05),且CCI组比HBO组降低显著(P<0.05)。CCI组、HBO组的磷酸化p38及P2X4受体含量较S组增加(P<0.05),且CCI组磷酸化p38及P2X4受体的表达比HBO组显著增加(P0.05),但与未给抑制剂第一部分实验的CCI组、HBO组比较明显增高(P<0.05);CCI组及HBO组的P2X4受体表达比S组显著增高(P0.05)。结论高压氧可能通过P2X4受体介导的p38
S6 Kinase 抑制剂 MAPK信号通路影响神经病理性疼痛大鼠。
目的分析胆酸降载脂蛋白A(Apo A)效应与miR-23b-3p的关系,研究胆酸降Apo A作用新机制。方法首先用生物信息学在线工具对miR-23b-3p与调控LPA基因的转录因子肝细胞核因子4γ(HNF4γ)进行靶基因分析,使用荧光素酶报告系统对miR-23b-3p与调控LPA基因的转录因子HNF4γ进行靶基因验证实验,Western blot检测Apo A表达水平、p38MAPK(MAPK:丝裂原活化蛋白激酶)及p-p38MAPK,实时定量PCR检测miR-23b-3p表达水平。结果生物信息学分析表明HNF4γ可作为miR-23b-3p的靶基因,荧光素酶报告系统转染miR-23b-3p处理组细胞裂解后荧光强度显著低于对照组,验证了HNF4γ可作为miR-23b-3p的靶基因。胆酸呈剂量和时间依赖性抑制Hep G2细胞Apo A的表达,以32 mg/L和24 h的作用最显著。胆酸抑制Apo A表达与活化MAPK和上调miR-23b-3p有关。结论胆酸呈剂量和时间依赖性地下调Hep G2细胞Apo A表达水平;胆酸降Apo A与上调miR-23b-3p有关。
分娩疼痛具有典型的内脏痛及躯体痛,电针分娩镇痛是一种安全有效、操作简单、对母婴无创伤的非药物治疗方法。在针灸镇痛领域,MAPKs是较为重要的研究对象。p38MAPK信号通路可被应激刺激激活,对疼痛发生、发展起着重要的作用,从基因水平及细胞分子学理论了解P38 TNF-alpha抑制剂 MAPK与分娩镇痛的关系,是研究电针分娩镇痛机制一个很好的侧重点,也为电针分娩镇痛的进一步研究提供科学依据和理论基础。
目的观察黄芩苷对宫颈癌HeLa细胞侵袭转移的作用及其相应机制。方法利用MTT法检测黄芩苷对HeLa细胞增殖的影响;Transwell小室法检测黄芩苷对HeLa细胞侵袭能力的影响;Real-time
PCR法检测黄芩苷对MMP-2、MMP-9RNA表达水平的影响;Western blot法检测黄芩苷对MMP-2、MMP-9蛋白表达的影响;Western blot法检测黄芩苷对P38和p-P38蛋白表达的影响;Real-time PCR法检测黄芩苷和sb203580联合应用对MMP-2和MMP-9RNA表达水平的影响。结果黄芩苷能够有效抑制HeLa细胞的增值,当质量浓度超过60μg/mL时,与对照组相比(0μg/mL)差异出现统计学意义。在低于细胞增殖抑制浓度时,黄芩苷也能够有效抑制HeLa细胞的侵袭,10、20、40μg/mL组穿过基质胶到达小室底端的细胞数目分别为对照组的(97.58±17.78)%、(67.95±49.75)%和(32.35±20.41)%。黄芩苷能够有效抑制HeLa细胞中MMP-2和MMP-9的表达及有效抑制HeLa细胞中P38的磷酸化水平;P38信号通路抑制剂预处理,能够增强黄芩苷对MMP-2和MMP-9表达的抑制作用。结论黄芩苷能够有效抑制HeLa细胞的侵袭转移,这种作用可能与其通过调节P38信号通路的活性进一步调节MMP-2和MMP-9的表达有关。
目的研究血管紧张素Ⅱ(Ang
Ⅱ)对大鼠心脏成纤维细胞(CFs)转录因子Ets-1及其下游促纤维化因子表达和细胞增殖的调节及相关的分子机制。方法将原代培养的大鼠CFs分为对照组,Ang Ⅱ处理不同时间组以及不同剂量组,采用实时定量RT-PCR及western blotting实验技术检测Ang Ⅱ对Ets-1mRNA及蛋白表达的影响。用Ang Ⅱ受体拮抗剂、MAPKs、PKC及PTK抑制剂预处理CFs,测定其对Ang Ⅱ诱导的Ets-1、结缔组织生长因子(CTGF)、纤溶酶原激活物抑制因子-1(PAI-1)表达及细胞增殖的影响。结果在CFs中,Ang Ⅱ可呈时间及浓度依赖性诱导Ets-1表达(P
目的探讨p38 {Selleck Anti-diabetic Compound Library|Selleck Antidiabetic Compound Library|Selleck Anti-diabetic Compound Library|Selleck Antidiabetic Compound Library|selleck Anti-diabetic Compound Library|selleck Antidiabetic Compound Library|selleck Anti-diabetic Compound Library|selleck Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|buy