蛋白激酶C信号传导通路在缺氧性心肌细胞凋亡中的作用

目的　研究蛋白激酶C信号通路在心肌细胞缺氧性凋亡中的作用。方法　将培养的大鼠心肌细胞随机分成 8组 :(1 )对照组 ;(2 )缺氧 6h组 ;(3)缺氧 1 2h组 ;(4 )缺氧 2 4h组 ;(5 )PMA1 0nM组 ;(6 )PMA1 0 0nM组 ;(7)CHE1 μM组 ;(8)CHE1mM组。对照组常氧培养 2 4h。缺氧培养即将心肌细胞 95 %N2 ～ 5 %CO2 下 37℃缺氧培养。 (5 )和 (6 )组即于缺氧培养前 ,加入PKC激动剂PMA(Phorbol 1 2 myristate 1 3 acetata) ,使其终浓度分别为 1 0nM、1 0 0nM ,预处理 1 0min后再缺氧 2 4h。 (7)和 (8)组即于缺氧培养前 1 0min ,加入PKC抑制剂CHE(chelerythrine) ,使其终浓度分别为 1 μM、1mM ,然后再缺氧培养 2 4h。其余各组缺氧不同的时间。终止培养后分别检测细胞的凋亡率和活性。结果　单纯缺氧能引起心肌细胞的凋亡和坏死 ,以缺氧 2 4h最显著。PMA1 0nM预处理能明显减少心肌细胞缺氧性凋亡 (P <0 .0 5 ) ,而PMA1 0 0nM组和CHE1 μM组心肌细胞凋亡率明显增加 (P <0 .0 5 )。PMA和CHE对 2 4h缺氧诱导的心肌细胞坏死无明显影响。结论　蛋白激酶C信号传导通路参与了抗心肌细胞缺氧性凋亡的信号传导 ,但可能与抗缺氧性坏死的信号传导之间存在差异     

缺氧和高浓度葡萄糖对体外培养人视网膜色素上皮衍生因子表达的影响

目的　探讨缺氧和高糖对体外培养的人视网膜色素上皮 (RPE)细胞血管内皮生长因子(VEGF)和色素上皮衍生因子 (PEDF)的影响。方法　我们通过实验性研究在氧正常或缺氧 (1%O2 )加或不加高浓度葡萄糖的条件下 ,培养的人RPE细胞 ,通过反转录PCR和实时定量分析检测PEDF和VEGF的表达 ,使用Western印迹分析检测PEDF和VEGF蛋白水平。结果　缺氧情况下 ,VEGF表达和蛋白水平增加 (P =0 .0 0 1) ;缺氧加 2 5mmol/L葡萄糖后增加更加明显 (P <0 .0 0 1)。缺氧情况下PEDF表达水平与正常氧环境比较无统计学意义 (P =0 .2 5 1) ;但加葡萄糖后PEDFmRNA表达水平低于正常对照。结论　体外培养的人RPE细胞在缺氧条件下PEDF表达降低不明显 ,这提示缺氧间接影响体外RPE细胞的PEDF下调 ,高葡萄糖直接下调PEDF的表达 ,同时增加VEGF的表达 ,这可能支持体内高血糖是糖尿病最危险的“糖毒性”观点。     

高浓度葡萄糖诱导大鼠肾小球系膜细胞VEGF的表达上调依赖于PKCβⅠ和RhoA的活化

目的:研究高浓度葡萄糖是否通过蛋白激酶C(PKC)βⅠ和RhoA信号通路介导大鼠肾小球系膜细胞血管内皮生长因子(VEGF)表达上调。方法:体外培养SD大鼠肾小球系膜细胞,给予葡萄糖和各种抑制剂处理细胞,提取细胞蛋白,采用Western免疫印迹检测PKCβⅠ及RhoA蛋白的表达量变化,同时提取RNA,采用实时定量PCR观察VEGF mRNA浓度变化。结果:高浓度葡萄糖(30mmol/L)诱导肾小球系膜细胞VEGF mRNA表达增加,而甘露醇对照组VEGF mRNA表达水平未见明显改变(P>0.05)。高浓度葡萄糖刺激系膜细胞RhoA和PKCβⅠ发生活化,RhoA-GTP蛋白和胞膜PKCβⅠ蛋白均呈时间依赖性增加。使用Rho激酶特异性抑制剂(HA-1077)预处理细胞后,VEGF mRNA表达量与高糖组相比明显下调(P<0.05)。进一步使用广谱PKC抑制剂(PMA)、传统PKC抑制剂(G6976)以及PKCβ特异性抑制剂(LY333531)预处理细胞后,VEGF mRNA和RhoAGTP蛋白表达量与高糖组相比均受到抑制(P<0.05)。结论:高浓度葡萄糖可能通过间接活化PKCβⅠ来激活RhoA信号通路,从而上调系膜细胞VEGF的表达,该信号通路在糖尿病肾病的病理过程中发挥着重要作用。     

