目的 探讨甘露聚糖结合凝集素(MBL)途径激活对糖尿病肾病(DN)合并高血压的影响,并探讨左旋氨氯地平对DN合并高血压患者的保护作用.方法 选择2012年9月至12月泸州医学院附属医院肾内科就诊的DN合并高血压患者40例,按机数字表法分为试验组30例,对照组10例.两组均给予DN的常规治疗,试验组在常规治疗基础上口服左旋氨氯地平2.5mg,每日1次,如果2周后血压仍未降至正常(＞140/90mmHg,1mmHg=0.133kPa)则增加左旋氨氯地平用量至5mg,并联合应用降压药物;两组均连续用药90d.观察两组患者治疗前和治疗后30d和90d血压的变化及治疗前后血脂、肝肾功指标、外周血尿白蛋白排泄率(UAER)、MBL、糖化血红蛋白(HbA1c)、膜攻击复合物(MAC)的变化,并评价MBL与DN的相关性.结果 试验组治疗后30d、60d血压均较治疗前下降[收缩压(mmHg):157.4±8.6、145.6±7.5比167.6±11.4,舒张压(mmHg):90.6±6.9、83.9±5.8比98.6±7.9,均P＜0.05].两组治疗前后总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白-C(HDL-C)、低密度脂蛋白-C(LDL-C)、糖化血红蛋白(HbA1c)、血肌酐(SCr)水平比较差异均无统计学意义(均P＞0.05).两组治疗后UAER、MBL和MAC均较治疗前明显下降,且试验组的下降程度较对照组更显著[UAER(mg/24h)为200.3±69.8比467.2±87.3,MBL(μg/L)为410±120比519±98,MAC(pg/L)为60±20比80±18,均P＜0.05].相关性分析显示,血清MBL及尿MAC水平均与UAER呈正相关(rMBL/UAER=0.894,P=0.041;rMAC/UAER=0.908,P=0.032).结论 左旋氨氯地平对DN合并高血压患者具有保护作用,其机制与MBL途径相关.

Objective To investigate effectiveness and safety of amlodipine besylate combined with enalapril on diabetic nephropathy complicated with hypertension. Methods From August 2012 to October 2014 in the Affiliated Hospital of Luzhou Medical College,a total of 118 diabetic nephropathy patients complicated with hypertension were divided into groups A (n = 35 ),B ( n = 39 ) and C ( n = 44 ) according to random number table. Patients of the three groups deactivate antihypertensive drugs before enrolling the study,and were given insulin and metformin to control blood glucose. Patients of A group were given enalapril,patients of B group were given amlodipine besylate,and patients of C group were given amlodipine besylate combined with enalapril,all of the three groups treated for 4 weeks. Blood pressure(including 24 h SBP,24 h DBP, 24 h MAP),glycemic indicators(FBG,2 h PBG,HbA1c ) before and after treatment,incidence of adverse reactions during treatment were compared among the three groups,renal function index ( including BUN, Scr,24 - hour urine protein quantitative). Results No statistically significant differences of 24 h SBP,24 h DBP,24 h MAP,BUN,Scr,24 - hour urine protein quantitative,FBG,2 h PBG or HbA1c was found among the three groups(P > 0. 05);after treatment,24 h SBP, 24 h DBP,24 h MAP,Scr and 24 - hour urine protein quantitative of C group were statistically significantly lower than those of groups A and B,while no statistically significant differences of BUN,FBG,2 h PBG or HbA1c was found among the three groups (P > 0. 05). The incidence of adverse reactions of A group was 11. 4% ,that of B group was 10. 3% ,of C group was 10. 3% , the difference was not statistically significantly different(P > 0. 05). Conclusion Amlodipine besylate combined with enalapril has better antihypertensive effect,hypoglycemic effect and renal protection effect than independent use of amlodipine besylate or enalapril in treating diabetic nephropathy complicated with hypertension,without increasing the incidence of adverse reactions.

目的 观察阿魏酸哌嗪片治疗狼疮肾炎的临床疗效.方法 将80例狼疮肾炎患者随机分为两组.对照组给予激素加免疫抑制剂常规治疗.治疗组在对照组基础上加用阿魏酸哌嗪片治疗.观察并比较两组的临床疗效及血肌酐、尿素氮、血浆白蛋白、血红蛋白、尿蛋白定量、补体C3、抗核抗体、抗双链DNA抗体等指标的改变情况.结果 治疗组在治疗后血尿素氮、血肌酐、尿蛋白定量均明显下降,血浆白蛋白、血红蛋白较治疗前明显上升,且与对照组比较有统计学差异.结论 阿魏酸哌嗪联合激素加免疫抑制剂治疗狼疮肾炎疗效优于常规治疗,对狼疮肾炎患者纠正贫血、改善肾功能、降低尿蛋白有一定疗效.

