5 mmol/L)和对照组(不含2APB),在糖氧剥夺情况下培养2 h,然后恢复正常全培养基复氧培养48 h。用Western blot检测星形胶质细胞神经生长因子的表达水平;用ELISA检测星形胶质细胞条件培养液中神经生长因子的含量。结果表明,0.5 mmol/L 2APB可以诱导正常情况下及糖氧剥夺再灌注情况下体外培养星形胶质细胞NGF的合成和释放(P<0.01)。此外,JNK阻滞剂可抑制糖氧剥夺再灌注情况下2APB诱导的星形胶质细胞神经生长因子的释放。综上,TRPV2激活可以影响糖氧剥夺再灌注情况下体外培养星形胶质细胞神经生长因子的合成和释放。TRPV2有可能成为脑缺血再灌注后的潜在治疗靶点。
云芝多糖简称PSK,是从担子菌亚门杂色云芝菌中提出的多糖,具有丰富的生物学功能,广泛应用于临床肿瘤治疗。本文就目前国内外对云芝多糖的抗肿瘤机制研究及临床应用研究进展做一综述。1对肿瘤免疫的影响1.1对DC细胞的影响DC细胞是人体最大的抗原呈递细胞,研究发现,在癌症患者体内,DC细胞的生物学功能表达降低。PSK可以促进DC细胞成熟,使其高表达MHCII、CD40、CD80、CD86、CD83及肿瘤坏死因子等[1]。PSK还可通过DC细胞刺激活化的毒性T细胞产生TNF-β及IL-
Objective:The

SB203580 anti-inflammatory effects of Ecklonia cava(EC)and its mechanism of action were examined in phorbol-12 myristate 13-acetate(30 nmol/L)and A23187(1μmol/L)(PMACI)stimulated human mast cell line-1 cells.Methods:Nitric oxide content,inducible nitric oxide synthase and cyclooxygenase-2 protein expression,pro-inflammatory

cytokines including IL-1β,TNF-α,and IL-6 mRNA and protein expressions were determined.In addition,extracellular regulated protein kinases/mitogen-activated Alectinib 而且 protein kinase(ERK/MAPK)activation was examined.Results:EC dose-dependently suppressed inducible nitric oxide synthase and cyclooxygenase-2 protein expression and subsequently it reduces nitric oxide content

in PMACI stimulated human mast cell line-1 cells.EC dose-dependently inhibited the mRNA as well as protein expression of TNF-α,IL—1β,and TL-6 in the PMACI stimulated human mast cell line-1 cells without any cytotoxic effect.Furthermore,EC significantly inhibited PMACI induced phosphorylation of ERK1/2 in a dose-dependent manner without affecting the total protein levels.Conclusions:EC exert its anti-inflammatory actions via inhibition of ERK/MAPK signalling pathway,suggesting that EC is a potent and efficacious anti-inflammatory agent for mast cellmediated inflammatory diseases.
目的:探讨养阴清肺方对钴60照射后肺成纤维细胞的生长周期及凋亡的影响。方法:制备实验用含药血清:空白组、中药组、激素组、中药加激素组;采用钴60射线照射肺成纤维细胞后,用不同含药血清培养细胞,分别于24、48、72 h后用流式细胞技术检测各组的细胞周期及细胞凋亡。结果:24 h,各药物组的细胞凋亡与空白组均有差异(P0.05)。72 h,各药物组细胞凋亡与空白组均有差异(P<0.