蛋白激酶C对哮喘患者T淋巴细胞核因子—кB活化的调控

为探讨蛋白激酶 C对哮喘患者 T淋巴细胞核因子 - кB(NF- кB)活化的调控作用 ,分别从 16例急性发作期哮喘患者及 16名正常对照者的外周血中分离出 T淋巴细胞并分成 3组培养 ,即空白对照组 ,加入 PKC激动剂 12 -肉豆蔻酰 - 13-乙酸佛波酯 (PMA)的 PMA组 ,同时加入 PMA和 PKC抑制剂 Ro31- 82 2 0的 PMA+Ro31- 82 2 0组。用免疫组织化学染色方法和 Western印迹检测 NF- кB和抑制蛋白 - кB(I- кB)的表达。结果显示 :哮喘 PMA组 NF- кB活化的细胞百分比显著高于空白对照组和正常 PMA组 (P<0 .0 1) ,且 I- кB水平显著低于上述 2组 (P<0 .0 1) ;而哮喘 PMA+Ro31- 82 2 0组 NF- кB活化的细胞百分比显著低于哮喘 PMA组 (P<0 .0 1) ,且 I- кB水平显著高于该组 (P<0 .0 1)。提示哮喘 T淋巴细胞 NF- кB的活化可能受 PKC调控 ,T淋巴细胞 PKC— NF- кB信号传导途径的激活可能是哮喘的发病机制之一     

缺氧促进牛视网膜血管内皮细胞VEGF的表达

目的探讨缺氧对视网膜血管内皮细胞VEGF表达的影响。方法采用细胞克隆、机械除杂法培养视网膜血管内皮细胞;四唑盐比色试验(MTT)比较正常和缺氧状态下牛视网膜血管内皮细胞的细胞数目。应用ELISA法检测正常和缺氧状态下牛视网膜血管内皮细胞VEGF的表达。缺氧状态下加入VEGF抗体后,检测VEGF的表达。结果正常状态下即可检测到VEGF的表达。缺氧状态下,牛视网膜血管内皮细胞VEGF的表达显著增加(P<0.01)。结论缺氧环境能刺激培养的牛视网膜血管内皮细胞的增殖。缺氧能刺激培养的牛视网膜血管内皮细胞VEGF的表达。     

蛋白激酶C活化对大鼠缺血/再灌注心肌细胞凋亡和Bcl-2表达的影响

目的 :　探讨PKC活化对大鼠I/R心肌细胞死亡和凋亡仰制基因Bcl 2表达的影响。方法 :采用TUNEL法以及免疫组化和原位杂交方法。结果 :(1)PMA +IR3h组IUNEL法阳性心肌细胞核数量及阳性心肌细胞核占总心肌细胞核数的百分比均明显少于IR3h组 (P <0 0 5 ,P <0 0 1) ;(2 )PMA +IR3h组表达Bcl 2蛋白阳性的心肌细胞数及阳性心肌细胞占心肌细胞总数的百分比均明显多于IR3h组 (P <0 0 1) ,PMA +IR1h组表达Bcl 2mPNA阳性的心肌细胞数及阳性心肌细胞占心肌细胞总数的百分比均明显多于IR1h组 (P <0 0 1)。结论 :(1)PKC活化能够显…     

缺氧条件下谷氨酸对鼠脑星形胶质细胞血管内皮生长因子表达的影响

目的观察谷氨酸在缺氧条件下对星形胶质细胞血管内皮生长因子(VEGF)表达的影响。方法原代培养SD大鼠星形胶质细胞,传代后分为4组:①对照组;②谷氨酸组(1μmol/L);③缺氧组;④缺氧+谷氨酸组。缺氧条件为:(94%N2,5%CO2和1%O2),每组包括6个时相点:0、2、4、6、8、12h(以缺氧后开始计时),②和④组加入1μmol/L的谷氨酸。在不同时间点提取细胞总RNA,用Real time FQ-PCR法检测VEGF mRNA表达变化;ELISA法检测培养上清液VEGF蛋白表达变化。结果对照组和谷氨酸组(1μmol/L)各实验时相点星形胶质细胞VEGF mRNA和蛋白表达无明显变化。而缺氧组和缺氧+谷氨酸组VEGF mRNA和蛋白表达却随实验时相逐步增高,分别在6和8h达最高,之后渐下降。缺氧+谷氨酸组VEGF mRNA和蛋白表达上调较单纯缺氧组更为显著。结论谷氨酸(1μmol/L)可在缺氧条件下增强星形胶质细胞VEGF mRNA和蛋白表达上调,这可能与缺氧状态下星形胶质细胞表面谷氨酸受体的表达变化有关。     

