发酵无花果香料的挥发性成分分析

利用微生物发酵无花果开发特色香料,并采用同时蒸馏萃取装置收集挥发性成分并用气相色谱一质谱仪对生物技术制备的无花果香料挥发性成分进行分离和鉴定,经毛细管色谱分离出47种组分,确认了其中的45种成分,并用面积归一化法测定了各种成分的百分含量,其主要成分为：9,12-十八碳二烯酸乙酯(27．34％)、十六酸乙酯(23．99％)、邻苯二甲酸二丁酯(6．18％)、邻苯二甲酸二异丁酯(5．52％)、9,12-十八碳二烯酸甲酯(4．72％)、十六酸甲酯(4．67％)、9,12,15-十八碳三烯酸乙酯(4．48％)、9-十八碳烯酸乙酯(3．80％)、糠醛(2．53％)、9,12,15-十八碳三烯酸甲酯(1．85％)、十八酸乙酯(1．42％)、9-十八碳烯酸甲酯(1．26％)等。     

红树植物红海榄脂肪酸的GC-MS分析

采用索氏提取法对红树植物红海榄(Rhizophora stylosa)叶中的脂肪酸进行提取,甲酯化后利用气相色谱-质谱联用仪对脂肪酸成分进行分离和鉴定,鉴定出了12种脂肪酸,占脂肪酸总量的84.95%,其中主要包括十六酸(棕榈酸)(40.49%),9-十八碳烯酸(油酸)(17.24%),9,12-十八碳二烯酸(亚油酸)(11.24%)等。     

金线莲挥发油化学成分的研究

采用水蒸气蒸馏法提取花叶开唇兰挥发油,用GC毛细管柱进行分析,归一化法测定其相对含量,并用GC-MS法鉴定化学成分。检出182个成分,鉴定出73个化合物,占挥发油总量的92.64%,主要成分为:正十六烷酸(25.22%)、(Z,Z)-9,12-十八碳二烯酸甲酯(6.47%)、11,14,17-二十碳三烯酸甲酯(4.42%)、(Z,Z)-9,12-十八碳二烯酸(15.35%)和(Z,Z,Z)-9,12,15-十八碳三烯酸甲酯(13.64%)。     

蝴蝶果茎挥发油的化学成分

采用水蒸汽蒸馏法从大戟科蝴蝶果茎中提取挥发油,用气相色谱-质谱联用技术对挥发油化学成分进行分析。分离出36个峰,鉴定出35种化合物,占总油量的98.34%,并应用面积归一化法测定各成分的相对百分含量。其主要成分为十六烷酸乙酯(13.19%)、正十六烷酸(11.11%)、十八碳烯酸乙酯(6.18%)、正十八烷(4.98%)、(Z,Z)-9,12-十八碳二烯酸(4.90%)及十八碳二烯酸乙酯(4.21%)。     

从华蟹甲草中分离的两种活性成分对家蝇的杀虫活性

研究了从我国特有植物华蟹甲草Sinacalia tangutica (Maxim.) B. Nord中经生物活性跟踪实验得出的杀虫活性成分Z,Z,Z-9,12,15-十八碳三烯酸和Z,Z-9,12-十八碳二烯酸对家蝇Musca domestica vicina的生物活性及对其生理生化指标的影响。结果表明,家蝇经该2种化合物1 mg/mL处理后表现出类似神经毒剂中毒的兴奋症状。这2种化合物对家蝇表现出毒杀作用,24 h时,Z,Z,Z-9,12,15-十八碳三烯酸和Z,Z-9,12-十八碳二烯酸对家蝇的LC₅₀值分别为0.26 mg/mL和0.43 mg/mL; 对家蝇触杀作用极低,以1 mg/mL分别点滴处理家蝇后48 h,死亡率分别为21.54%和4.08%。这2种化合物对家蝇的AChE影响不明显,但可引起家蝇的过氧化物酶的活性发生紊乱,对家蝇总糖含量也有一定的影响。Z,Z-9,12-十八碳二烯酸可引起家蝇的Mg-ATPase的比活力降低,而Z,Z,Z-9,12,15-十八碳三烯酸引起家蝇的Na-K-Mg-ATPase和Ca-ATPase的比活力较对照上升。     

