人高密度脂蛋白受体CLA-1表达上调剂4776B和4776C的分离、结构鉴定及生物活性研究

目的 从微生物代谢产物中筛选和分离能够上调人高密度脂蛋白受体（CLA-1）表达的新型活性化合物。方法 应用本实验室已经建立的CLA-1表达上调剂的高通量筛选模型，从6000多株微生物中筛选出8株能使CLA-1表达上调的阳性菌株。对其中一株阳性菌株放线菌04-4776发酵产物的活性成分进行活性跟踪分离纯化，从中获得CLA-1表达上调的化合物4776B和4776C，并测定了化合物的理化特性和波谱学数据及相关的生物活性。结果通过理化性质、质谱、紫外和核磁等波谱学数据的分析，确定了化合物4776B和4776C的结构；4776B和4776C对CLA-1的上调率分别在2．08和3．26μmol／L时达到最大，与对照相比分别上调了60％和78％。结论 放线菌04-4776产生的两个活性化合物分别与文献报道的红车轴草素和（9R，13S）-7-脱氧-13-二氢道诺霉素酮结构一致；两个化合物均具有强的上调CLA-1的表达活性，属首次报道。     

化合物E0869体外抗动脉粥样硬化的活性研究

ATP结合盒转运体A1(ATP-binding cassette transporter A1,ABCA1)和清道夫受体B型I(scavenger receptor class B type I,SR-BI/CLA-1)是胆固醇逆转运过程中的重要蛋白。ABCA1和SR-BI/CLA-1的高表达能降低动脉粥样硬化的危险性。因此,本研究利用前期已建立的人ABCA1和CLA-1表达上调剂筛选模型,对20 000个化合物进行筛选,获得能上调ABCA1和CLA-1表达的化合物E0869[4-甲磺酰甲基苯甲酸-1-(3,4-二甲基苯基)-1-丙酮-2-酯],其上调活性分别为160%和175%,EC50值分别为3.79和1.42μmol·L-1;进一步研究发现,活性化合物E0869能上调肝细胞Hep G2以及巨噬细胞RAW264.7中ABCA1、SR-BI/CLA-1以及ABCG1的m RNA和蛋白水平,但不影响FAS、SREBP-1c、CD36的表达;E0869能使泡沫化巨噬细胞RAW264.7胞内脂滴量明显减少,并能增加其胆固醇的流出。因此,化合物E0869能够上调ABCA1和CLA-1活性,并且具有较好的体外抗动脉粥样硬化效果。     

抗MRSA抗生素FW99501的分离纯化、结构鉴定和生物学活性

在筛选微生物来源抗M RSA抗生素中从一株链霉菌F IM 99501的发酵产物中分离纯化到一个具有抗M RSA的化合物FW 99501,经理化性质研究和光谱分析,证实它与尼日利亚菌素同质。FW 99501对几株耐不同抗生素的M RSA菌株和革兰氏阳性菌有很强抗菌活性,此外它还具有免疫抑制活性。     

深海冷泉链霉菌OUCLQ19-3次级代谢产物的研究

目的 探究深海冷泉来源微生物产生丰富次级代谢产物的潜力,挖掘具有抗多重耐药(multi-drug resistant, MDR)菌活性的次级代谢产物,为新型海洋药物研发提供先导化合物。方法 采用大规模发酵积累粗提物,利用有机溶剂萃取、C18反相硅胶开放柱层析、半制备高效液相等分离手段对发酵产物进行分离纯化,通过MS、NMR数据以及文献比对进行化合物的结构鉴定,进而对化合物进行抗MDR菌活性测试。结果 从深海冷泉来源链霉菌Streptomyces sp. OUCLQ19-3发酵产物中分离得到2个xiamycin类化合物,分别为xiamycin B(1)和xiamycin A(2);活性结果显示,化合物1和2均无抗MDR菌活性。结论 深海冷泉来源链霉菌Streptomyces sp. OUCLQ19-3能够产生一系列丰富的次级代谢产物,具有潜在的药用价值,其活性化合物有待进一步挖掘。     