金丝桃素对培养的人视网膜色素上皮细胞钙离子内流的抑制

目的研究蛋白激酶C (PKC) 抑制剂金丝桃素对视网膜色素上皮细胞(RPE cells)钙离子信号共聚成像的影响. 方法使用钙荧光指示剂fluo-3 AM和激光扫描共聚焦显微镜(LSCM),分析在100 nmol*L-1 佛波酯(PMA)和(或)5个浓度的金丝桃素(1, 2, 3, 4和5 μmol*L-1)刺激时培养的人RPE细胞的钙离子信号的变化. 结果 RPE细胞荧光着色很强,遍布整个细胞,其中细胞核比细胞质更强. 只用PMA或金丝桃素刺激时,可以观察到荧光强度迅速下降,并且5个浓度金丝桃素之间的下降曲线无明显差异. 用PMA预先处理细胞24 h后,再给予金丝桃素刺激发现荧光强度并没有进一步下降. 结论 fluo-3 AM 是人RPE细胞钙离子良好的指示剂,金丝桃素能强力抑制钙离子内流,它作为治疗增殖性玻璃体视网膜病变的潜在药物可能是因为能抑制PKC活性和钙离子内流.     

二甲双胍对缺氧环境中RPMI 8226细胞新生血管生成的影响

目的 探讨缺氧条件下二甲双胍对多发性骨髓瘤(MM)细胞株RPMI 8226新生血管生成的影响。方法 选取常氧和缺氧条件下RPMI 8226细胞的基因表达综合数据库(GEO)数据集GSE110113进行差异表达基因(DEGs)和相关信号通路富集分析。采用100μmol/L氯化钴(CoCl₂)构建化学缺氧模型;采用CCK-8试剂盒检测不同浓度的二甲双胍作用于缺氧条件下MM细胞株RPMI 8226后的细胞增殖活力;采用Western-blot检测缺氧诱导因子-1α(HIF-1α)和血管内皮生长因子(VEGF)蛋白的表达情况;采用ELISA检测培养基上清液VEGF蛋白的表达含量;采用体外新生血管生成实验检测新生血管生成。结果 基因本体论(GO)、京都基因和基因组百科全书(KEGG)信号富集分析显示,DEGs富集在“缺氧反应”和“HIF-1信号通路”;RPMI 8226细胞中HIF-1α和VEGF蛋白的表达随CoCl₂作用时间增加而增加;二甲双胍以剂量依赖性方式降低缺氧诱导RPMI 8226细胞中HIF-1α和VEGF蛋白的表达及培养上清液中VEGF蛋...     

金雀异黄素抑制缺氧人视网膜色素上皮细胞VEGF表达机制的初步研究

目的:进一步明确金雀异黄素(Gen)抑制缺氧人视网膜色素上皮细胞(RPE)血管内皮生长因子(VEGF)表达的机制。方法:以体外正常情况为对照,建立人RPE缺氧模型并经不同浓度Gen干预后,通过RT-PCR检测VEGF及其转录调节因子c-fos、c-jun、缺氧诱导因子(HIF)-1α、HIF-2α、HIF-3αmRNA的表达水平,了解Gen是否通过对VEGF的转录因子活性调节而影响VEGF的表达。结果:缺氧能使人RPE细胞的VEGF、c-fos、c-jun及HIF-2α、HIF-3αmRNA水平增高,对HIF-1α无影响;Gen能抑制缺氧诱导的VEGF表达;在所检测的VEGF转录因子中,Gen只对HIF-2α的转录有抑制作用。结论:Gen抑制VEGF表达的作用部分是通过抑制其转录调节因子HIF-2α转录实现的。     

