p38 MAPK信号传导通路

丝裂原活化蛋白激酶（ｍｉｔｏｇｅｎ－ａｃｔｉｖａｔｅｄｐｏｒｏｔｅｉｎｋｉｎａｓｅ,ＭＡＰＫ）介导了生长、发育,分裂,死亡,以及细胞间的功能同步等多种细胞生理功能,在哺乳动物细胞中已发现和克隆了ＥＲＫ、ＪＮＫ／ＳＡＰＫ,ＥＲＫ５／ＢＭＫ１和ｐ３８／ＲＫ四个ＭＡＰＫ亚族,这些新的ＭＡＰＫ介导了物理,化学反激,细菌产物,炎性细胞因子等多种刺激引起的细胞反应,ｐ３８亚族至少包括ｐ３８（α）,ｐ３８β,ｐ     

BIV—1—gp120在重组杆状病毒系统中的表达

将中国株ＨＩＶ－１Ｂ亚型ｇｐ１２０全基因序列克隆到杆状病毒转座载体ｐＦａｓｔＢａｃＩ中多角体启动子下游,构建成重组转座载体ｐＦａｓｔＢａｃＩ－ｇｐ１２０,利用细菌／杆状病毒（Ｂａｃ ｔｏ Ｂａｃ）表达系统筛选重组杆状病毒,在昆虫细胞Ｓｆ９中高效表达了ＨＩＶ－１的外膜糖蛋白ｇｐ１２０,ＳＤＳ－ＰＡＧＥ和Ｗｅｓｔｅｒｎ ｂｌｏｔ分析结果一致,证明表达了２种糖基化程度不同的ｇｐ１２０。     

NEW SPECIES OF GENUS MANSONIELLA POPPIUS FROM CHINA (HEMIPTERA: MIRIDAE: BRYOCORINAE)

本文记述了曼盲蝽属ＭａｎｓｏｎｉｅｌａＰｏｐｐｉｕｓ,１９１５的７个新种：环曼盲蝽Ｍ．ａｎｎｕｌａｔａｓｐ．ｎｏｖ．;脊曼盲蝽Ｍ．ｃｒｉｓｔａｔａｓｐ．ｎｏｖ．;狭长曼盲蝽Ｍ．ｅｌｏｎｇａｔａｓｐ．ｎｏｖ．;黄翅曼盲蝽Ｍ．ｆｌａｖａｓｐ．ｎｏｖ．;胡桃曼盲蝽Ｍ．ｊｕｇｌａｎｄｉｓｓｐ．ｎｏｖ．;瑰环曼盲蝽Ｍ．ｒｏｓａｃｅａｓｐ．ｎｏｖ．;赤环曼盲蝽Ｍ．ｒｕｂｉｄａｓｐ．ｎｏｖ．。提出３个新组合：Ｍ．ｃｉｎｎａｍｏｍｉ（ＺｈｅｎｇｅｔＬｉｕ,１９９２）,ｃｏｍｂ．ｎｏｖ．;Ｍ．ｓａｓａｆｒｉ（ＺｈｅｎｇｅｔＬｉｕ,１９９２）,ｃｏｍｂ．ｎｏｖ．;Ｍ．ｗａｎｇｉ（ＺｈｅｎｇｅｔＬｉ,１９９２）,ｃｏｍｂ．ｎｏｖ．,均由ＰａｃｈｙｐｅｌｔｉｓＳｉｇｎｏｒｅｔ属移入本属,模式标本存放于南开大学生物系昆虫标本室     

亚渊产透骨草属植物的修订

对Ｐｈｙｍａ ｌｅｐｔｏｓｔａｃｈｙａ Ｌ．的亚洲产亚种,即ｓｓｐ．ａｓｉａｔｉｃａ（Ｈａｒａ）Ｋｉｔａｍｕｒａ作了分类修订,列出了显示两个亚种本质区别的表,并提供了ｓｓｐ．ａｓｉａｔｉｃａｘ的详细的地理分布资料。     

横断山地区的伏绕眼果蝇亚属及三新种(双翅目:果蝇科)

本文记述分布在中国横断山地区绕眼果蝇属伏绕眼果蝇亚属［Ａｍｉｏｔａ（Ｐｈｏｒｔｉｃａ）］的１１个物种，其中包括３个新种：不对称绕眼果蝇Ａ．（Ｐ．）ａｃｏｎｇｒｕｅｎｓｓｐ．ｎ．、突绕眼果蝇Ａ．（Ｐ．）ｐｒｏｔｒｕｓａｓｐ．ｎ．、韩氏绕眼果蝇Ａ．（Ｐ．）ｈａｎｉｓｐ．ｎ．。     