目的 探讨辛伐他汀联合氯吡格雷对糖尿病肾病合并高脂血症的血液透析患者动静脉内瘘血栓形成的预防作用及可能机制. 方法 选取65例维持性透析的糖尿病肾病合并高脂血症的动静脉内瘘患者,随机分为对照组,治疗组,治疗组患者予以口服“辛伐他汀20mg,qd及氯吡格雷50mg,qd”,对照组不使用任何调脂和抗血小板药物,观察12个月,统计内瘘总通畅率.结果 治疗组内瘘通畅率明显高于对照组,治疗组明显减少了内瘘血栓的形成.结论 联合使用辛伐他汀及氯吡格雷对预防糖尿病肾病合并高脂血症的血液透析患者动静脉内瘘血栓形成具有显著效果,其操作简单,费用少,有较高的临床应用价值.

目的 观察舒洛地特治疗非糖尿病性慢性肾脏病(CKD) 2～3期的临床疗效及安全性.方法 将40例非糖尿病性CKD 2～3期患者随机分为对照组和治疗组,每组20例.对照组进行常规治疗(包括降压、肠道排毒及纠正贫血等处理)；治疗组在对照组治疗的基础上加服舒洛地特胶囊25 mg/次,2次/d,共50 d.比较2组治疗后血肌酐、24 h尿蛋白定量及纤维蛋白原含量.结果 治疗组血肌酐、24 h尿蛋白定量及纤维蛋白原含量明显低于对照组(P＜0.05).结论 舒洛地特治疗非糖尿病性CKD 2～3期效果好,具有临床应用价值.

Objective To observe the effects of Shenxiong glucose injection in the treatment of chronic renal failure.Methods 60 patients with chronic renal failure were randomly divided into control group(rourine treatment) and treatmental group(routine treatment added with Shenxiong glucose injection).Results The serum creatinine,the urine protein quantitiative and fibrinogen of treatmental group were decreased greater than that in the control group,there was obviously difference in two groups(P<0.05).Conclusion Shenxiong glucose injection is effective in the treatment of chronic renal failure.

目的探讨脱氧核苷酸钠注射液对急性肾损伤患者的肾功能恢复是否有促进作用。方法将60例急性肾损伤患者随机分为两组:(1)对照组:进行常规治疗(包括病因、对症治疗以及血液透析);(2)治疗组:在上述对照组疗法基础上加用脱氧核苷酸钠注射液200mg静滴,每天一次,共15天。比较两组患者治疗后肾功的恢复情况。结果治疗15天后治疗组患者血肌酐水平明显低于对照组(P<0.01)。结论脱氧核苷酸钠注射液对急性肾损伤患者肾功的恢复有促进作用。

原发性肾病综合征(primary nephon systom)是一种肾脏的常见病、多发病.大剂量激素常用于原发性肾病综合征患者,会引起感染加重、严重高血压、糖尿病、精神性疾病、骨质疏松、消化道出血等并发症,多以高血压、高血糖、加重感染等常见,而上消化道出血则鲜为报道.现将我院收治的1例原发性肾病综合征患者在使用激素过程中出现上消化道出血病例进行报道分析,以期望引起临床医师对同类病例的重视.

目的探讨立普妥对维持性血透(MHD)患者微炎症状态的影响。方法选择我院肾内科维持性血透患者40例,随机分为对照组和立普妥治疗组。检测治疗前后患者炎症因子高敏-C反应蛋白(hs-CRP)及白细胞介素-6(IL-6)的变化。结果治疗组患者用立普妥20mg/d治疗3月,其hs-CRP及IL-6含量较对照组显著减少(P<0.05)。结论立普妥可改善维持性血透患者微炎症状态。

