罗格列酮对多囊肾囊肿衬里上皮细胞p38促分裂原活化蛋白激酶信号通路的影响

Objective To investigate the effect of rosiglitazone on p38 mitogen-activated protein kinase (p38MAPK) pathway in polycystic kidney cyst-lining epithelial cells. Methods The cyst-lining epithelial cells (PKD cells) from human polycystic kidney were treated with rosiglitazone (10 μmol/L), peroxisome proliferator-activated receptor-γ (PPARγ) inhibitor GW9662 (10 μmol/L), rosiglitazone (10 μmol/L) +GW9662 (10 μmol/L), p38MAPK specific inhibitor SB203580 (10 μmol/L), SB203580 (10 μmol/L)+ rosiglitazone(10 μmol/L) for 2 hours followed by epidermal growth factor (EGF) stimulation. Protein expressions of p38, phuspho-p38 (p-p38) and proliferating cell nuclear antigen (PCNA) were detected by Western blot. p38 mRNA was examined by RT-PCR. Expression of c-fos and c-jun was observed by immunocytochemistry. Results (1) EGF markedly up-regulated the expressions of p38, p-p38, PCNA, c-fos anti c-jun compared with control group (P<0.01). (2) Compared with EGF treated group, rosiglitazone significantly reduced p38 activation and mRNA expression (P<0.01, respectively). Rosiglitazone, rosiglitazone+SB203580 could significantly down-regulated p-p38, PCNA, c-fos and c-jun expression (P<0.01, respectively) with no significant difference between these two groups. (3) GW9662 partially reversed the reduction effect of rosiglitazone. Conclusions Rosiglitazone can inhibit proliferation of autosomal dominant polycystic kidney disease cyst-lining epithelial cells partially through down-regulating p38 activation and reducing c-fos, c-jun and PCNA expression. The above effect of rosiglitazone is in part PPARγ-independcnt.     

多囊肾肾功能衰竭患者发生心肌梗死行PCI治疗1例

<正>1临床资料患者男性,57岁,主因"间断胸痛5年,加重2月"入院。患者源于5年前活动后出现心前区闷痛,放射至后背,伴心悸,持续3分钟左右可自行缓解。2月前因"多囊肾"于当地医院行右肾切除术,术后5天突发胸痛,呈压榨样,放射至后背,伴胸闷、大汗,诊断为急性心肌梗死,因合并消化道出血未行冠状动脉造影及介入治疗。此后活动耐量进行性下降,步行数步即出现喘憋,常伴夜间阵发性呼     

利用凝集素芯片检测多囊肾病特异iPS细胞表面糖谱的研究

目的:建立一套凝集素芯片检测活体iPS细胞表面糖谱的方法。方法:以ADPKD-iPS为对象,运用不同活细胞染料,尝试不同的染色时间,找到最佳的iPS细胞与凝集素芯片结合的实验方案。结果:利用SYBR green,染色30min可以获得最佳的信号强度和信噪比。结论:已成功建立了一套利用凝集素芯片对活体iPS细胞进行表面糖谱检测的方法。     

常染色体显性遗传性多囊肾——病因,发病机制的研究进展

随着分子生物学技术的飞速发展及其在医学研究领域的广泛应用，有关常染色体显性遗传性多囊肾（ＡＤＰＫＤ）这一最常见的单基因病的研究成果越来越多。研究者们将由既往数十年缓慢进展的临床和病理生理学研究所积累的知识，已经与迅速发展的分子生物学技术相互结合，用来...     

肝肾囊性疾病，当明确诊断；临床干预治疗，应中西融合

肝肾囊肿是临床常见的囊性疾病,CT、核磁、B超等影像学检查有利于明确其诊断及鉴别诊断。单纯性的肝囊肿是肝脏最常见的良性病变之一,病位主要在肝,与脾、肾有关。单纯性的肾囊肿为良性的上皮囊肿,病位主要在肾,与肝、脾有关。肝肾囊肿病性皆为本虚标实。一般来说,囊肿体积较小,无压迫症状及肝肾功能障碍,仅需随访观察即可。若囊肿较大或多发囊肿,或病理性质倾向于恶性,损伤肝肾功能,或出现压迫症状,甚至引起肝肾功能衰竭,则应积极干预。治疗此类疾病之前,首先要明确诊断,明确病变病因,注意将单纯性囊肿与肝肾脏其他肿块相鉴别。临床在分期辨证的同时,将辨病与辨症相结合,采用中西医结合疗法可确保疗效。具体治疗,可采用外科手术改善压迫症状。中医治疗则可在辨证论治基础上,选用中药或针灸治疗,补虚祛邪并重,以恢复脏腑功能,延缓肝肾功能衰竭进展。     