卷丝苣苔和勐醒芒毛苣苔脂肪酸成分的研究

用索氏提取法提取,甲酯化处理后采用气相色谱-质谱联用技术首次对卷丝苣苔(Corallodiscus kingianus)和勐醒芒毛苣苔(Aeschynanthus mengxingensis)中脂肪酸成分进行了分析.从卷丝苣苔的脂肪酸成分中鉴定出33个化合物,占检出物总质量分数的95.44%,主要成分为9,12-十八碳二烯酸、(Z,Z,Z)-9,12,15-十八碳三烯酸、十六烷酸.从勐醒芒毛苣苔的脂肪酸成分中鉴定出30个化合物,占检出物总质量分数的94.23%,主要成分为14-甲基-十五烷酸、(E)-9-十八碳烯酸、10,13-十八碳二烯酸.二者有15个组分是相同的.     

乳突果苗的组织培养及脂氧合酶的诱导

脂氧合酶(LOX)是植物十八碳酸途径中一个很重要的酶,该酶作用的产物在植物生长发育过程以及在植物对环境胁迫反应中起着重要作用。首次建立了萝藦科植物乳突果苗的培养体系,并用仿真菌环境(几丁质)对乳突果组培苗进行刺激诱导,通过LC-ESI-MS检测脂氧合酶反应的产物。粗酶活性鉴定结果显示,经150mg/L几丁质诱导9h的乳突果组培苗产生了9-LOX,该酶可催化亚油酸生成9,10,11-三羟基-12-十八碳烯酸。推测在乳突果组培苗中,几丁质诱导的十八碳酸代谢途径沿着9-LOX方向进行。     

瑞香狼毒茎叶化学成分研究

新鲜瑞香狼毒(Stellera chamaejasme)茎叶经正已烷提取,脱腊后进行GC-MS-DS联用分析,鉴定出20个化合物。主要成分为正十八烷;正十九烷;2,6,10,14 — 四甲基十六烷;十六烷酸;十六烷酸甲酯;十六烷酸乙酯;9,12,15-十八碳三烯酸甲酯;9,12-+八碳二烯酸;9,12,15-十八碳三烯酸和十八烷酸。     

青阳参组织培养及愈伤组织的成分分析

用青阳参(Cynanchum otophyllum)的嫩枝和芽在Ms 2．0mg／L2,4-D 0．1mg／L KIN的培养基上诱导愈伤组织。通过不同的培养基和激素配比实验,发现6,7-V 2．0mg／L2,4．D 0．3mg／LKIN最适合愈伤组织的生长。但在6,7-V 1．0mg／L2,4．D 0．1mg／L KIN培养基中的愈伤组织次生代谢物含量最高。愈伤组织的生长周期为27d,但在33d时次生代谢产物的含量最高。从愈伤组织中分离到7个化合物：(1)9,10,11-三羟基-十八碳-12(Z)-烯酸甲酯(methyl9,10,11-trihydroxy-12-octadecencate),(2)胡萝卜甙(daucosterol),(3)β-谷甾醇(β-sitoster01),(4)华木酸(betuliniic acid),(5)齐端果酸(oleamlic acid),(6)棕榈酸(hexadecanoic acid),(7)十八碳-9-烯酸(9-octadecenoic acid)。首次报道从植物愈伤组织中分离到多羟基十八碳烯酸,并讨论了化合物（1）对植物细胞生长的可能影响。     

共轭亚油酸生理功能及微生物合成调控研究进展

共轭亚油酸(conjugated linoleic acid,CLA)是一种新型功能性油脂,顺9,反11-十八碳二烯酸(c9,t11-CLA)和反10,顺12-十八碳二烯酸(t10,c12-CLA)由于具有比其他异构体更强的生理功能得到广泛关注和研究.微生物合成CLA具有安全性高、选择特异性强等特点,研究CLA产量提高...     