微生物来源白细胞介素-4受体拮抗剂的筛选*

目的：从链霉菌4849的代谢产物中分离白细胞介素4受体（IL-4R）拮抗剂。方法：采用大孔吸附，溶媒萃取，硅胶柱色谱，重结晶等方法进行分离和纯化，以酶联免疫法进行活性跟踪，通过UV，ESIMS和NMR进行化合物的结构鉴定。结果：分离得到化合物4849A，4849B和4849C，根据波谱解析，确定其分别为金丝菌素、硫藤黄菌素和4’，7-二甲氧基异黄酮，其中4’，7-二甲氧基异黄酮的拮抗活性比较明显。结论：从链霉菌4849的代谢产物中首次筛选出白细胞介素4受体拮抗剂4’，7-二甲氧基异黄酮。     

海洋链霉菌Streptomyces sp. S598中抗菌活性产物的研究

目的 对海洋链霉菌Streptomyces sp. S598固体发酵提取物的抗菌成分进行研究。方法 采用葡聚糖凝胶Sephadex LH-20、反相柱色谱、硅胶柱层析及半制备HPLC等方法分离纯化该菌株的活性次级代谢产物,并通过ESI-MS、NMR等波谱技术结合文献对比鉴定其结构。结果 从10L固体发酵提取物中分离得到5个单体化合物,分别鉴定为缬氨霉素(1)、二活菌素(2)、亚油酸(3)、亚油酸甲酯(4)和油酸(5)。结论 海洋链霉菌Streptomyces sp. S598能代谢产生具有多种生物活性的化合物。化合物1对MRSA 28300和白念珠菌(ATCC10231)的MIC为1μg/mL,化合物2具有较强的广谱抗细菌活性,对肺炎链球菌、流感嗜血菌的MIC为0.125μg/mL,尤其具有显著的抗MRSA的活性,对MRSA     

海洋链霉菌Streptomyces sp. S598中抗菌活性产物的研究

目的 对海洋链霉菌Streptomyces sp. S598固体发酵提取物的抗菌成分进行研究。方法 采用葡聚糖凝胶Sephadex LH-20、反相柱色谱、硅胶柱层析及半制备HPLC等方法分离纯化该菌株的活性次级代谢产物,并通过ESI-MS、NMR等波谱技术结合文献对比鉴定其结构。结果 从10L固体发酵提取物中分离得到5个单体化合物,分别鉴定为缬氨霉素(1)、二活菌素(2)、亚油酸(3)、亚油酸甲酯(4)和油酸(5)。结论 海洋链霉菌Streptomyces sp. S598能代谢产生具有多种生物活性的化合物。化合物1对MRSA 28300和白念珠菌(ATCC10231)的MIC为1μg/mL,化合物2具有较强的广谱抗细菌活性,对肺炎链球菌、流感嗜血菌的MIC为0.125μg/mL,尤其具有显著的抗MRSA的活性,对MRSA 28300的MIC<0.125μg/mL。化合物1和2均为首次从该种放线菌中分离得到,且本文首次报道其对MRSA均具有抑制活性。     

弗氏链霉菌泰乐菌素还原酶基因编辑及其对泰乐菌素发酵产物的影响

目的 对弗氏链霉菌(Streptomyces fradiae)泰乐菌素还原酶(tylosin reductase,SFR)进行改造以抑制其对泰乐菌素(tylosin)的还原作用，提高泰乐菌素发酵产量和产品质量。方法 在前期对泰乐菌素还原酶编码基因第642位碱基进行定点突变形成终止密码子的基础上，对该基因642位后碱基进行敲除；对基因敲除菌株的生长以及发酵产物中泰乐菌素(A组分)和雷诺菌素(relomycin,D组分)含量进行分析。结果 获得了泰乐菌素还原酶基因部分序列敲除的弗氏链霉菌菌株M1-d1；该菌株培养过程中生长状态及稳定期生物量与原始菌株基本一致，菌落形态正常；泰乐菌素发酵产物中敲除菌株A组分相对含量较原始菌株相比增加了10.08%，而D组分相对含量较原始菌株减少68.75%。结论 弗氏链霉菌泰乐菌素还原酶基因部分序列敲除不影响菌体正常生长，但能够抑制泰乐菌素还原酶对A组分的还原作用，提高泰乐菌素发酵产物中A组分含量，显著降低D组分含量。     