PKC信号传导通路在缺氧心肌细胞表达VEGF中的作用

目的：明确缺氧对心肌细胞表达血管内皮生长因子（ＶＥＧＦ）的影响及蛋白激酶Ｃ（ＰＫＣ）信号传导通路在其中的作用。方法：将原代培养大鼠心肌细胞模型分组：①正常缺氧４组：Ａ组正常对照;Ｒ组缺氧６ｈ;Ｃ组缺氧１２ｈ：Ｄ组缺氧２４ｈ。②ＰＫＣ激动剂４组;Ａ组缺氧２４ｂ对照;Ｂ组加入ＰＭＡ１０ｎｇ／ｍｌ缺氧２４ｈ;Ｃ组加入ＰＭＡ１００ｎｇ／ｍｌ缺氧２４ｈ;Ｄ组加入ＰＭＡ１０００ｍｇ／ｍｌ缺氧２４ｈ。③ＰＫＣ抑     

The effect of protein kinase C on voltage-gated potassium channel in pulmonary artery smooth muscle cells from rats exposed to chronic hypoxia

Background Chronic hypoxia can cause pulmonary hypertension and pulmonary heart disease with high mortality.The signal transduction pathway of protein kinase C (PKC) plays an important role in chronic pulmonary hypertension. So it is necessary to investigate the effect of PKC on voltage-gated potassium (K+) channels in pulmonary artery smooth muscle cells of rats exposed to chronic hypoxia.Methods Male Wistar rats were randomly divided into a control group (group A) and a chronic hypoxia group (group B). Group B received hypoxia ［oxygen concentration （10±1）%］ eight hours per day for four consecutive weeks. Single pulmonary artery smooth muscle cells were obtained using an acute enzyme separation method. Conventional whole cell patch clamp technique was used to record resting membrane potential, membrane capacitance and voltage-gated K+ currents. The changes in voltage-gated K+ currents before and after applying paramethoxyamphetamine (PMA) (500 nmol/L), an agonist of PKC, and PMA plus carbohydrate mixture of glucose, fructose and xylitol (GFX) (30 nmol/L), an inhibitor of PKC, were compared between the two groups.Results The resting membrane potential in group B was significantly lower than that of group A: －(29.0±4.8) mV (n=18) vs －(42.5±4.6) mV (n=35) (P&lt;0.01). But there was no change in membrane capacitance between the two groups: (17.9±4.6) pF (n=40) vs (19.7±5.8) pF (n=31) (P&gt;0.05). The voltage-gated K+ currents were significantly inhibited by PMA in group A, and this effect was reversed by GFX. However, the voltage-gated K+ currents in group B were not affected by PMA.Conclusions The resting membrane potential and voltage-gated K+ currents in pulmonary artery smooth muscle cells from rats exposed to chronic hypoxia decreased significantly. It seems that PKC has different effects on the voltage-gated K+ currents of pulmonary artery smooth muscle cells under different conditions.     

Local tissue hypoxia and formation of nasal polyps

Objective To explore the response of nasal mucosa epithelial cells to hypoxia in terms of formation of nasal polyps (NP). Methods Epithelial cells of NP and inferior turbinate (IT) were cultured serum-free under normal oxygen and hypoxic circumstances with stimulation of IL-1β and TNFα. The vascular endothelial growth factor (VEGF)mRNA and VEGF protein levels of the cultured cells were detected using in situ hybridization and ELISA, respectively. Results The expression of VEGF mRNA was significantly higher in epithelial cells of NP than in IT exposed to pro-inflammatory cytokines or hypoxia ( P &lt;0.01). VEGF levels were higher in NP epithelial cells than those of IT ( P &lt;0.01) under hypoxia. Conclusion VEGF-induced by hypoxia is very important for the early stages of forming polyps.     

The signal transduction pathway in the proliferation of airway smooth muscle cells induced by urotensin Ⅱ