罗格列酮对多囊肾囊肿衬里上皮细胞p38促分裂原活化蛋白激酶信号通路的影响

Objective To investigate the effect of rosiglitazone on p38 mitogen-activated protein kinase (p38MAPK) pathway in polycystic kidney cyst-lining epithelial cells. Methods The cyst-lining epithelial cells (PKD cells) from human polycystic kidney were treated with rosiglitazone (10 μmol/L), peroxisome proliferator-activated receptor-γ (PPARγ) inhibitor GW9662 (10 μmol/L), rosiglitazone (10 μmol/L) +GW9662 (10 μmol/L), p38MAPK specific inhibitor SB203580 (10 μmol/L), SB203580 (10 μmol/L)+ rosiglitazone(10 μmol/L) for 2 hours followed by epidermal growth factor (EGF) stimulation. Protein expressions of p38, phuspho-p38 (p-p38) and proliferating cell nuclear antigen (PCNA) were detected by Western blot. p38 mRNA was examined by RT-PCR. Expression of c-fos and c-jun was observed by immunocytochemistry. Results (1) EGF markedly up-regulated the expressions of p38, p-p38, PCNA, c-fos anti c-jun compared with control group (P<0.01). (2) Compared with EGF treated group, rosiglitazone significantly reduced p38 activation and mRNA expression (P<0.01, respectively). Rosiglitazone, rosiglitazone+SB203580 could significantly down-regulated p-p38, PCNA, c-fos and c-jun expression (P<0.01, respectively) with no significant difference between these two groups. (3) GW9662 partially reversed the reduction effect of rosiglitazone. Conclusions Rosiglitazone can inhibit proliferation of autosomal dominant polycystic kidney disease cyst-lining epithelial cells partially through down-regulating p38 activation and reducing c-fos, c-jun and PCNA expression. The above effect of rosiglitazone is in part PPARγ-independcnt.     

罗格列酮对多囊肾囊肿衬里上皮细胞p38促分裂原活化蛋白激酶信号通路的影响

Objective To investigate the effect of rosiglitazone on p38 mitogen-activated protein kinase (p38MAPK) pathway in polycystic kidney cyst-lining epithelial cells. Methods The cyst-lining epithelial cells (PKD cells) from human polycystic kidney were treated with rosiglitazone (10 μmol/L), peroxisome proliferator-activated receptor-γ (PPARγ) inhibitor GW9662 (10 μmol/L), rosiglitazone (10 μmol/L) +GW9662 (10 μmol/L), p38MAPK specific inhibitor SB203580 (10 μmol/L), SB203580 (10 μmol/L)+ rosiglitazone(10 μmol/L) for 2 hours followed by epidermal growth factor (EGF) stimulation. Protein expressions of p38, phuspho-p38 (p-p38) and proliferating cell nuclear antigen (PCNA) were detected by Western blot. p38 mRNA was examined by RT-PCR. Expression of c-fos and c-jun was observed by immunocytochemistry. Results (1) EGF markedly up-regulated the expressions of p38, p-p38, PCNA, c-fos anti c-jun compared with control group (P<0.01). (2) Compared with EGF treated group, rosiglitazone significantly reduced p38 activation and mRNA expression (P<0.01, respectively). Rosiglitazone, rosiglitazone+SB203580 could significantly down-regulated p-p38, PCNA, c-fos and c-jun expression (P<0.01, respectively) with no significant difference between these two groups. (3) GW9662 partially reversed the reduction effect of rosiglitazone. Conclusions Rosiglitazone can inhibit proliferation of autosomal dominant polycystic kidney disease cyst-lining epithelial cells partially through down-regulating p38 activation and reducing c-fos, c-jun and PCNA expression. The above effect of rosiglitazone is in part PPARγ-independcnt.     

产气性肾周脓肿1例

患者,男,41岁.入院前6天起无明显诱因出现左腰部胀痛,呈持续性阵发性加重,无放射痛,期间伴有寒战、高热,体温最高41℃,不伴有恶心、呕吐,无尿频、尿急、尿痛、脓尿及肉眼血尿,在外院按"肾结石"给予止痛、解痉、抗感染治疗,症状无明显缓解,急诊入我院.体检:心、肺、腹正常,肾区、输尿管走行区无压痛,左肾区叩击痛.既往有先天性多囊肾病史,右肾萎缩,发现血糖升高1年,未予治疗.实验室检查:白细胞为10.6×109/L,GR89.4%,血糖25.01 mmol/L,肌酐165.9 μmol/L;尿糖( ),尿白细胞和尿细菌培养均阴性.     

成年型多囊肾一家系六例

先证者（Ⅱ7）男，59岁，自觉双侧腰部不适，疼痛6年，加重伴水肿2年。该患者于6年前无明显诱因出现双侧腰部不适，疼痛，遂于当地市医院检查，诊断为“先天性多囊肾”，未给予特殊治疗。近2年来该患者上述症状渐加重，出现颜面部水肿，晨起时明显，同时出现血尿、头晕、头胀痛等症状，查体：血压190／105mmHg（1mmHg=0．133kPa），肾功能检查：血尿素氮20．5mmol／L，