辽西义县组长节锯蜂科(昆虫纲,膜翅目)昆虫化石

描述产自辽宁西部北票上园地区和凌源大王杖子义县组长节锯蜂科（Ｘｙｅｌｉｄａｅ）巨长节锯蜂亚科（Ｍａｃｒｏｘｙｅｌｉｎａｅ）昆虫化石１２种,归于４族８属,其中６新属１２新种,包括Ａｎｇａｒｉｄｙｅｌａ ｒｏｂｕｓｔａ ｓｐ．ｎｏｖ．,Ａｎｇａｒｉｄｙｅｌａ ｅｘｃｕｌｐｔａ ｓｐ．ｎｏｖ．,Ａｎｇａｒｉｄｙｅｌａ ｓｕｓｐｅｃｔａ ｓｐ．ｎｏｖ．,Ａｎｇａｒｉｄｙｅｌａ ｅｎｄｅｍｉｃａ ｓｐ．ｎｏ     

横断山地区的伏绕眼果蝇亚属及三新种

本文记述分布在中国樱花断山地区绕眼果蝇属伏绕眼果蝇亚属「Ａｍｉｏｔａ（Ｐｈｏｒｔｉｃａ）」的１１个物种,其中包括３个新种,不对称绕眼果蝇Ａ．（Ｐ．）ａｃｏｎｇｒｕｅｎｓ ｓｐ．ｎ．、突绕眼果蝇Ａ．（Ｐ．）ｐｒｏｔｒｕｓａ ｓｐ．ｎ．、韩氏绕眼果蝇Ａ．（Ｐ．）ｈａｎｉ ｓｐ．ｎ。     

根癌土壤杆菌介导的水稻高效转化和转基因植株的高频再生

利用根襄封杆菌（Ａｇｒｏｂａｃｔｅｒｕｍ ｔｕｍｅｆａｃｉｅｎｓ（Ｓｍｉｔｈ ｅｔ Ｔｏｗｎｓｅｎｄ）Ｃｏｎｎ）介导的转化方法对４个粳稻（Ｏｒｙｚａ ｓａｔｉｖａ Ｌ．ｓｓｐ．ｊａｐｏｎｉｃａ）品种和２个灿稻（Ｏ．ｓａｔｉｖａ ｓｓｐ．ｉｎｄｉｃａ）品种进行了转化。在对影响根癌土壤杆菌转化水稻效率的多种因素进行比较研究后,建立了根癌土壤杆菌介导的水稻高效转化和再生系统。将水稻成熟胚和未成熟胚来源的     

重组家蚕病毒表达传染性法氏囊病病毒VP2蛋白

将传染性囊病病毒ＨＺ９６株主要宿主保护性抗原ＶＰ２的ｃＤＮＡ基因克隆到杆状病毒转移载体ｐＢａｃ－ＰＡＫ８中,获得重组转移载体ｐＢａｃＰＡＫ－ＶＰ２,载体ｐＢａｃＰＡＫ－ＶＰ２与修饰病毒Ｂｍ－ＢａｃＰＡＫ６线性化基因组ＤＮＡ共转染单层家蚕Ｂｏｍｂｙｘ ｍｏｒｉ（Ｂｍ）Ｎ细胞,经细胞内同源重组,筛选到重组病毒。ＥＬＩＳＡ和Ｗｅｓｔｅｒｎ免疫鲩迹结果表明,ＶＰ２在家蚕培养细胞和家蚕幼虫中均得到了表达。     

云南鹤庆盆地晚第四纪介形类新属种

云南鹤庆盆地晚第四纪（１５ ０００－１２ ０００ａＢＰ）ＨＱ钻孔剖面建立介形类２新属６新种,即玻璃介科的Ｃａｎｄｏｎａ ｐａｒｕａ ｓｐ．ｎｏｖ．,Ｙｕｎｎａｎｉｃａｎｄｏｎａ ｏｂｌｏｎｇａ ｓｐ．ｎｏｖ．,Ｌｉｎｅｏｃｙｐｒｉｓ ｇｒａｎｕｌｏｓａ ｓｐ．ｎｏｖ．,Ｌ．ｇｉｂｂａ ｓｐ．ｎｏｖ．以及湖花介科的Ｐａｒａｃｈｉｎｏｃｙｔｈｅｒｅ ｒｅｔｉｃｕｌａｔａ ｇｅｎ．ｅｔ ｓｐ．ｎｏｖ．,     

LPS诱导乳鼠心肌细胞p38蛋白激酶的激活与转位

探讨p38蛋白激酶信号传导通路在细胞中的特异性作用机制。应用共聚焦激光扫描技术观察心肌细胞中p38蛋白激酶的分布及LPS对其分布的影响。结果提示未受刺激静止的及EGF刺激的心肌细胞中,p38在胞浆和胞核中荧光强度呈散性分布。LPS刺激30分钟后,细胞核区的荧光强度明显增强,而胞浆区域的荧光强度降低,心肌细胞受LPS刺激激活后,其p38蛋白激酶由胞浆转位到胞核。     