Background Human urotensin Ⅱ (UⅡ) is the most potent mammalian vasoconstrictor identified so far. Our previous study showed that UⅡ is a potent mitogen of airway smooth muscle cells (ASMC) inducing ASMC proliferation in a dose-dependent manner. The signal transduction pathway of UⅡ mitogenic effect remains to be clarified. This study was conducted to investigate the signal transduction pathway in the proliferation of ASMC induced by UⅡ. Methods In primary cultures of rat ASMCs, activities of protein kinase C (PKC), mitogen-activated protein kinase (MAPK) and calcineurin (CaN) induced by UⅡ were measured. The effect of CaN on PKC and MAPK was studied by adding cyclosporin A (CsA), a specific inhibitor of CaN. Using H7 and PD98059, inhibitors of PKC and MAPK, respectively, to study the effect of PKC and MAPK on CaN. The cytosolic free calcium concentration induced by UⅡ was measured using Fura-2/AM. Results UⅡ 10-7 mol/L stimulated ASMC PKC and MAPK activities by 44% and 24% (P&lt;0.01), respectively, after incubating for 20 minutes. It increased CaN activity in a time-dependent manner, being 1.68 times as that of control for 24 hours (P&lt;0.01). It promoted the cytosolic free calcium concentration increase of 18% (P&lt;0.01). CsA 10-6 mol/L and H7 50 μmol/L inhibited UⅡ-stimulated CaN activity by 45% (P&lt;0.01) and 21% (P&lt;0.05), respectively, while PD98059 50 μmol/L had no effect on CaN activity (P&gt;0.05). CsA 10-6 mol/L inhibited UⅡ-stimulated PKC activity by 14% (P&lt;0.05), while having no effect on MAPK activity (P&gt;0.05). Conclusions UⅡ increases cytosolic free calcium concentration and activates PKC, MAPK and CaN. The signal transduction pathway between PKC and CaN has cross-talk.     

血管内皮生长因子干扰RNA对人鼻咽癌CNE一2Z细胞VEGF表达调控的实验研究

目的：研究血管内皮生长因子（VEGF）的特异性小片段干扰RNA（siRNA）对低分化人鼻咽癌CNE-2Z细胞VEGF表达的抑制作用，为鼻咽癌的治疗提供新的途径。方法：体外培养人鼻咽癌细胞CNE-2Z，并分成正常氧状态培养组（20％）和低氧（1％）培养组。采用脂质体（LF2000）将VEGF siRNA转染两组细胞，并采用RT—PCR、ELISA检测鼻咽癌细胞在正常氧状态和低氧状态下VEGF mRNA和蛋白质表达的差异。结果：与未转染组和转染空载体组相比，在正常氧和低氧状态下，VEGFsiRNA均能明显抑制VEGFmRNA的表达（P〈0．01）；正常氧状态下VEGFsiRNA的抑制效率比低氧状态高。正常氧状态下：未转染组、转染空载体组、转染VEGFsiRNA组CNE-2Z细胞培养上清液中VEGF165的含量分别为：423．92、419．68和328．86pg／mL；低氧状态下VEGF165的含量分别为：813．62、799．89和500．96pg／mL，转染VEGF siRNA组VEGF的表达下调。结论：VEGF siRNA能有效地、特异地抑制人鼻咽癌CNE-2Z细胞VEGF mRNA和蛋白质的表达，因而有望成为治疗鼻咽癌的一种有效方法。     

氧化修饰低密度脂蛋白对培养人动脉平滑肌细胞周期及增殖 …

应用流式细胞仪对氧化修饰低密度脂蛋白刺激动脉平滑肌细胞增殖，细胞周期及增细胞核原、Ｐ５３、Ｐ２７及ｃ－ｅｒｂＢ蛋白表达的影响进行了观察。结果发现：Ｏｘ－ＬＤＬ和天然低密度脂蛋白刺激培养人动脉ＳＭＣ细胞增殖时其Ｓ期细胞百分率增加，且Ｏｘ－ＬＤＬ的作用比Ｎ－ＬＤＬ强。     

肺动脉内皮细胞缺氧时内皮型一氧化氮合酶基因表达的变化及蛋白激酶C亚型的作用

目的　研究蛋白激酶C(PKC)及其亚型对缺氧引起的肺动脉内皮细胞内皮型一氧化氮合酶 (eNOS)基因表达变化的调控作用。方法　将原代培养的猪肺动脉内皮细胞置于缺氧 (5 %O2 )条件培养 2、6、12、2 4、4 8h ,用RT PCR的方法检测eNOSmRNA的含量。用蛋白质免疫印迹技术检测eNOS和 8种PKC亚型的表达水平。加入选择性PKC抑制剂BIMⅠ (1μmol/L)和G 6 983(1μmol/L) 后观察其对 5 %O2 所引起的eNOSmRNA水平变化的影响。采用瞬时转染的方法 ,通过荧光素酶报告基因实验检测eNOS基因转录起始点上游长 1 6kb启动子区域的活性。加入转录抑制剂放线菌素D后比较不同时间点常氧培养组和 5 %O2 培养组eNOSmRNA的含量。结果　 5 %O2培养 12h可使肺动脉内皮细胞eNOS表达增加 ,2 4h达高峰。缺氧 2 4h组eNOSmRNA和蛋白质水平分别是常氧组的 171%± 18% (P <0 0 1)和 16 6 %± 2 1% (P <0 0 5 )。BIMⅠ和G 6 983可抑制缺氧 2 4h引起的eNOSmRNA表达上调。缺氧时新型蛋白激酶Cε(nPKCε)发生了膜转位。报告基因实验表明 ,缺氧 2 4h肺动脉内皮细胞eNOS基因启动子活性明显增加 ,为常氧组的 (2 2 9± 0 73)倍。放线菌素D实验表明缺氧对肺动脉内皮细胞eNOSmRNA的稳定性无明显影响。结果表明 ,缺氧上调eNOSmRNA是由于基因转录增强     