海洋链霉菌Streptomyces sp. rssa2的次生代谢产物及其抗菌活性研究

目的 研究1株珊瑚来源的共附生链霉菌菌株Streptomyces sp. rssa2的次生代谢产物及其抗菌活性。方法 采用正相硅胶柱色谱、ODS反相硅胶柱色谱、Sephadex LH-20凝胶柱色谱以及半制备高效液相色谱（HPLC）等手段对rssa2的发酵产物进行分离纯化，通过核磁、质谱数据并结合文献数据鉴定化合物结构；通过滤纸片法和稀释法对化合物的抗菌活性进行测定。结果 从海洋链霉菌Streptomyces sp. rssa2的液体麦芽提取物培养基发酵产物中分离得到3个主要成分，其结构分别鉴定为大环内酯类化合物aldgamycin G(1)、aldgamycin E(2)、swalpamycin(3)。抗菌活性测试结果显示，化合物1～3均对溶藻弧菌（Vibrio alginolyticus）的生长具有弱抑制活性。结论 化合物1～3均为首次从珊瑚共附生链霉菌中分离获得，并且发现它们具有一定程度的抗菌活性，具有潜在的研究价值。     

基因组信息指导下茂源链霉菌代谢产物研究

目的在基因组信息指导下,研究茂源链霉菌Streptomyces mobaraensis US-43的代谢产物。方法采用16S r RNA基因序列分析对菌株US-43进行初步分类鉴定,应用anti SMASH分析菌株US-43的基因组序列并预测其可能含有的代谢产物;采用正向硅胶柱色谱、凝胶柱色谱以及高效液相色谱等分离技术对该菌株的代谢产物进行分离纯化,利用核磁共振和质谱鉴定化合物结构;通过改变培养条件对其发酵稳定性进行考察,通过HPLC-UV方法建立标准曲线,研究代谢产物的产量。结果在基因组信息指导下从茂源链霉菌Streptomyces mobaraensis US-43中分离鉴定了一个α-吡啶酮类化合物杀粉蝶菌素A1,且该菌株的发酵稳定性良好,最高产量为144mg/L。结论茂源链霉菌Streptomyces mobaraensis US-43能够稳定产生杀粉蝶菌素A1。     

Evaluation and validation of multiple cell lines and primary mouse macrophages to predict phospholipidosis potential

Phospholipidosis (PLD) in preclinical species can lead to regulatory delays thereby creating incentives to screen for PLD during drug discovery. The objective of this work was to compare, optimize, and validate in vitro PLD assays in primary mouse macrophages and hepatocyte- (HepG2, HuH7) or macrophage-derived cells lines (I.13.35, RAW264.7) and to evaluate whether primary cells were better at predicting PLD. Assay precision, determined by a measure of signal to noise window (Z′), within assay variability, and day-to-day variability, using amiodarone, was generally acceptable for all cell types; however, precision limits for HepG2 and HuH7 were slightly below assay acceptance criteria. Up to 66 known PLD inducers and non-inducers were subsequently tested to validate the assays. The concordance for predicting PLD in primary macrophages, I-13.35, RAW264.7, HuH7, and HepG2 cells was 91%, 74%, 73%, 62%, and 62% respectively using a decision limit of EC₅₀ ? 125 μM as a positive finding. Increasing the number of negative controls tested in RAW264.7 cells and changing the decision limit to ?4-fold increase in PLD, improved the specificity and overall concordance to 88%. RAW264.7 cells were selected as the primary screen for predicting PLD, and together with the primary macrophages, were integrated into an overall testing paradigm proposed for use in PLD risk identification.     

1-苯甲酰基-4-(4-氯苄基)哌嗪衍生物的设计、合成以及抗炎活性研究

目的:以1-苯甲酰基-4-(4-氯苄基)哌嗪为先导化合物,经进一步的结构优化,期望获得一类抗炎活性更好的多靶点抑制剂。方法:以取代苯甲酸为起始原料,经取代、酰化反应合成18个目标化合物。测定所有化合物对脂多糖(lipopolysaccharide,LPS)诱导RAW264.7细胞分泌肿瘤坏死因子(tumor necrosis factor,TNF)-α和白细胞介素(interleukin,IL)-6的抑制作用,并对活性较好的化合物进行分子对接。结果:所有化合物均经¹H NMR,¹³C NMR,HRMS确定其结构,化合物3d,8k对TNF-α的分泌具有较好的抑制活性,化合物3b,3d对IL-6的分泌具有较好的抑制活性。结论:化合物3d对LPS诱导RAW264.7细胞分泌TNF-α和IL-6具有较好的抑制活性,有进一步研究的价值。     