OBJECTIVE To study the effects of transforming growth factor-beta1/integrin-linked kinase (TGF-beta1/ILK) signal way in interleukin-1beta (IL-1beta)-induced rat tubular epithelial-myofibroblast transdifferentiation (TEMT), and to investigate whether emodin inhibits IL-1beta-induced TEMT through the TGF-beta1/ILK signal way-dependent mechanism. METHODS Normal rat kidney epithelial cell line (NRK52E) was used in this study. NRK52E cells were divided into blank control group, emodin control group, IL-1beta-induced group, emodin-inhibited group, SB431542 (TGF-beta 1 type I receptor blocker)-inhibited group, emodin plus SB431542-inhibited group, emodin-pretreated group and emodin-reversed group. After 48-hour culture, morphological changes of the NRK52E cells were observed by an inverted phase contrast microscope. The expressions of alpha-smooth muscle actin (alpha-SMA) and E-cadherin were detected by two-color immunohistochemical staining, while the expressions of TGF-beta1 and ILK were detected by one-color immunohistochemical staining. We also performed the imaging analysis to quantitatively analyze the result of the immunohistochemical staining. The secretion of fibronectin (FN) was analyzed by enzyme-linked immunosorbent assay. RESULTS Compared with the blank control group, IL-1beta might induce TEMT, which was showed in increasing expression of alpha-SMA, increasing secreting of FN and decreasing expression of E-cadherin, and at the same time the expressions of TGF-beta1 and ILK were enhanced (P<0.05). Emodin might inhibit all of those changes induced by IL-1beta (P<0.05). When TGF-beta1 signal way was intercepted, IL-1beta induced-TEMT was suppressed and the expression of ILK was decreased, however, there was no significant difference in expression of TGF-beta1 between the SB431542 group and the IL-1beta-induced group. Compared with emodin-inhibited group, emodin-pretreatment could not prevent IL-1beta induced-TEMT in a certain extent, but emodin could not revert IL-1beta-induced TEMT. Spearman correlation analysis showed that TGF-beta1 expression had positive correlation with expressions of alpha-SMA, FN, ILK and negative correlation with E-cadherin expression, and the expression of ILK was positively correlated with the expressions of alpha-SMA and FN and negatively correlated with E-cadherin expression. CONCLUSION IL-1beta induces TEMT partly depending on TGF-beta1/ILK signal way, partly via which emodin inhibits the TEMT induced by IL-1beta.

Objective It is to explore the role of p38 mitogenactivated protein kinase(p38MAPK) on the IL-1β-induced tubular epithelial-myofibroblast transdifferentiation(TEMT) and to explore intervention of Emodin(EMD).Methods The cultured NRK52E cells in vitro were divided into control group,IL-1β-induced group,IL-1β+SB203580 group and IL-1β+EMD group.After the cells had been cultured for 48 hours,the morphology of cells was observed under the inverted phase-contrast microscope and the expressions of α-SMA,CK,p38MAPK and p-p38MAPK were measured by immuno-cytochemistry method.Results IL-1β could induce some NRK52E became fibroblast-like-shaped and the expressions of CK decreased significantly,but α-SMA p38MAPK and p-p38MAPK increased respectively.After p38MAPK been blocked by SB 203580,the changes of morphology induced by IL-1β were inhibited,and the expressions of α-SMA and p-p38MAPK decreased respectively,CK increased significantly.EMD could significantly inhibit the morphologic changes and the expressions of α-SMA p38MAPK and p-p38MAPK.The inhibitory effects of EMD were similar to that of SB 203580.Conclusion p38MAPK takes a part in the process of TMET induced by IL-1β.EMD can inhibit the process of TMET through interventing the p38MAPK signaling pathway.

AIMTo observe the change of ILK expression in interleukin-1beta(IL-1beta)-induced tubular epithelial-myofibroblast transdifferentiation, and to investigate whether emodin inhibit IL-1beta-induced tubular epithelial-myofibroblast transdifferentiation through an intergern linked kinase-dependent mechanism.METHODSNormal rat kidney epithelial cell line (NRK52E) was cultured and then divided into blank group, emodin control group, IL-1beta-induced group and emodin-inhibited group. When the cells were cultured for 48 h, their morphological changes were observed by an inverted phase contrast microscope. The expression of a-smooth muscle actin (a-SMA) and E-cadherin were detected using a two-color immunohistochemistry staining technique, while the expression of integrin-linked kinase (ILK) was detected using a one-color immunohistochemistry staining technique. The secretion of fibronectin (FN) was analyzed by ELISA.RESULTSNRK52E cells cultured with IL-1 became fibroblast-like in appearance. The expression of a-SMA was enhanced (65h5+/-1h7 vs 140h4+/-3h0, P<0h05), the expression of E-cadherin was decreased (82h5+/-1h0 vs 36h0+/-2h8, P<0h05), the expression of ILK was enhanced (36h1+/-3h1 vs 82h4+/-1h2, P<0h05), and the secretion of FN was increased (54h6+/-3h1 vs 124h8+/-3h2 mg/L, P<0h05). Emodin markedly inhibited all of those changes induced by IL-1beta.CONCLUSIONThe expression of ILK is up-regulated in IL-1beta-induced tubular epithelial-myofibroblast transdifferentiation. Emodin might inhibit TEMT by a down-regulation the expression of ILK.

Objective To observe the effect of Emodin(EMD)on the tubular epithelial-myofibroblast transdifferentiation(TEMT)induced by IL-1β in vitro.Methods The cultured NRK52E cells were induced by IL-1β,and at the same time co-incubated with different concentrations EMS.After cells had been cultured for 12、24、48 and 72 hours respectively,the morphology of cells was observed under the inverted phase-contrast microscope;the expressions of a-SMA,CK were measured by immuno-cytochemistry method and semiquantified by mean intergrated opitical density(IOD).Results Compared with IL-1β group,the expressions of a-SMA and CK of NRK52E cells treated only with different concentrations EMD have not significant difference.EMD can reduce the IL-1β-induced NRK52E cells' morphology changes,and up-regulate the expression of CK but down-rugulate a-SMA's significantly.Conclusion EMD can inhibit partly the process of TMET induced by IL-1β.