中药组方黄芩汤抑制胃癌细胞增殖的实验研究

目的探讨黄芩汤对胃癌细胞生长增殖及干细胞标志物表达的影响。 方法采用体外优化培养的胃癌细胞株SGC-7901模型,分别加入生理盐水、5-FU、黄岑汤和5-FU+黄芪汤干预,MTT法检测胃癌细胞增殖情况,Real-time PCR检测胃癌干细胞相关表面标志物CD44、EpCAM、CD90的表达情况;并进一步利用胃癌细胞裸鼠荷瘤模型,观察黄岑汤协同5-FU对体内肿瘤生长的抑制效果。细胞增殖曲线多组间数据比较采用重复测量数据方差分析,单时间点多组数据采用单因素方差分析,组间比较采用Tukey法。 结果优化培养的胃癌细胞SGC- 7901呈球形生长,细胞活性染色显示良好的活性状态;MTT结果显示,黄岑汤组（0.44±0.04）能够抑制胃癌细胞的增殖,从第4天起与对照组（0.59±0.02）相比,差异具有统计学意义（F = 39.550,P < 0.01）;黄岑汤联合5-FU组（0.36±0.04）加强5-FU对肿瘤细胞的抑制作用,从第3天起与对照组（0.50±0.01）相比,差异具有统计学意义（F = 10.670,P < 0.01）,与5-FU组（0.42±0.03）对比,差异具有统计学意义（F = 10.670,P < 0.05）;Real-time PCR结果显示黄岑汤联合5-FU可抑制胃癌细胞中肿瘤干细胞相关表面标志物CD44、EpCAM、CD90表达（P < 0.01）;移植瘤生长抑制实验发现黄芪汤组对荷瘤鼠移植瘤的生长具有抑制作用,与对照组相比移植瘤体积减小,差异具有统计学意义（P < 0.01）,黄岑汤联合5-FU组与5-FU组相比对移植瘤抑制效果更明显,差异具有统计学意义（P < 0.01）。 结论黄芪汤能抑制胃癌细胞的生长和增殖,并能协同5-FU产生抗肿瘤作用。     

大蒜阿霍烯抗胃癌的作用及分子机制*

目的: 探讨大蒜阿霍烯对胃癌细胞MGC-803的作用及相关分子机制。方法: 终浓度分别为0、1、5、25和125 μmol/L大蒜阿霍烯作用于细胞MGC-803 24 h、48 h和72 h,各设3复孔,MTS法检测细胞增殖活性,JC-1和Hoechst染色法观察线粒体膜电位和核型改变,LDH释放法检测细胞毒性,流式法分析细胞的凋亡和周期改变,RT-qPCR和Western blot检测P53、Caspase-3、RAS、ERK、BCL-2、AKT、mTOR、PI3K基因的表达,同时,取4周龄雄性BALB/C鼠随机分成5组,20只/组,腹股沟皮下接种胃癌细胞MGC-803,2 d后各组分别经皮下注射浓度为0 μmol/L、1 μmol/L、5 μmol/L、25 μmol/L、125 μmol/L的大蒜阿霍烯,0.1 ml/次,隔天注射一次,并于首次注射肿瘤细胞的第20日每组杀10只,取瘤组织,称重。记录剩余小鼠的存活期,观察大蒜阿霍烯对荷瘤小鼠胃癌生长及生存期的影响。结果: 大蒜阿霍烯可明显抑制MGC-803细胞增殖活性,诱导细胞凋亡(P＜0.01),显著上调P53、Caspase-3、BAX基因的转录和表达水平,抑制基因RAS、ERK1、BCL-2、AKT、mTOR和PI3K的表达(P＜0.01),显著抑制小鼠胃癌移植瘤生长,并延长荷瘤小鼠存活期(P＜0.01)。结论: 大蒜阿霍烯对胃癌有治疗作用,可通过调节PI3K-AKT-mTOR、RAS-RAF-MEK-ERK信号通路而抑制胃癌细胞增殖,诱导细胞凋亡。     

苯污染对大鼠脑组织环核苷酸与相关蛋白水平的影响

为了探索苯污染对人类健康损伤作用的因素, 选用SPF级Wistar大鼠为实验对象, 分为4组: 低剂量组灌胃苯 0.19 g·kg-1, 中剂量组灌胃苯 0.38 g·kg-1, 高剂量组灌胃苯 0.76 g·kg-1, 对照组灌胃菜籽油2 mL·kg-1;用酶联免疫吸附法(ELISA)检测脑组织中环核苷酸和相关蛋白的水平。结果发现, 连续给予大鼠不同剂量苯21 d, 低、中、高剂量大脑皮质cAMP、c-fos、Bax和caspase-9水平比对照组分别升高了22.41%-59.53%, 38.28%-81.34%, 29.08%-63.04%和44.53%-70.07%; cGMP、Bcl-2水平比对照组分别降低了15.20%-49.79% 和13.42%-46.98%。丘脑组织cAMP、c-fos、Bax和caspase-9水平比对照组分别升高了34.71%-63.34%, 28.32%-78.04%, 16.54%-49.46% 和9.10%-61.57%; cGMP、Bcl-2水平比对照组分别降低了20.00%-33.83% 和8.53%-39.53%。结果提示, 苯污染引起脑组织损伤和细胞凋亡主要与cAMP、c-fos、Bax、caspase-9水平升高及cGMP和Bcl-2水平降低有关。     