八肽胆囊收缩素抑制LPS诱导的RAW264.7细胞AP-1活性及IL-6表达

目的研究八肽胆囊收缩素(CCK-8)对LPS诱导RAW264.7细胞IL-6表达的影响及相关机制。方法用ELISA及RT-PCR法检测RAW264.7细胞IL-6蛋白及mR-NA表达;用EMSA方法检测RAW264.7细胞AP-1 DNA结合活性。结果①LPS可时间依赖性的诱导RAW264.7细胞IL-6蛋白及mRNA表达;②10-10 mol.L-1 CCK-8对LPS诱导的RAW264.7细胞IL-6表达无明显影响;10-8、10-6 mol.L-1 CCK-8浓度依赖性地抑制了LPS诱导的RAW264.7细胞IL-6表达;③10-10 mol.L-1 CCK-8未影响LPS诱导的AP-1活性,10-8、10-6 mol.L-1 CCK-8浓度依赖性地抑制了LPS诱导的AP-1活性。结论 CCK-8通过抑制AP-1 DNA结合活性而抑制了LPS诱导的RAW264.7细胞IL-6表达,这可能是CCK-8发挥抗炎作用的信号转导机制之一。     

Inhibition of lipopolysaccharide-induced nitric oxide production by flavonoids in RAW264.7 macrophages involves heme oxygenase-1

The role of heme oxygenase-1 (HO-1) played in the inhibitory mechanism of flavonoids in lipopolysaccharide (LPS)-induced responses remained unresolved. In the present study, flavonoids, including 3-OH flavone, baicalein, kaempferol, and quercetin, induced HO-1 gene expression at the protein and mRNA levels in the presence or absence of LPS in RAW264.7 macrophages. This effect was associated with suppression of LPS-induced nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) protein expression. Hemin induced HO-1 protein expression and this was associated with the suppression of LPS-induced NO production and iNOS protein expression in a dose-dependent manner. In addition, an increase in bilirubin production was found in flavonoid- and hemin-treated cells. Hemin, at the doses of 10, 20, and 50 microM, dose-dependently stimulated the flavonoid (50 microM)-induced HO-1 protein expression, and enhanced their inhibitory effects on LPS-induced NO production and iNOS protein expression. Pretreatment of the HO-1 inhibitor, tin protoporphyrin (10 microM), attenuated the inhibitory activities of the indicated flavonoids on LPS-induced NO production. Morphologic analysis showed that 3-OH flavone, baicalein, kaempferol, quercetin, hemin, and tin protoporphyrin did not cause any change in cell viability in the presence or absence of LPS. In contrast, only 3-OH flavone showed a significant inhibition of cell growth using the MTT assay. Transfection of an HO-1 vector in macrophages (HO-1/RAW264.7) resulted in a 3-fold increase in HO-1 protein compared with that the parental RAW264.7 cells. NO production mediated by LPS in HO-1 over-expressed RAW264.7 cells (HO-1/RAW264.7) was significant less than that in parental RAW264.7 cells. 3-OH Flavone, baicalein, kaempferol, and quercetin showed a more significant inhibition on LPS-induced NO production in HO-1/RAW264.7 cells than in parental RAW264.7 cells. These results provide evidence on the role of HO-1 in the inhibition of LPS-induced NO production by flavonoids. A combination of HO-1 inducers (i.e. hemin) and flavonoids might be an effective strategy for the suppression of LPS-induced NO production.     

β1-Adrenergic receptor-mediated HO-1 induction, via PI3K and p38 MAPK, by isoproterenol in RAW 264.7 cells leads to inhibition of HMGB1 release in LPS-activated RAW 264.7 cells and increases in survival rate of CLP-induced septic mice

High mobility group box (HMGB)-1 plays an important role in sepsis-associated death in experimental studies. Heme oxygenase-1 (HO-1) inducers were reported to reduce HMGB1 release in experimental sepsis. Previously, we reported on the importance of the β1-adrenergic receptor and protein kinase A pathway in the regulation of HO-1 expression by isoproterenol (ISO) in RAW 264.7 cells. We investigated whether ISO reduces HMGB1 release in LPS-activated RAW 264.7 cells and improves survival rate in septic mice due to HO-1 induction. ISO concentration-dependently increased HO-1 via Nrf-2 translocation and inhibited release of HMGB1 through the β₁-adrenergic receptor (β₁-AR) in LPS-activated RAW 264.7 cells. This conclusion was supported by the finding that dobutamine but not salbutamol increased HO-1 expression in both RAW 264.7 cells. ISO failed to inhibit HMGB1 release when HO-1 expression was suppressed by ZnPPIX, an HO-1 inhibitor in RAW 264.7 cells. ISO significantly inhibited phosphorylation of IκB-α and NF-κB-driven luciferase activity in LPS-activated RAW 264.7 cells. In addition, LY294002, a PI3K inhibitor, and SB203580, a p38 MAPK inhibitor, significantly inhibited not only HO-1 induction but also HMGB1 release by ISO. Importantly, ISO increased HO-1 protein expression in heart and lung tissues, reduced HMGB1 in plasma and increased survival rate in CLP-treated septic mice, which was significantly reversed by co-treatment with ZnPPIX. Taken together, we conclude that inhibition of HMGB1 release during sepsis via β₁-AR-mediated HO-1 induction is a novel mechanism for the beneficial effects of ISO in the treatment of sepsis.     