Aim: To observe the influence of interleukin (IL)-1β on tubular epithelial-myofibroblast transdifferentiation (TEMT) and the secretion of fibronectin (FN) in cells. Methods: The experiment was carried out in the Staff Room of Infection Immunity, Affiliated Hospital of Luzhou Medical College from June 2005 to January 2006. The normal rat kidney epithelial cell line (NRK52E) was cultured In Vitro and then co-incubated with IL-1β (10 μg/L), When the cells were cultured for 12, 24, 48, 72 hours, their morphological changes were observed through inverted phase contrast microscope; The expressions of α-smooth muscle actin (α-SMA) and E-cadherin were detected by a two-color immunohistochemistry staining technique; Supernatant liquid of every well was analyzed for secretion of FN by ELISA. Results: NRK52E cells cultured with IL-1β for 48 hours became fibroblast-like in appearance; when the cells were cultured With IL-1β for 12 and 72 hours, the expression of α-SMA were enhanced (64.80±2.19, 83.23±2.71, 170.53±3.94, P < 0.05), the expression of E-cadherin was decreased (81.77±1.27, 64.50±1.31, 26.20±2.32, P < 0.05). These changes were time-dependent. The secretion of FN was increased with the time prolonged (P < 0.05) and doubled at 72 hours of culture. Conclusion: IL-1β can induce TEMT and enhance the secretion of FN in cultured NRK52E cells.

AIM:Emodin could significantly inhibit the differentiation of NRK52F cell induced by interleukin-1β(IL-1β).In this study,we investigate the effects of transforming growth factor β1(TGF-β1) on the differentiation of tubular epithelial-myofibroblast transdifferentiation(TEMT) induced by IL-1β and on the inhibition of emodin.METHODS:The experiment was carried out in Immunity Laboratory of Affiliated Hospital of Luzhou Medical College from October 2006 to May 2007.The cultured NRK52E cells of rats were divided into ①control group,in which the cells were cultured in high glucose DMEM medium added by 0.05 volume fraction calf serum,②IL-1β induction group,in which the high glucose DMEM medium containing 10 μg/L IL-1β was used,③SB431542 blocking group,in which the cells were cultured in high glucose DMEM medium containing 10 μg/L IL-1β and 10 μmol/LSB431542,and ④IL-1β+emodin group,in which the cells were cultured in high glucose DMEM medium containing 10 μg/L IL-1β and 25 mg/L emodin.After the cells were treated for 48 hours,the morphology of NRK52E cells was observed under the inverted phase-contrast microscope and the expressions of creatine kinase(CK),α-smooth muscle actin(α-SMA) and TGF-β1 were measured by immunocytochemistry method.RESULTS:①Some cells became fibroblast-like-shaped after induced by IL-1β,and the expressions of CK decreased significantly(P < 0.01),but α-SMA and TGF-β1 increased(P < 0.01).②In SB431542 blocking group,the percentage of elongated cells was less than that of IL-1β group and the expression of α-SMA was decreased(P < 0.01),but CK increased significantly(P < 0.01).No obvious change was found in the expression of TGF-β1.③The inhibitory effect of emodin on the morphous of IL-1β induced cells and the expressions of CK and α-SMA was significantly and similar to that of SB431542.Meanwhile,emodin remarkably inhibited the expression of TGF-β1 induced by IL-1β.CONCLUSION:TGF-β1 may mediate the process of TMET induced by IL-1β,and the inhibitory effect of emodin on the process of TMET induced by IL-1β.

丝裂原活化蛋白激酶(mitogen activated protein kinases,MAPKs)是一类存在于大多数真核细胞内,转导胞外信号引起细胞反应的丝/苏氨酸蛋白激酶,是细胞内一重要信号系统.其中,p38MAPK信号通路是MAPKs家族的重要组成部分,它经外界刺激应激而激活,故又称为MAPK应急信号通路,其在全身炎性反应、细胞分化及凋亡等方面具有十分重要的作用,近年研究发现p38MAPK信号通路也参与细胞迁移的调控.现就p38MAPK及其在细胞迁移中的作用的研究进展进行综述.

肾间质纤维化几乎是所有原发或继发肾脏疾病进展到终末期肾衰竭的共同途径.大黄素为大黄的有效成分之一,其药理作用广泛.近年研究表明大黄素有抗肾间质纤维化作用,本文就大黄素药理作用机制及其抗间质纤维化研究进展进行综述.