6%)高于对照组(80.0%),差异有统计学意义(P<0.05)。观察组患者血淀粉酶以及白细胞达到正常范围的时间、腹痛症状改善时间与住院天数方面显著短于对照组,差异有高度统计学意义(P<0.01)。结论参麦注射液联合生长抑素治疗重症急性胰腺炎效果显著,可以明显改善患者血清TNF-α、IL-6及IL-10水平。
目的探讨Src酪氨酸激酶抑制剂Ⅱ对Src蛋白及其下游信号作用。方法采用半定量RT-PCR法检测Src酪氨酸激酶抑制剂Ⅱ处理后的人膀胱癌细胞T24各浓度组(0、0.2、1.0、5.0μmol/mL组)的c-Src、p38MAPK基因表达的变化情况,使用Western blot检测Src酪氨酸激酶抑制剂Ⅱ处理后T24细胞内的c-Src蛋白磷酸化类型与非磷酸化类型的表达情况。结果 Src酪氨酸激酶抑制剂Ⅱ处理有下调后的人膀胱癌细胞T24各浓度组的c-Src mRNA的表达下调;p38基因的表达呈逐渐下调趋势。处理后T24细胞内c-Src基因在蛋白表达水平上其磷酸化类型随Src酪氨酸激酶抑制剂Ⅱ浓度的增高表达逐渐下降,并且呈剂量效应关系。结论 Src酪氨酸激酶抑制剂Ⅱ可能通过竞争Src蛋白磷酸化位点,使其不能激活,导致下游的细胞传导途径失活使得T24细胞增殖得到抑制,认为Src蛋白具有作为膀胱移行细胞癌分子靶向治疗的潜在靶点的可能性。Src酪氨酸激酶抑制剂Ⅱ可能可以通过阻止Src蛋白激活影响其下游的Ras/Raf/MEK/MAPK(ERK1/2或p38)通路和ERK1/2和p38细胞信号传导通路,下调p38表达不仅直接和间接地诱导T24细胞凋亡,而且可以阻止或减少T24细胞的迁移、扩散和穿膜侵袭的发生。
目的分析并探讨支气管哮喘患儿吸入糖皮质激素对生长发育的影响情况。方法择取我院所收治的支气管哮喘患儿60例作为研究对象,均接受小剂量糖皮质激素吸入治疗。选择同期健康儿童60例作为对照组。对两组进行为期1年的随访调查,就身高、体重、骨代谢水平进行综合对比与分析。结果哮喘组患儿1年内身高增长均值、体重增长均值、骨密度水平均值与对照组对比无明显差异(P>0.05),无统计学意义。结论以小剂量吸入糖皮质激素方法对支气管哮喘患儿进行治疗,对儿童生长发育无明显不良影响,可作为临床常规用药方案,具有安全性优势,值得进一步推广。
目的通过分析丝裂原和应激激活蛋白激酶1(MSK1)在实验性自身免疫性脑脊髓炎(EAE)中的表达情况探讨中药复方益肾达络饮保护小鼠损伤脑组织的机制。方法利用蛋白印迹技术,检测小鼠脑组织中MSK1、CREB的含量。结果脑组织中MSK1表达显示,正常组和中药组、激素组、抑制剂组均有显著性差异(均P<0.01);模型组和抑制剂组有显著性差异(均P<0.01);中药组和激素组、抑制剂组有显著性差异(P<0.01);中药组和模型组、中药加激素组有差异(均P<0.05)。CREB表达显示:中药组CREB的表达与其余各组相比均显著升高(P<0.01);中药组、中药加激素组和激素组的CREB水平依次降低。结论复方益肾达络饮治疗EAE与MSK1升高有关,p38MAPK信号通路下游因子MSK1表达与其底物CREB表达呈相同态势。
Colorectal

点击此处 通常 cancer(CRC)remains one of the most common malignancies in 很少 the world.Although surgical resection combined with adjuvant therapy is effective at the early stages of the disease,resistance to conventional therapies is frequently observed in advanced stages,where

treatments become ineffective.Resistance to cisplatin,irinotecan and 5-fluorouracil chemotherapy has been shown to involve mitogen-activated protein kinase(MAPK)signaling and recent studies identified p38αMAPK as a mediator of resistance to various agents in CRC patients.Studies published in the last decade showed a dual role for the p38αpathway in mammals.Its role as a negative regulator of proliferation has been reported in both normal(including cardiomyocytes,hepatocytes,fibroblasts,hematopoietic and lung cells)and cancer cells(colon,prostate,breast,lung tumor cells).This function is mediated by the negative regulation of cell cycle progression and the transduction of some apoptotic stimuli.However,despite its anti-proliferative and tumor suppressor activity in some tissues,the p38αpathway may also acquire an oncogenic role involving cancer related-processes such as cell metabolism,invasion,inflammation and angiogenesis.In this review,we summarize current knowledge about the predominant role of the p38αMAPK pathway in CRC development and chemoresistance.In our view,this might help establish the therapeutic potential of the targeted manipulation of this pathway in clinical settings.