携带小鼠 KLF4 基因重组慢病毒的构建及对 RAW264.7 细胞增殖的影响

目的 构建小鼠 Krüppel 样因子 4（KLF4）慢病毒表达载体,并建立 KLF4 过表达小鼠腹腔巨噬细胞 RAW264.7 细胞株。方法 采用聚合酶链式反应（PCR）技术扩增目的基因 KLF4 后,构建重组质粒 pLVX-KLF4,并 通过 PCR、双酶切和测序方法对其进行鉴定。重组质粒与 pSPAX2、pMD2.G 辅助质粒通过 Lipofectamine® 3000 共转 染 293T 细胞,包装病毒并测定病毒滴度。将获得的慢病毒感染 RAW264.7 细胞,实时定量 PCR 法检测 KLF4 mRNA 的表达。分选流式细胞仪分选 GFP 阳性 RAW264.7 细胞。流式细胞术检测 KLF4 对 RAW264.7 细胞周期的影响。 EdU 法检测 KLF4 对 RAW264.7 细胞增殖的影响。结果 经 PCR、双酶切鉴定和测序证实,成功构建了包含小鼠 KLF4 基因的慢病毒穿梭质粒,RT-PCR 证实 Lenti-KLF4 感染的 RAW264.7 细胞中 KLF4 mRNA 表达高于未感染的 对照组 RAW264.7 细胞（P＜0.05）。初次浓缩后测定小鼠 KLF4 基因重组慢病毒的滴度为 2.05×108 TU/mL。分选出 KLF4 过表达的 RAW264.7 细胞。KLF4 过表达的 RAW264.7 细胞周期变化显示为 S 期延长,G0/G1 期缩短。EdU 检 测显示 KLF4 过表达的 RAW264.7 细胞增殖活性增高。结论 成功构建了 KLF4 的慢病毒表达载体,并建立 KLF4 过表达的 RAW264.7 细胞株,KLF4 过表达促进了 RAW264.7 细胞的增殖。     

丹参酮II-A通过调控TLR4/IκBα/NFκB信号通路抑制LPS诱导的细胞炎症

目的建立脂多糖(LPS)诱导的小鼠单核巨噬细胞(RAW264.7)炎症模型,探究丹参酮II-A(Tan IIA)的抗炎活性及其机制。方法CCK-8法测定Tan IIA对细胞活力的影响;迁移小室测定Tan IIA对LPS诱导细胞迁移能力作用;ELISA法测定细胞上清液中小鼠肿瘤坏死因子α(tumor necrosis factoralpha,TNF-α)、白介素6(interleukin 6,IL-6)、IL^-1β、单核细胞趋化蛋白-1(monocyte chemoattractant protein,MCP-1)的含量;Western blot法检测基质金属蛋白酶2(matrix metalloproteinases,MMP-2)、MMP-9、Toll样受体-4(TLR4)、IκB-α、p-IκB-α、NFκB和p-NFκB蛋白的表达。结果Tan IIA对LPS诱导的RAW264.7细胞培养液中炎症因子TNF-α、IL-6、IL^-1β和MCP-1的分泌有明显的抑制作用;明显下调MMP-2、MMP-9、TLR4、p-IκB-α和p-NFκB的蛋白的表达,抑制IκB-α磷酸化和NFκB的入核和活化。结论Tan IIA可通过抑制MMP-2和MMP-9的表达以及TLR4/κB-α/NF-κB信号通路,调控TNF-α、IL-6、IL^-1β等炎症因子的释放而发挥抗炎活性。     