Anti-diabetic Compound Library|Anti-diabetic Compound Library半抑制浓度|Anti-diabetic Compound Library价格|Anti-diabetic Compound Library花费|Anti-diabetic Compound Library溶解度|Anti-diabetic Compound Library购买|Anti-diabetic Compound Library制造商|Anti-diabetic Compound Library查找购买|Anti-diabetic Compound Library订单|Anti-diabetic Compound Library mouse|Anti-diabetic Compound Library chemical structure|Anti-diabetic Compound Library分子量|Anti-diabetic Compound Library molecular weight|Anti-diabetic Compound Library数据表|Anti-diabetic Compound Library supplier|Anti-diabetic Compound Library体外|Anti-diabetic Compound Library细胞系|Anti-diabetic Compound Library concentration|Anti-diabetic Compound Library nmr|Anti-diabetic Compound Library体内|Anti-diabetic Compound Library clinical trial|Anti-diabetic Compound Library cell assay|Anti-diabetic Compound Library screening|Anti-diabetic Compound Library high throughput|buy Antidiabetic Compound Library|Antidiabetic Compound Library半抑制浓度|Antidiabetic Compound Library价格|Antidiabetic Compound Library花费|Antidiabetic Compound Library溶解度|Antidiabetic Compound Library购买|Antidiabetic Compound Library制造商|Antidiabetic Compound Library查找购买|Antidiabetic Compound Library订单|Antidiabetic Compound Library chemical structure|Antidiabetic Compound Library数据表|Antidiabetic Compound Library supplier|Antidiabetic Compound Library体外|Antidiabetic Compound Library细胞系|Antidiabetic Compound Library concentration|Antidiabetic Compound Library clinical trial|Antidiabetic Compound Library cell assay|Antidiabetic Compound Library screening|Antidiabetic Compound Library high throughput|Anti-diabetic Compound high throughput screening| MAPK对人主动脉平滑肌细胞Ⅰ型和Ⅲ型胶原表达的影响。方法分别使用药理学抑制剂和siRNA干预细胞。药理学抑制剂试验细胞分为:1正常对照组,平滑肌细胞完全培养基正常培养;2 DMSO(p38 MAPK抑制剂溶剂)对照组,0.01%DMSO处理;3 p38 MAPK抑制剂组,0.01%p38 MAPK抑制剂(20 mg/m L)处理。基因沉默试验细胞分为:1静态对照组,平滑肌细胞完全培养基正常培养;2阴性对照siRNA组,M ACSfectin试剂转染阴性对照siRNA 48 h;3 p38 M APK siRNA组,M ACSfectin试剂转染p38 M APK siRNA 48 h。采用qRT-PCR法检测Ⅰ型和Ⅲ型胶原mRNA表达;采用Western blotting法检测Ⅰ型和Ⅲ型胶原蛋白表达以及p38 MAPK转染效率;荧光显微镜观察siRNA转染效率。结果与正常对照组相比,DMSO对照组细胞Ⅰ型和Ⅲ型胶原mRNA和蛋白表达无明显变化(P>0.05),p38 MAPK抑制剂组细胞Ⅰ型和Ⅲ型胶原mRNA和蛋白表达显著降低(P0.