目的:分析非小细胞肺癌(NSCLC)中黑素瘤相关抗原D4(MAGE-D4)基因启动子甲基化程度与MAGE-D4 mRNA表达水平及患者临床病理特征的关系.方法:采用甲基化特异性PCR(MSP)法检测38例NSCLC患者癌组织及其癌旁组织中MAGE-D4启动子甲基化程度,实时荧光定量PCR(qPCR)法检测组织中MAGE-D4 mRNA相对表达量,分析MAGE-D4启动子甲基化频率与患者临床病理特征的关系.结果:肺癌组织中MAGE-D4基因甲基化频率为23.68％,明显低于癌旁组织的86.84％(P<0.05);而癌组织中MAGE-D4 mRNA表达水平则显著高于癌旁组织(5.49±5.65 vs.1.44±1.08,P<0.05),MAGE-D4表达量与启动子甲期化程度呈负相关关系(r=-0.663,P<0.05).肿瘤直径>3 cm的肺癌患者MAGE-D4甲基化发生率明显低于肿瘤直径≤3 cm患者(P<0.05).结论:NSCLC中MAGE-D4基因转录活性的增强与其启动子低甲基化相关;肿瘤直径较大的NSCLC患者MAGE-D4甲基化发生率较低.

Objective To investigate effect of berberine on fasting glucose , fasting serum insulin, islet morphology, and ex-pression of glucose transporter 4 (GLU-4) of islet in type 2 diabetes mellitus (T2DM) rats.The present study aimed to evaluate the ually, especially for high-dose group ( P <0.01).⑷Compared with normal group , INS of diabetic control group was significantly de-creased ( P <0.05), INS of low-dose, middle-dose, and high-dose groups were all increased gradually , especially for high-dose group ( P <0.01 ) .Conclusions Berberine has the effects of antidiabetes via ameliorate insulin sensitivity , and promotes GLUT-4 protein expression .

Objective Pancreatic duodenal homeobox-1 ( PDX-1) plays an important role in the occurrence and development of diabetes.More importantly,its potential application in insulin resistance (IR) improvement is attracting further attention .Berberine has been shown to improve glucose metabolism and insulin resistance .In this study,rat models of type 2 diabetes mellitus ( T2DM) were established by combination of intraperitoneal injection of low -dose streptozotocin and highg-lucose-high-fat diet induction .The effect of berberine on fasting glucose , fasting serum insulin , homeostasis model assessment of insulin resistance ( HOMAI-R) , and ex-pression of PDX -1 of islet in T2DM rats were analyzed .The present study aimed to evaluate the anti-diabetic efficacy of berberine and study the mechanism of its preliminary therapeutic effects .Methods Twenty healthy adult male Sprague Dawley ( SD) rats were di-vided by random number table into the normal control group ( n =6) feeding with a standard diet ,and the experimental group ( n =14 ) given an intraperitoneal injection of streptozotocin .The rats with fasting blood glucose ( FBG) greater than 13.8 mmol/L were ran-domly divided into diabetes mellitus group feeding high sugar high fat diet for two weeks and then continuing with a standard diet , and the berberine group given berberine [180 mg /(kg· d)] every day.The normal control group and diabetes mellitus group were given physiological saline for every day 6 weeks.At the end of 6th week, the rats were executed , and the levels of fasting glucose, fasting se-rum insulin, HOMA-IR, and expression of PDX-1 in pancreas islet of each group were detected .The expression of PDX1-in pancreas islet was examined by immunohistochemistry .The image pro plus 6.0software was used to calculate the integrated optical density ( IOD) of positive expression .Results Compared with the normal control group , FBG, fasting insulin levels ( FINS) , and HOMA-IR of the diabetes mellitus group and berberine group were significantly increased ( P <0.05 ) .Compared with the diabetes mellitus&nbsp;group, FBG, FINS, and HOMA-IR of the berberine group were statistically significantly decreased [ ( 13.11 ±6.87 ) mmol/L vs (18.45 ±4.69) mmol L/, (2.58 ±0.34) μIU/ml vs (2.98 ±0.40) μIU/ml, 1.60 ±0.91 vs 2.75 ±0.28, P <0.05].Compared with the normal control group , the expression of PDX-1 of the islet in the diabetes mellitus group and berberine group was statistically significantly decreased ( P <0.05).After treatment with berberine, FBG, FINS, HOMA-IR, and IOD of PDX-1 in pancreas islet of berberine treatment rats were significantly increased compared with the diabetes mellitus group ( 9.14 ±1.51 vs 6.79 ±0.98 , P <0.01 ) .Conclusions The increases of PDX-1 in islet may be one of the mechanism in the improvement of hyperglycemia .

目的:探讨黄连素对2型糖尿病(T2DM)大鼠空腹血糖(FBG)、空腹胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)及胰岛素生长因子-1(IGF-1)表达的影响.方法:SD雄性大鼠40只,随机取6只作为正常对照组,34只用链脲佐菌素(STZ)诱导T2DM大鼠模型,造模成功后随机分为T2DM模型组及T2DM治疗组.正常对照组始终予普通饲料喂养,T2DM模型组及T2DM治疗组予高糖高脂饲料喂养2周后予普通饲料喂养.T2DM治疗组予黄连素180 mg/(kg·d)灌胃,正常对照组及T2DM模型组给予生理盐水灌胃,共6周.第6周末处死各组大鼠,留取血清标本测定FBG、FINS水平,计算HOMAIR;留取各组大鼠胰腺组织,应用免疫组织化学法检测胰岛中IGF-1的表达,并使用Image pro plus 6.0软件计算IGF-1阳性表达的累计光密度值(IOD值).结果:T2DM模型组及T2DM治疗组FBG、FINS、HOMA-IR均高于正常对照组(P＜0.01),T2DM治疗组FBG、FINS、HOMA-IR均较T2DM模型组改善(P＜0.05或P＜0.01).T2DM治疗组及T2DM模型组IGF 1表达较正常对照组减少(P＜0.05).T2DM治疗组中IGF-1值较T2DM模型组有所下降,但差异无统计学意义(P＞0.05).结论:黄连素能改善T2DM大鼠的胰岛素抵抗,IGF-1可能与黄连素改善T2DM大鼠的胰岛素抵抗无关.

目的:评价不同腰围2型糖尿患者胰岛素抵抗的程度。方法:92例2型糖尿病患者根据2005年国际糖尿病联盟关于代谢综合征中心性肥胖的华人定义进行分组,按女性腰围<80 cm、男性腰围<90 cm,女性腰围≥80 cm、男性腰围≥90 cm分别分成2型糖尿病非肥胖组及2型糖尿病肥胖组,均测定其空腹血糖(FBG)、餐后2 h血糖(PBG2h)、空腹胰岛素水平(FINS)、胆固醇(TC)、甘油三酯(TG),计算胰岛素抵抗指数(HOMA-IR),比较不同腰围2型糖尿患者胰岛素抵抗程度。结果:HOMA-IR随腰围的增加而增大,2型糖尿病肥胖组较非肥胖组显著升高(P<0.01)。多元线性回归显示,影响HOMA-IR的因素分别为腰围和FBG。结论:腰围是影响胰岛素抵抗的重要因素,腰围、FBG增加均可加重胰岛素抵抗程度。女性腰围≥80 cm、男性腰围≥90 cm较女性腰围<80 cm、男性腰围<90 cm的2型糖尿病患者胰岛素抵抗程度严重。