Combined effect of sCD40L and PI3K siRNA on transplanted tumours growth and microenvironment in nude mice with gastric cancer

The objective of the paper is to investigate the combined effect of sCD40L and phosphatidylinositol 3-kinase (PI3K) siRNA on transplanted tumours growth and microenvironment in nude mice with gastric cancer. 48 h after modeling, the animals were randomly divided into saline + AGS group (A), sCD40L + AGS group (B), saline + PI3K siRNA group (C) and sCD40L + PI3K siRNA group (D), six mice in each group. The mouse in the groups was inoculated with exponential phase AGS cell or PI3K gene silencing cells (100 μl, 5 × 10(6)). After tumour size reaches 0.2-0.3 cm, Tumours in animals of groups were injected with sCD40L (100 μl, 10 mg/kg) or equal volume of saline, thrice each day, respectively. Microvessel density (MVD), apoptosis index, and expression levels of PI3K, Survivin and vascular endothelial growth factor (VEGF) proteins in transplanted tumor cells in gastric cancer nude mice were analyzed by utilizing Immunohistochemistry, western blot, terminal deoxynucleotidyl transferase dUTP nick end labeling assays. Results showed that combination of sCD40L with PI3K siRNA could significantly decrease tumour size, MVD, expression levels of PI3K, Survivin and VEGF proteins, and increase apoptosis index. It can be concluded that combination of sCD40L with PI3K siRNA provides a promising future for gastric cancer therapy.     

Regulation of protein kinase B activity by PTEN and SHIP2 in human prostate-derived cell lines

Protein Kinase B (PKB/Akt) is a key regulator of cell proliferation, motility and survival. The activation status of PKB is regulated by phosphatidylinositol 3-kinase (PI3K) via the synthesis of phosphatidylinositol-3,4,5-trisphosphate (PI(3,4,5)P3, PIP3). PTEN antagonises PI3K by degrading PIP3 to phosphatidylinositol-4,5-bisphosphate (PI(4,5)P2). Deregulation of PKB through loss of functional PTEN has frequently been implicated in the progression of tumours, including prostate cancer, and the PTEN-negative prostate cancer cell lines LNCaP and PC3 have been widely used as models for this mechanism of constitutive PKB activation. However, other enzymes in addition to PTEN can antagonise PI3K, including SHIP2, which degrades PIP3 to phosphatidylinositol-3,4-bisphosphate (PI(3,4)P2). We investigated the role of PTEN and SHIP2 in the regulation of PKB phosphorylation in a panel of human prostate-derived epithelial cell lines. In the PTEN-positive prostate-derived cell lines PNT2, PNT1a and P4E6, PI3K inhibition by LY294002 caused rapid dephosphorylation of PKB at ser473 (T(1/2)<2 min), leading to its inactivation. In the PTEN-null line LNCaP, LY294002-induced PKB dephosphorylation was much slower (T(1/2)>20 min), but in PC3 cells (also PTEN-null) it was only slightly slower than in PTEN-positive cells (T(1/2)=3 min). PKB dephosphorylation paralleled loss of plasma membrane PIP3. PNT1a, P4E6 and PC3, but not PNT2 or LNCaP, expressed SHIP2. SiRNA-mediated knockdown of SHIP2 expression markedly slowed PKB inactivation in response to LY294002 in PC3 but not in other SHIP2-positive cells, whereas knockdown of PTEN expression in PNT2, PNT1a and P4E6 resulted in higher steady-state levels of PKB phosphorylation and slowed, but did not prevent, LY294002-induced PKB inactivation. Thus SHIP2 substitutes for PTEN in the acute regulation of PKB in PC3 cells but not other prostate cell lines, where PTEN may share this role with further PIP3-degrading mechanisms.     

Phosphatidylinositol (3,4,5)P3 is essential but not sufficient for protein kinase B (PKB) activation; phosphatidylinositol (3,4)P2 is required for PKB phosphorylation at Ser-473: studies using cells from SH2-containing inositol-5-phosphatase knockout mice.