Role of p38 mitogen-activated protein kinase (MAPK) for vacuole formation in lipopolysaccharide (LPS)-stimulated macrophages

The role of p38 mitogen-activated protein kinase (MAPK) on vacuole formation in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells was examined. LPS definitely induced the formation of vacuoles in RAW 264.7 cells and SB202190 as a p38 specific inhibitor also induced slight vacuole formation. The simultaneous treatment with LPS and SB202190 induced many more vacuoles in RAW 264.7 cells than the treatment with LPS or SB202190 alone, and the vacuoles were extraordinarily large in size. On the other hand, an inactive inhibitor of p38 MAPK did not augment LPS-induced vacuole formation. Further, the inhibitors of other MAPKs and nuclear factor (NF)-kappaB pathways did not affect it. The extraordinarily large vacuoles in RAW 264.7 cells treated with LPS and SB202190 were possibly formed via fusion of small vacuoles. However, SB202190 did not augment vacuole formation in CpG DNA or interferon (IFN)-gamma-stimulated RAW 264.7 cells. The role of p38 MAPK in the vacuole formation in LPS-stimulated macrophages is discussed.     

Ganglioside GM3 suppresses lipopolysaccharide‐induced inflammatory responses in rAW 264.7 macrophage cells through NF‐κB,AP‐1, and MAPKs signaling

Gangliosides are known to specifically inhibit vascular leukocyte recruitment and consequent interaction with the injured endothelium, the basic inflammatory process. In this study, we have found that the production of nitric oxide (NO), a main regulator of inflammation, is suppressed by GM3 on murine macrophage RAW 264.7 cells, when induced by LPS. In addition, GM3 attenuated the increase in cyclooxyenase‐2 (COX‐2) protein and mRNA levels in lipopolysaccharide (LPS)‐activated RAW 264.7 cells in a dose‐dependent manner. Moreover, GM3 inhibited the expression and release of pro‐inflammatory cytokines of tumor necrosis factor‐alpha (TNF‐α), interleukin‐6 (IL‐6), and interleukin‐1β (IL‐1β) in RAW 264.7 macrophages. At the intracellular level, GM3 inhibited LPS‐induced nuclear translocation of nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) and activator protein (AP)‐1 in RAW 264.7 macrophages. We, therefore, investigated whether GM3 affects mitogen‐activated protein kinase (MAPK) phosphorylation, a process known as the upstream signaling regulator. GM3 dramatically reduced the expression levels of the phosphorylated forms of ERK, JNK, and p38 in LPS‐activated RAW 264.7 cells. These results indicate that GM3 is a promising suppressor of the vascular inflammatory responses and ganglioside GM3 suppresses the LPS‐induced inflammatory response in RAW 264.7 macrophages by suppression of NF‐κB, AP‐1, and MAPKs signaling. Accordingly, GM3 is suggested as a beneficial agent for the treatment of diseases that are associated with inflammation.     

Naringin lauroyl ester inhibits lipopolysaccharide-induced activation of nuclear factor κB signaling in macrophages

Naringin (Nar) has antioxidant and anti-inflammatory properties. It was recently reported that enzymatic modification of Nar enhanced its functions. Here, we acylated Nar with fatty acids of different sizes (C2–C18) using immobilized lipase from Rhizomucor miehei and investigated the anti-inflammatory effects of these molecules. Treatment of murine macrophage RAW264.7 cells with Nar alkyl esters inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO) production, with Nar lauroyl ester (Nar-C12) showing the strongest effect. Furthermore, Nar-C12 suppressed the LPS-induced expression of inducible NO synthase by blocking the phosphorylation of inhibitor of nuclear factor (NF)-κB-α as well as the nuclear translocation of NF-κB subunit p65 in macrophage cells. Analysis of Nar-C12 uptake in macrophage cells revealed that Nar-C12 ester bond was partially degraded in the cell membrane and free Nar was translocated to the cytosol. These results indicate that Nar released from Nar-C12 exerts anti-inflammatory effects by suppressing NF-κB signaling pathway.     

