the acute stage and recovery stage of DSS-mice. Both B. Adoleseentis and L. Acidophilus had more effective than SASP on decreasing the proportion of Th1/Th2 at two stages,ospecially L. Acidophilus.     

青春双歧杆菌和嗜酸乳酸杆菌对急性期和恢复期结肠炎小鼠Th1/Th2亚群的影响

Objective To observe and analyze the effect of B. Adolescentis and L. Acidophilus on the proportion of Th cell Th1/Th2 in peripheral blood of UC-mice in acute stage and recovery stage. Method 40 BABL/c mice were induced by 3% DSS water for 7 clays free drinking and then with distilled water for 10 days. They were randomly allocated in 4 groups: NS group, SASP group, BF0624 group and LT0637 group, also the fifth group-10 normal animals. The blood of mice were collected by removing their eyes at day 8 and day 18, and then the mononuclear cells were iso]atecl. The proportion of Th1/Th2 was analyze through flow eytometry,hy labeling the specific antibody ot Th cellular membrane with the CD4 antibody, and the cytoplastie antigen of Thl or Th2 with IIA antibody or IF'N-γ antibody. Result The proportion of Th1/Th2 in normal mouse was 0. 84 -0. 94,and it raised up in DSS-mice at both acute stage and recovery stage. It decreased unequally after 7 or 17 days'B, adoleseentis, L. Acidophilus and SASP treatment, but that of all three groups were lower than NS group (2.21±0. 83). Even the proportion got close to the normal animals after 17 days'L. Acidophilus -treated. Conclusion The proportion of Thl/Th2 increased at the acute stage and recovery stage of DSS-mice. Both B. Adoleseentis and L. Acidophilus had more effective than SASP on decreasing the proportion of Th1/Th2 at two stages,ospecially L. Acidophilus.     

青春双歧杆菌和嗜酸乳酸杆菌对急性期和恢复期结肠炎小鼠Th1/Th2亚群的影响

Objective To observe and analyze the effect of B. Adolescentis and L. Acidophilus on the proportion of Th cell Th1/Th2 in peripheral blood of UC-mice in acute stage and recovery stage. Method 40 BABL/c mice were induced by 3% DSS water for 7 clays free drinking and then with distilled water for 10 days. They were randomly allocated in 4 groups: NS group, SASP group, BF0624 group and LT0637 group, also the fifth group-10 normal animals. The blood of mice were collected by removing their eyes at day 8 and day 18, and then the mononuclear cells were iso]atecl. The proportion of Th1/Th2 was analyze through flow eytometry,hy labeling the specific antibody ot Th cellular membrane with the CD4 antibody, and the cytoplastie antigen of Thl or Th2 with IIA antibody or IF'N-γ antibody. Result The proportion of Th1/Th2 in normal mouse was 0. 84 -0. 94,and it raised up in DSS-mice at both acute stage and recovery stage. It decreased unequally after 7 or 17 days'B, adoleseentis, L. Acidophilus and SASP treatment, but that of all three groups were lower than NS group (2.21±0. 83). Even the proportion got close to the normal animals after 17 days'L. Acidophilus -treated. Conclusion The proportion of Thl/Th2 increased at the acute stage and recovery stage of DSS-mice. Both B. Adoleseentis and L. Acidophilus had more effective than SASP on decreasing the proportion of Th1/Th2 at two stages,ospecially L. Acidophilus.     

Ginsenoside Rh4 Suppresses Metastasis of Gastric Cancer via SIX1-Dependent TGF-β/Smad2/3 Signaling Pathway

Gastric cancer (GC) is the leading causes of cancer-related death worldwide. Surgery remains the cornerstone of gastric cancer treatment, and new strategies with adjuvant chemotherapy are currently gaining more and more acceptance. Ginsenoside Rh4 has excellent antitumor activity. Conversely, the mechanisms involved in treatment of GC are not completely understood. In this study, we certified that Rh4 showed strong anti-GC efficiency in vitro and in vivo. MTT and colony formation assays were performed to exhibit that Rh4 significantly inhibited cellular proliferation and colony formation. Results from the wound healing assay, transwell assays, and Western blotting indicated that Rh4 restrained GC cell migration and invasion by reversing epithelial–mesenchymal transition (EMT). Further validation by proteomic screening, co-treatment with disitertide, and SIX1 signal silencing revealed that SIX1, a target of Rh4, induced EMT by activating the TGF-β/Smad2/3 signaling pathway. In summary, our discoveries demonstrated the essential basis of the anti-GC metastatic effects of Rh4 via suppressing the SIX1–TGF-β/Smad2/3 signaling axis, which delivers a new idea for the clinical treatment of GC.     

青春双歧杆菌和嗜酸乳酸杆菌对急性期和恢复期结肠炎小鼠Th1/Th2亚群的影响

Objective To observe and analyze the effect of B. Adolescentis and L. Acidophilus on the proportion of Th cell Th1/Th2 in peripheral blood of UC-mice in acute stage and recovery stage. Method 40 BABL/c mice were induced by 3% DSS water for 7 clays free drinking and then with distilled water for 10 days. They were randomly allocated in 4 groups: NS group, SASP group, BF0624 group and LT0637 group, also the fifth group-10 normal animals. The blood of mice were collected by removing their eyes at day 8 and day 18, and then the mononuclear cells were iso]atecl. The proportion of Th1/Th2 was analyze through flow eytometry,hy labeling the specific antibody ot Th cellular membrane with the CD4 antibody, and the cytoplastie antigen of Thl or Th2 with IIA antibody or IF'N-γ antibody. Result The proportion of Th1/Th2 in normal mouse was 0. 84 -0. 94,and it raised up in DSS-mice at both acute stage and recovery stage. It decreased unequally after 7 or 17 days'B, adoleseentis, L. Acidophilus and SASP treatment, but that of all three groups were lower than NS group (2.21±0. 83). Even the proportion got close to the normal animals after 17 days'L. Acidophilus -treated. Conclusion The proportion of Thl/Th2 increased at the acute stage and recovery stage of DSS-mice. Both B. Adoleseentis and L. Acidophilus had more effective than SASP on decreasing the proportion of Th1/Th2 at two stages,ospecially L. Acidophilus.