Using bone marrow derived mast cells from SH2-containing inositol-5-phosphatase (SHIP) +/+ and minus sign/minus sign mice, we found that the loss of SHIP leads to a dramatic increase in Steel Factor (SF)-stimulated phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P(3)), a substantial reduction in PI(3,4)P(2), and no change in PI(4,5)P(2) levels. We also found that SF-induced activation of protein kinase B (PKB) is increased and prolonged in SHIP -/- cells, due in large part to more PKB associating with the plasma membrane in these cells. Pretreatment of SHIP -/- cells with 25 microm LY294002 resulted in complete inhibition of SF-induced PI(3,4)P(2), while still yielding PI(3,4,5)P(3) levels similar to those achieved in SHIP+/+ cells. This offered a unique opportunity to study the regulation of PKB by PI(3,4,5)P(3), in the absence of PI(3,4)P(2). Under these conditions, PKB activity was markedly reduced compared with that in SF-stimulated SHIP+/+ cells, even though more PKB localized to the plasma membrane. Although phosphoinositide-dependent kinase 1 mediated phosphorylation of PKB at Thr-308 was unaffected by LY294002, phosphorylation at Ser-473 was dramatically reduced. Moreover, intracellular delivery of PI(3,4)P(2) to LY294002-pretreated, SF-stimulated SHIP -/- cells increased phosphorylation of PKB at Ser-473 and increased PKB activity. These results are consistent with a model in which SHIP serves as a regulator of both activity and subcellular localization of PKB.     

PI(3,4,5)P3 and PI(3,4)P2 levels correlate with PKB/akt phosphorylation at Thr308 and Ser473, respectively; PI(3,4)P2 levels determine PKB activity

The PI3K-PKB pathway is an important and widely studied pathway in cell signaling. The enzyme activity of PI3K produces D-3 phosphoinositides, including the lipid second messengers PI(3,4,5)P3 and PI(3,4)P2. PI(3,4,5)P3 has been deemed to be the most important second messenger for triggering PKB phosphorylation. PKB has two regulatory phosphorylation sites, Thr308 and Ser473, both of which contribute to its full activity. The direct relationship between PI3K lipid products and PKB phosphorylation is still not entirely clear. Our previous study showed that PI(3,4)P2 has a specific role in contributing to PKB phosphorylation on Ser473 sites in mast cells. In this study, we used two strategies to further elucidate this question in a well-established B cell system. First, by SHIP overexpression, we examined PKB activation under conditions where PI(3,4,5)P3 accumulation is largely suppressed. Second, we used dose response of different forms of B-cell receptor ligands to manipulate the relative levels of PI(3,4,5)P3 and PI(3,4)P2. Our results demonstrate a close relationship between PI(3,4,5)P3 levels and Thr308 phosphorylation levels, and PI(3,4)P2 levels and Ser473 phosphorylation levels, respectively. Furthermore, overall PKB activity, primarily consisting of cytosolic enzyme, was dependent upon levels of PI(3,4)P2, while only membrane-associated PKB activity was dependent upon PI(3,4,5)P3 levels. We conclude that PI(3,4,5)P3 and PI(3,4)P2 have distinct roles in determining PKB phosphorylation and activity. Thus, when investigating PI3K-PKB pathways, the importance of both lipids must be considered.     

Novel functional PI 3-kinase antagonists inhibit cell growth and tumorigenicity in human cancer cell lines.