腺病毒载体介导的VEGF基因转染对C17．2神经干细胞凋亡的影响

OBJECTIVE: To study the effects of vascular endothelial growth factor (VEGF) gene transfer on hypoxia-induced apoptosis of neural stem cells in vitro. METHODS: C17.2 neural stem cells cultured in vitro were infected by recombinant adenovirus containing VEGF gene and cultured under hypoxic condition. VEGF expression in these cells was detected by Western blotting, and the apoptotic index was calculated from results of triphosphate-biotin nick end-labeling (TUNEL) assay. Flow cytometry was employed to examine the changes in the cell apoptotic rate after VEGF gene transfer, and the apoptotic bodies were observed under fluorescence microscope with Hoechst33342 staining. RESULTS: The expression of VEGF was significantly increased in pAdCMV VEGF(165)-infected cells, resulting in inhibition of the apoptosis of C17.2 neural stem cells induced by hypoxia manifested by a significantly lower apoptotic rate of the stem cells transfected by pAdCMV VEGF(165) than that of the untransfected cells (10.38%;+/-0.48%; vs 19.98 %;+/-0.55%;, P<0.01) and of the cells transfected with pAdCMV VEGF(165) along with VEGF anti-sense oligodeoxynucleotide (19.07%;+/-0.64%;, <0.01) after hypoxia. CONCLUSIONS: Recombinant adenovirus can efficiently mediate VEGF gene transfer into C17.2 neural stem cells, resulting in high expression of the exogenous VEGF in vitro, which effectively reduces C17.2 neural stem cell apoptosis induced by hypoxia.     

Nuclear factor- κB in signal conduction of protein kinase C in T lymphocytes from an asthmatic guinea pig model

Objective To explore the role of nuclear factor- κB (NF- κB) in the signal conduction of protein kinase C (PKC) regulated proliferation, apoptosis and expression of Th2 cytokines - interleukin- 4 (IL- 4) and interleukin- 5 (IL- 5) of T lymphocytes in the bronchial alveolus lavage fluid (BALF).Methods T lymphocytes were isolated and purified from BALF of asthmatic guinea pigs in normal and asthmatic groups, and were stimulated with PKC agitator phorbol 12- myristate 13- acetate (PMA) and NF- κB inhibitor pyrrolidine dithiocarbamate (PDTC), respectively.The expressions of NF- κB, IL- 4 and IL- 5 mRNA and protein, the proliferation and apoptosis of T lymphocytes were observed by immunohistochemistry, in situ hybridization, ELISA, MTT and TUNEL, respectively. Results The activation of NF- κB, proliferation response, and expression of IL- 4 and IL- 5 mRNA and protein in T lymphocytes stimulated by PMA were significantly higher than those of their blank control (P&lt;0.01), while those indexes of T lymphocytes stimulated by PMA and PDTC simultaneously were significantly lower than those stimulated by PMA alone (P&lt;0.01).The apoptotic index of T lymphocytes stimulated with PMA were significantly lower than that of their blank control (P&lt;0.01), and the apoptotic index of asthmatic guinea pig T lymphocytes stimulated with PMA and PDTC simultaneously were significantly higher than that stimulated by PMA alone (P&lt;0.01).The significant positive correlations were found between the activation of NF- κB and the proliferation (r=0.64, P&lt;0.001), and the expression of IL- 4 and IL- 5 mRNA and protein of T lymphocytes, respectively (r=0.55-0.68, P&lt;0.001).There was also significant negative correlation between the activation of NF- κB and apoptosis of T lymphocytes (r=0.62, P&lt;0.001). Conclusions NF- κB may participate in the signal conduction of PKC regulated proliferation, apoptosis and expression of IL- 4 and IL- 5 of T lymphocytes in asthma.The activation of NF- κB in PKC signal conduction pathway of T lymphocytes may play an important role in the pathogenesis of asthma.