Sphingosine kinase protects lipopolysaccharide-activated macrophages from apoptosis

Lipopolysaccharide (LPS) signaling is critical for the innate immune response to gram-negative bacteria. Here, evidence is presented for LPS stimulation of sphingosine kinase (SPK) in the RAW 264.7 murine macrophage cell line and rat primary hepatic macrophages (HMs). LPS treatment of RAW 264.7 cells resulted in a time- and dose-dependent activation of SPK and membrane translocation of SPK1. Further, LPS-induced SPK activation was blocked by SPK1-specific small interfering RNA (siRNA). Overexpression of Toll-like receptor 4 and MD2, the receptor and coreceptor of LPS, in HEK 293 cells activated SPK activity in the absence of LPS treatment. Inhibition of SPK by the pharmacological inhibitor N,N-dimethylsphingosine (DMS) or SPK1-specific siRNA blocked LPS stimulation of extracellular signal-regulated kinase 1/2 and p38 but enhanced LPS-induced c-Jun N-terminal kinase activation. The SPK inhibitor DMS and dominant-negative SPK1 also blocked LPS activation of Elk-1 and NF-kappaB reporters in RAW 264.7 cells. Inhibition of SPK sensitized RAW 264.7 cells and HMs to LPS-induced apoptosis. These data demonstrate the critical role of SPK1 in LPS signaling in macrophages and suggest that SPK1 is a potential therapeutic target to block hyperimmune responses induced by gram-negative bacteria.     

Interleukin-10 inhibits tumor necrosis factor-alpha production in lipopolysaccharide-stimulated RAW 264.7 cells through reduced MyD88 expression

The mechanism of interleukin (IL)-10-mediated inhibition of tumor necrosis factor (TNF)-alpha production was studied by lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. IL-10 inhibited TNF-alpha production transiently at an early stage after LPS stimulation. IL-10 inhibited the activation of nuclear factor (NF)-kappaB, p38 and stress-activated protein kinase (SAPK) in LPS-stimulated RAW 264.7 cells. Although the level of MyD88 protein increased in response to LPS, IL-10 prevented the LPS-induced MyD88 augmentation. There was no significant difference in the MyD88 mRNA expression between the cells pretreated with or without IL-10 in response to LPS. Therefore, IL-10 was suggested to inhibit LPS-induced TNF-alpha production via reduced MyD88 expression.     

Ceramide inhibits lipopolysaccharide-mediated nitric oxide synthase and cyclooxygenase-2 induction in macrophages: effects on protein kinases and transcription factors

The goal of this study was to elucidate whether triggering the sphingomyelin pathway modulates LPS-initiated responses. For this purpose we investigated the effects of N-acetylsphingosine (C(2)-ceramide) on LPS-induced production of NO and PGE(2) in murine RAW 264.7 macrophages and explored the signaling pathways involved. We found that within a range of 10-50 microM, C(2)-ceramide inhibited LPS-elicited NO synthase and cyclooxygenase-2 induction accompanied by a reduction in NO and PGE(2) formation. By contrast, a structural analog of C(2)-ceramide that does not elicit functional activity, C(2)-dihydroceramide, did not affect the LPS response. The nuclear translocation and DNA binding study revealed that ceramide can inhibit LPS-induced NF-kappaB and AP-1 activation. The immunocomplex kinase assay indicated that IkappaB kinase activity stimulated by LPS was inhibited by ceramide, which concomitantly reduced the IkappaBalpha degradation caused by LPS within 1-6 h. In concert with the decreased cytosolic p65 protein level, LPS treatment resulted in rapid nuclear accumulation of NF-kappaB subunit p65 and its association with the cAMP-responsive element binding protein. Ceramide coaddition inhibited all the LPS responses. In addition, LPS-induced PKC and p38 mitogen-activated protein kinase activation were overcome by ceramide. In conclusion, we suggest that ceramide inhibition of LPS-mediated induction of inducible NO synthase and cyclooxygenase-2 is due to reduction of the activation of NF-kappaB and AP-1, which might result from ceramide's inhibition of LPS-stimulated IkappaB kinase, p38 mitogen-activated protein kinase, and protein kinase C.     

Nasunin inhibits the lipopolysaccharide-induced pro-inflammatory mediator production in RAW264 mouse macrophages by suppressing ROS-mediated activation of PI3 K/Akt/NF-κB and p38 signaling pathways

Nasunin is a major anthocyanin in eggplant peel. The purpose of this study was to examine the anti-inflammatory effects of nasunin in lipopolysaccharide (LPS)-stimulated RAW264 macrophages and to identify the molecular mechanisms underlying these effects. We found that nasunin reduced the LPS-induced secretion of tumor necrosis factor-α, interleukin-6 and nitric oxide, and expression of inducible nitric oxide synthase in a dose-dependent manner. Nasunin diminished LPS-induced nuclear factor-κB (NF-κB) activation by suppressing the degradation of inhibitor of κB-α and nuclear translocation of p65 subunit of NF-κB. Nasunin also attenuated the phosphorylation of Akt and p38, signaling molecules involved in pro-inflammatory mediator production. Moreover, nasunin inhibited the intracellular accumulation of ROS, leading to the suppression of NF-κB activation, Akt and p38 phosphorylation, and subsequent pro-inflammatory mediator production. These findings suggest that nasunin exerts an anti-inflammatory effect and this effect is mediated, at least in part, by its antioxidant activity.