八肽胆囊收缩素通过p38MAPK通路抑制LPS诱导的RAW264.7细胞IL-1β表达

目的研究八肽胆囊收缩素(CCK-8)对LPS诱导RAW264.7细胞IL-1β表达的影响及相关机制。方法用ELISA及RT-PCR法检测RAW264.7细胞IL-1βmRNA及蛋白表达;用Western blot检测RAW264.7细胞p38 MAPK的磷酸化水平。结果①LPS可时间依赖性的诱导RAW264.7细胞IL-1βmRNA及蛋白的表达,分别于刺激后3 h及6 h达到高峰;②10-10 mol.L-1 CCK-8对LPS诱导的RAW264.7细胞IL-1β表达无影响;10-8、10-6 mol.L-1CCK-8浓度依赖性地抑制了LPS诱导的RAW264.7细胞IL-1β表达;③10-10 mol.L-1 CCK-8未影响LPS诱导的p-p38MAPK水平,10-8、10-6 mol.L-1 CCK-8浓度依赖性地抑制了LPS诱导的p-p38 MAPK水平;④p38 MAPK特异性抑制剂SB203580可抑制LPS诱导的RAW264.7细胞IL-1β表达,与CCK-8共同作用后,抑制作用进一步加强。结论 CCK-8通过抑制p38 MAPK磷酸化而抑制了LPS诱导的RAW264.7细胞IL-1β表达,这可能是CCK-8发挥抗炎作用的信号转导机制之一。     

穿心莲内酯对脂多糖诱导RAW264.7细胞炎症反应的抑制作用

目的探讨穿心莲内酯对脂多糖诱导RAW264.7细胞炎症反应的抑制作用及其作用机制。方法采用噻唑蓝比色(MTT)法分析穿心莲内酯对RAW264.7细胞活力的影响。通过脂多糖处理RAW264.7细胞24 h建立细胞炎症模型,造模前1 h用穿心莲内酯2.5、5、10、20μmol/L预处理。荧光定量PCR法检测RAW264.7细胞内相关抗氧化应激酶基因和i NOS水平。穿心莲内酯单独处理RAW264.7细胞24 h,Western blotting法检测Keap1/Nrf2/HO-1信号通路相关蛋白和Keap1、Nrf2、HO-1蛋白水平。免疫荧光检测转录因子Nrf2在胞质及核内的分布情况。结果与对照组比较,穿心莲内酯剂量相关性地抑制RAW264.7细胞活力,差异具有统计学意义(P0.05、0.01、0.001)。穿心莲内酯显著抑制脂多糖诱导RAW264.7细胞的i NOS水平(P0.001),增加相关抗氧化酶基因HO-1、NQO1 m RNA水平。穿心莲内酯抑制Keap1表达,增加Nrf2和HO-1蛋白水平的表达。结论穿心莲内酯可抑制脂多糖诱导的炎症反应,其作用机制可能与激活Keap1/Nrf2/HO-1信号通路从而调控抗氧化酶HO-1、NQO1 m RNA表达水平相关。     

Isolation of endophytic fungi with anti-inflammatory effect in vitro from Zanthoxylum armatum

Endophytic fungus is a rich source of bioactive metabolites with multiple activities. In the present study, eight endophytic fungal strains (Z-1 to Z-8) from Zanthoxylum armatum DC. were isolated and identified, and the anti-inflammatory effect of their extracts was evaluated in vitro. The results showed that four endophytic fungal extracts (Fusarium oxysporum Schlecht. (Z-1), Alternaria arborescens E.G Simmons (Z-3), Mucor fragilis Bainier (Z-4) and Aspergillus terreus Thom (Z-6)) displayed good activities in inhibition of excessive production of nitric oxide in lipopolysaccharide-activated mouse macrophage RAW264.7 cells. Among them, the extracts of Fusarium oxysporum Schlecht showed the maximum inhibition activity with a half maximal inhibitory concentration of 174.0 μg/mL. The underlying mechanism of the anti-inflammatory effect of Fusarium oxysporum Schlecht extract was associated with its inhibition on the release of several inflammatory factors. The mRNA expression of interleukin 1β, interleukin 6, inducible nitric oxide synthase in lipopolysaccharide-activated mouse macrophage RAW264.7 cells were all inhibited by Z-1 extract detected by real-time polymerase chain reaction. In summary, several endophytic fungal from Zanthoxylum armatum have good anti-inflammatory activity and Fusarium oxysporum Schlecht possesses a promising potential to be developed to a novel anti-inflammatory agent.