After per-meabilization of muscle cells, the Gi3 antibody inhibited bombesin-induced smooth muscle cell contraction. RESULTS: Incubation of http://www.selleckchem.cn/products/Fludarabine(Fludara).html permeabilized circular muscle cells with PLC-β3 antibody could inhibit bombesin-induced contraction. H-7, chelerythrine (PKC inhibitor) and genistein (protein tyrosine kinase inhibitor) inhibited bombesin-induced contraction, but DAG kinase inhibitor, R59949, could not inhibit it. To examine which mitogen-activated protein kinase (MAPK) was involved in bombesin-induced contraction, the specific MAPK inhibitors (MEK inhibitor, PD98059 and p38 MAPK inhibitor, SB202190) were used. Preincubation of PD98059

blocked the contraction induced by bombesin in a concentration-dependent manner. However,

SB202190 had no effects on contraction. CONCLUSION: Bombesin-induced circular muscle cell contraction in cat esophagus is madiated via a PKC or a PTK-dependent pathway 已经 or p44/p42 MAPK pathway.
目的:观察p38MAPK信号转导通路在17β-雌二醇和雷洛昔芬促成骨细胞增殖和分化过程中的作用。方法:取第一继代BALB/c小鼠头盖骨成骨细胞,药物刺激组分别加入不同浓度17β-雌二醇或雷洛昔芬;含阻断剂组预先添加不同浓度的SB202190(p38MAPK的阻断剂)阻断信号转导通路,再加17β-雌二醇或雷洛昔芬,作用72h后用MTT法与PNPP法测定细胞的增殖能力和碱性磷酸酶活性。结果:加入雌激素或雷洛昔芬后,成骨细胞的增殖和分化明显增强,与空白对照组比较差异具有显著性意义(P<0·05);阻断p38MAPK信号转导通路后,细胞增殖分化受到明显抑制,与未阻断组比较差异具有非常显著性意义(P<0.01)。结论:p38MAPK在17β-雌二醇和雷洛昔芬诱导的小鼠成骨细胞的増殖和分化过程中发挥重要作用。
目的:观察牛磺酸(Tau)对烧伤后心肌细胞凋亡的影响并探讨其作用机制。方法:选健康W istar大鼠50只,随机分为对照组、烧伤组(造成30%TBSAⅢ度烧伤)、烧伤+牛磺酸组(烫伤后即刻腹腔注射牛磺酸,200 mg/kg)、烧伤+牛磺酸(Tau)+SB202190组及烧伤+SB202190组(烫伤后立即注射SB202190,10 mg/kg)。末端标记(TUNEL)法检测凋亡细胞,放射免疫法测定TNFα含量,荧光分析法测定caspase-3活性及免疫组化分析心肌Fas、caspase-8、Bc l-2和Bax蛋白的表达。结果:烧伤组心肌细胞凋亡指数(18.69±2.47)显著高于对照组(0.48±0.05)(P<0.01)。Tau组和Tau+SB202190组心肌细胞凋亡指数分别为3.15±0.41和1.63±0.31,显著低于烧伤组。心肌TNFα、Fas、caspase-8和Bax蛋白表达及caspase-3活性均不同程度低于烧伤组(P<0.05)。结论:牛磺酸对烧伤后心肌细胞凋亡有较好的抑制作用,其机制可能是牛磺酸调控了部分凋亡相关基因的表达和减少TNF-α的生成。
AIM:To

examine the pathway related to the IL-1β-induced PD0325901 activation of mitogen-activated protein(MAP)kinases in cat esophageal smooth muscle cells.METHODS:Culture of the esophageal smooth musclecells from cat was prepared.Specific inhibitors weretreated before applying the IL-1β.Western blot analysiswas performed to detect the expressions of COX,iNOSand MAP kinases.RESULTS:In the primary cultured cells,although IL-1βfailed to upregulate the COX and iNOS levels,the levelsof the phosphorylated forms of p44/42 MAP kinase andp38 MAP kinase increased in both concentration-andtime-dependent manner,of which the level of activationreached a maximum within 3 and 18 h,respectively.The pertussis toxin reduced the level of p44/42 MAPkinase phosphorylation.Tyrphostin 51 and genistein alsoinhibited this activation.Neomycin decreased the densityof the p44/42 MAP kinase band to the basal level.Phosphokinase C(PKC)was found to play a mediatingrole in the IL-1β-induced p44/42 MAP kinase activity.In contrast,the activation of p38 MAP kinase wasinhibited only by a pretreatment with forskolin,and wasunaffected by the other compounds.