目的 明确Wnt/PCP-JNK通路在牛磺酸预防神经畸形中的介导作用及机制.方法 采用维甲酸诱导昆明小鼠胚胎神经管畸形模型及设立应用牛磺酸预防的动物模型,采用免疫组化、蛋白质印迹法(Western blot)检测Wnt/PCP-JNK通路中Dvl、RhoA、p-JNK/JNK在胚胎发育神经管中的表达变化,及各个蛋白表达变化的相互关系.结果 健康对照组中未见神经管畸形胚胎;采用免疫组化、Western Blot检测Dvl、RhoA、p-JNK/JNK表达较低.维甲酸致畸组神经畸形发生率为57.1％,较健康对照组明显增高(P＜0.05);Dvl、RhoA、p-JNK/JNK表达较健康对照组明显增高(P＜0.05).牛磺酸干预组神经畸形发生率为31.7％,较维甲酸致畸组明显减低(P＜0.05);Dvl、RhoA、p-JNK/JNK表达较维甲酸致畸组明显降低(P＜0.05).结论 Wnt/PCP-JNK通路介导了牛磺酸预防神经管畸形发生的过程

Objective To clarify the mediating role and mechanism of Wnt/PCP-JNK pathway in prevention of neural malformation of taurine.Methods Kunming mouse model of embryonic neural tube defects were induced by using retinoic acid and the animal models of these defects were established by using taurine.Immunohistochemistry,Western Blotting were used to detect Dvl,RhoA,p-JNK/JNK expression of Wnt/PCP-JNK pathway in the neural tube during embryonic development and the relationships among expression changes of various proteins.Results In the control group,no embryos with neural tube defects were observed and low expressions of Dvl,RhoA and p-JNK/JNK were detected by using immunohistochemistry and Western blotting.In the teratogenic group,the incidence of neurological malformation (57.1％) was significantly higher than that in the control group (P ＜ 0.05).Compared with the control group,the expressions of Dvl,RhoA and p-JNK/JNK significantly increased (P ＜ 0.05).The incidence of neurolo

研究c-jun氨基末端激酶(JNK)参与三丁基锡(Tributyltin,TBT)诱导正常人羊膜细胞FL凋亡的分子机制。方法:FL细胞经不同浓度TBT染毒1h后,PI/Annexin V双染色法检测FL细胞凋亡率。Western blot检测FL细胞JNK的磷酸化水平,Bax定位、Bcl-2的磷酸化水平及总Bax和Bcl-2表达水平。结果:与对照组相比,4μmol/L和6μmol/L的TBT染毒剂量组细胞凋亡率明显升高,2μmol/L~6μmol/L剂量组JNK磷酸化水平升高,差异有统计学意义(P0.01)。JNK特异抑制剂SP600125明显降低TBT诱导的FL细胞凋亡率,而JNK特异抑制剂SP600125对Bax定位、Bcl-2的磷酸化水平及总的Bax和Bcl-2表达量无影响。结论:JNK的活化是TBT诱导FL细胞凋亡的重要因素,但JNK介导凋亡的途径并非通过调控凋亡相关因子Bax和Bcl-2。

Objective:To study the effects of JNK activation on TBT-induced apoptosis and investigate the underly-ing mechanism in human amnionic cells. Methods:In the study, PI/Annexin V staining assay was applied to detect apopto-sis induced by TBT in FL cells. The phosphorylation of JNK, expression and localization of Bax, and the expression and phosphorylation of the Bcl-2, respectively, were measured by Western blot. Results:Compared with the control group, the proportion of apoptotic FL cells were increased in the 4 and 6 μmol/L TBT-treated groups, and the phosphorylation of JNK was markedly increased in the 2, 3, 4 and 6 μmol/L TBT-treated groups (P<0.01). JNK-specific inhibitor attenuated the TBT-mediated elevation of apoptotic rates. However, JNK-specific inhibitor had no effect on the expression and localiza-tion of Bax, as well as the expression and phosphorylation of the Bcl-2. Conclusion:JNK activation in apoptotic human amnion cells is not involved in the upstream signali

JNK信号通路在组织器官的形态发生、结构维持以及损伤修复中发挥重要的调节功能，其基本构成、调节方式、胞内其他信号通路间相互作用及其在生理与肿瘤的的发生中作用。JNK信号传导通路与肿瘤侵袭演进起重要作用，对肿瘤发生、发展机制研究中也有重要的作用。

JNK signaling pathways in tissue organ morphogenesis, structure to maintain and repair damage play an important regulating function .JNK signaling pathways basic structure, control mode, intracellular signaling pathways other interaction and the physiological and the occurrence of cancer role. The JNK signal transduction pathway plays an important role in tumor invasion and evolution,research on the mechanism of JNK signaling pathway in tumorigenesis, also has an important role.