New efforts in cancer therapy are being focused at various levels of signaling pathways. With phosphoinositide 3-kinase (PI3-K) potentially being necessary for a range of cancer-related functions, we have investigated the influence of selected inositol tris- to hexakisphosphates on cell growth and tumorigenicity. We show that micromolar concentrations of inositol 1,3,4,5,6-pentakisphosphate and inositol 1,4,5,6-tetrakisphosphate [Ins(1,4,5,6)P(4)] inhibit IGF-1-induced [(3)H]-thymidine incorporation in human breast cancer (MCF-7) cells and the ability to grow in liquid medium and form colonies in agarose semisolid medium by small cell lung cancer (SCLC) cells, a human cancer cell line containing a constitutively active PI3-K. In an ovarian cancer cell line that also contains a constitutively active PI3-K (SKOV-3 cells), Ins(1,4,5,6)P(4) again inhibited liquid medium growth. Furthermore, when applied extracellularly, inositol 1,3,4,5-tetrakisphosphate was shown indeed to enter SCLC cells. These effects appeared specifically related to PH domains known to bind to phosphatidylinositol 3,4-bisphosphate [PtdIns(3,4)P(2)] and phosphatidylinositol 3,4,5-trisphosphate [PtdIns(3,4,5)P(3)], indicating involvement of the PI3-K downstream target protein kinase B (PKB/Akt). This was further supported by inhibition of PKB/Akt PH domain membrane targeting in COS-7 cells by Ins(1,4,5,6)P(4). Thus, we propose that specific inositol polyphosphates inhibit PI3-K by competing with PtdIns(3,4, 5)P(3)-binding PH domains and that this occurs mainly at the level of the downstream PI3-K target, PKB/Akt.     

5' phospholipid phosphatase SHIP-2 causes protein kinase B inactivation and cell cycle arrest in glioblastoma cells

The tumor suppressor protein PTEN is mutated in glioblastoma multiform brain tumors, resulting in deregulated signaling through the phosphoinositide 3-kinase (PI3K)-protein kinase B (PKB) pathway, which is critical for maintaining proliferation and survival. We have examined the relative roles of the two major phospholipid products of PI3K activity, phosphatidylinositol 3,4-biphosphate [PtdIns(3,4)P2] and phosphatidylinositol 3,4,5-triphosphate [PtdIns(3,4,5)P3], in the regulation of PKB activity in glioblastoma cells containing high levels of both of these lipids due to defective PTEN expression. Reexpression of PTEN or treatment with the PI3K inhibitor LY294002 abolished the levels of both PtdIns(3, 4)P2 and PtdIns(3,4,5)P3, reduced phosphorylation of PKB on Thr308 and Ser473, and inhibited PKB activity. Overexpression of SHIP-2 abolished the levels of PtdIns(3,4,5)P3, whereas PtdIns(3,4)P2 levels remained high. However, PKB phosphorylation and activity were reduced to the same extent as they were with PTEN expression. PTEN and SHIP-2 also significantly decreased the amount of PKB associated with cell membranes. Reduction of SHIP-2 levels using antisense oligonucleotides increased PKB activity. SHIP-2 became tyrosine phosphorylated following stimulation by growth factors, but this did not significantly alter its phosphatase activity or ability to antagonize PKB activation. Finally we found that SHIP-2, like PTEN, caused a potent cell cycle arrest in G(1) in glioblastoma cells, which is associated with an increase in the stability of expression of the cell cycle inhibitor p27(KIP1). Our results suggest that SHIP-2 plays a negative role in regulating the PI3K-PKB pathway.     

川楝素诱导人胃癌MGC-803细胞凋亡及其机制

目的: 本研究旨在探讨川楝素诱导人胃癌MGC-803细胞凋亡及其机制。方法: 将人胃癌MGC-803细胞分为5组,每组3个复孔,采用氟尿嘧啶(5-FU)和0 nmol/L川楝素(TSN)分别作为阳性对照和阴性对照。其余3组分别加入终浓度为30 nmol/L、50 nmol/L、70 nmol/L的川楝素。川楝素处理细胞48 h后,利用激光共聚焦显微镜观察细胞形态结构变化;流式细胞术检测线粒体膜电位变化;酶标法检测Caspase-3和Caspase-9活性;利用qRT-PCR和Western blot检测凋亡相关基因Bcl-2、Bax、Cyt c和APAF-1 mRNA和蛋白水平。结果: 与0 nmol/L TSN组相比,30 nmol/L、50 nmol/L、70 nmol/L的川楝素作用于人胃癌MGC-803细胞48 h,可见细胞体积缩小,细胞核裂解,部分染色质凝集等形态学变化;Caspase-3和Caspase-9活性升高(P＜0.05);而线粒体膜电位明显下降(P＜ 0.05);Bax、Cyt c和APAF-1 基因mRNA及蛋白表达量显著升高(P＜0.05),Bcl-2 基因mRNA及蛋白表达量显著降低(P＜0.05)。结论: 川楝素通过上调Bax、Cyt c和APAF-1的表达,下调Bcl-2基因表达,增强Caspase-3、Caspase-9活性诱导人胃癌MGC-803细胞凋亡。