目的：观察缓激肽（bradykinin,BK）对高糖诱导肾系膜细胞产生C-Jun氨基末端激酶（C-JunNH2-terminal kinase,JNK）通路活化的影响,探讨BK对高糖诱导肾系膜细胞的影响与JNK通路的相关性。方法：用Western Blotting法检测BK（100ng/mL）对JNK磷酸化蛋白瞬间表达的影响。结果：BK可抑制高糖诱导的JNK磷酸化蛋白的表达,与未加BK组比较,差异有统计学意义（P〈0.01）。结论：BK可抑制高糖诱导肾系膜细胞JNK磷酸化蛋白的表达,可能是其延缓糖尿病肾病进展的作用机制。

Objective:To observe the effect of bradykinin(BK)on activation of C-jun NH2-terminal kinase(JNK)sig-nal pathway in mesangial cells induced by high glucose and the correlation between them. Methods: Mesangial cells were pretreated by BK with a concentration of 100 ng/ml for 15 min and then were cocultured with high glucose(30 mmol/L). Transient expression of JNK phosphorylation protein were detected with Western blotting. Re-sults: Compared with that in mesangial cells cultured with glucose and high glucose, the expression of JNK phos-phorylation protein was less in mesangial cells pretreated with BK, with a significant difference (P<0.01). Conclu-sion: BK can inhibit the expression of JNK phosphorylation protein in mesangial cells cultured with high glucose. This may be the underlying mechanism of BK involved in delaying the progression of diabetic nephropathy.

目的：探讨芪蓟肾康方通过JNK信号通路对大鼠肾小球系膜细胞的影响。方法：体外培养大鼠肾小球系膜细胞，用血管紧张素Ⅱ刺激系膜细胞增生，给予芪蓟肾康方黄酮干预，用酶联免疫吸附（ELISA）法检测肾小球系膜细胞上清液 c-Jun 氨基末端激酶（JNK）、活化蛋白1（AP-1）、纤维粘连蛋白（FN）蛋白表达；实时定量 PCR 法检测 JNK、AP-1 mRNA 的表达。结果：与正常组比较，模型组及治疗组大鼠肾小球系膜细胞中 JNK、AP-1及 FN 蛋白表达明显升高（P约0.05或 P约0.01）；与模型组比较，治疗组大鼠肾小球系膜细胞中 JNK、AP-1及 FN 蛋白表达明显降低（P约0.05或 P约0.01）。与正常组比较，模型组及治疗组大鼠肾小球系膜细胞中 JNK、AP-1及 FN mRNA 表达明显升高（P约0.05或 P约0.01）；与模型组比较，治疗组大鼠肾小球系膜细胞中 JNK、AP-1及 FN mRNA明显降低（P约0.05）。结论：芪蓟肾康方可以通过下调肾小球系膜细胞JNK、AP-1 mRNA及蛋白的表达水平，抑制 JNK 信号转导，降低 AP-1的活性，减少 FN 的增殖，从而减轻 GMC 增生，延缓肾小球的损伤，防止肾小球的硬化。

This study was aimed to investigate the effects of Qi-Ji Shen-Kang (QJSK) on glomerular mesangial cell (GMC) through the c-Jun N-terminal kinase (JNK) signal pathway. GMC was cultured in vitro and the proliferation was induced with Angiotensin II (AngII). Then, QJSK was used to inhibit the proliferation. ELISA was used in the detection of protein expressions of JNK, activator protein-1 (AP-1) and fibronectin (FN). Q-PCR was used in the de-tection of expression of JNK and AP-1mRNA. The results showed that compared with the normal group, protein ex-pressions of JNK, AP-1 and FN of GMC among rats in the model group and the treatment group were obviously in-creased (P< 0.05 or P< 0.01). Compared with the model group, protein expressions of JNK, AP-1 and FN of GMC among rats in the treatment group were obviously decreased (P < 0.05 or P < 0.01). Compared with the normal group, expressions of JNK, AP-1 and FN mRNA of GMC among rats in the model group and the treatment group were obviously in