中国实用医刊
中國實用醫刊
중국실용의간
CENTRAL PLAINS MEDICAL JOURNAL
2009年
10期
1-4
,共4页
陈白莉%柯春龙%何瑶%贺青%聂小英%廖山婴
陳白莉%柯春龍%何瑤%賀青%聶小英%廖山嬰
진백리%가춘룡%하요%하청%섭소영%료산영
过氧化酶体增殖因子活化受体γ%胃癌%大鼠模型%环氧化酶-2%血管内生长因子
過氧化酶體增殖因子活化受體γ%胃癌%大鼠模型%環氧化酶-2%血管內生長因子
과양화매체증식인자활화수체γ%위암%대서모형%배양화매-2%혈관내생장인자
Peroxisome proliferator - activated receptor - γ%Gastric cancer%Rat model%Cycloox-ygenase -2%Vascular endothelial growth factor
目的 研究证实过氧化酶体增殖因子活化受体γ(PPAR-γ)配体罗格列酮(RSG)具有预防化学致癌剂N-甲基-N'-硝基-亚硝基胍(MNNG)诱导大鼠胃癌发生的作用,本研究拟探讨罗格列酮预防大鼠胃癌形成的可能机制.方法 采用RT-PCR及免疫组化法检测罗格列酮处理后大鼠胃癌组织环氧化酶-2(COX-2)、血管内皮生长因子(VEGF)、基质金属蛋白酶-9(MMP-9)mRNA及蛋白的表达.结果 MNNG诱癌组14例大鼠胃癌组织VEGF、COX-2 mRNA的表达明显高于癌旁组织(P<0.01),而MMP-9的表达在大鼠胃癌及癌旁组织中差异无统计学意义(P>0.05),RSG处理组(15例)大鼠胃癌组织VEGF、COX-2 mRNA的表达明显低于MNNG诱癌组大鼠胃癌组织,免疫组化显示MNNG诱癌组大鼠胃癌组织COX-2阳性物质主要分布在癌细胞胞浆或沿核膜周边,在问质的血管内皮细胞、成纤维细胞及单核细胞中亦可见阳性表达;VEGF阳性细胞主要位于癌细胞胞浆内,血管内皮细胞也有阳性表达.罗格列酮处理后大鼠胃癌组织的COX-2阳性细胞分布与MNNG诱癌组胃癌组织相似,而VEGF阳性细胞主要位于癌细胞胞浆内,血管内皮细胞未见明显VEGF表达.结论 罗格列酮可下调大鼠胃癌组织COX-2及VEGF的表达,促进肿瘤细胞凋亡、减少肿瘤血管生成可能是罗格列酮预防大鼠胃癌发生的机制之一.
目的 研究證實過氧化酶體增殖因子活化受體γ(PPAR-γ)配體囉格列酮(RSG)具有預防化學緻癌劑N-甲基-N'-硝基-亞硝基胍(MNNG)誘導大鼠胃癌髮生的作用,本研究擬探討囉格列酮預防大鼠胃癌形成的可能機製.方法 採用RT-PCR及免疫組化法檢測囉格列酮處理後大鼠胃癌組織環氧化酶-2(COX-2)、血管內皮生長因子(VEGF)、基質金屬蛋白酶-9(MMP-9)mRNA及蛋白的錶達.結果 MNNG誘癌組14例大鼠胃癌組織VEGF、COX-2 mRNA的錶達明顯高于癌徬組織(P<0.01),而MMP-9的錶達在大鼠胃癌及癌徬組織中差異無統計學意義(P>0.05),RSG處理組(15例)大鼠胃癌組織VEGF、COX-2 mRNA的錶達明顯低于MNNG誘癌組大鼠胃癌組織,免疫組化顯示MNNG誘癌組大鼠胃癌組織COX-2暘性物質主要分佈在癌細胞胞漿或沿覈膜週邊,在問質的血管內皮細胞、成纖維細胞及單覈細胞中亦可見暘性錶達;VEGF暘性細胞主要位于癌細胞胞漿內,血管內皮細胞也有暘性錶達.囉格列酮處理後大鼠胃癌組織的COX-2暘性細胞分佈與MNNG誘癌組胃癌組織相似,而VEGF暘性細胞主要位于癌細胞胞漿內,血管內皮細胞未見明顯VEGF錶達.結論 囉格列酮可下調大鼠胃癌組織COX-2及VEGF的錶達,促進腫瘤細胞凋亡、減少腫瘤血管生成可能是囉格列酮預防大鼠胃癌髮生的機製之一.
목적 연구증실과양화매체증식인자활화수체γ(PPAR-γ)배체라격렬동(RSG)구유예방화학치암제N-갑기-N'-초기-아초기고(MNNG)유도대서위암발생적작용,본연구의탐토라격렬동예방대서위암형성적가능궤제.방법 채용RT-PCR급면역조화법검측라격렬동처리후대서위암조직배양화매-2(COX-2)、혈관내피생장인자(VEGF)、기질금속단백매-9(MMP-9)mRNA급단백적표체.결과 MNNG유암조14례대서위암조직VEGF、COX-2 mRNA적표체명현고우암방조직(P<0.01),이MMP-9적표체재대서위암급암방조직중차이무통계학의의(P>0.05),RSG처리조(15례)대서위암조직VEGF、COX-2 mRNA적표체명현저우MNNG유암조대서위암조직,면역조화현시MNNG유암조대서위암조직COX-2양성물질주요분포재암세포포장혹연핵막주변,재문질적혈관내피세포、성섬유세포급단핵세포중역가견양성표체;VEGF양성세포주요위우암세포포장내,혈관내피세포야유양성표체.라격렬동처리후대서위암조직적COX-2양성세포분포여MNNG유암조위암조직상사,이VEGF양성세포주요위우암세포포장내,혈관내피세포미견명현VEGF표체.결론 라격렬동가하조대서위암조직COX-2급VEGF적표체,촉진종류세포조망、감소종류혈관생성가능시라격렬동예방대서위암발생적궤제지일.
Objective To demonstrat that PPARγ ligand rosiglitazone prevents gastric carcino-genesis in rats induced by chemical carcinogen N - methyl - N' - nitro - N - nitrosoguanidine (MNNG).We attempted to determinepossible anti - cancer mechanisms of rosiglitazone. Methods By examining COX -2, VEGF and MMP- 9 expression in MNNG induced gastric cancer and the rosiglitazone treated gastric cancer with RT -PCR and immunohistochemistry. Results The COX -2 and VEGF mRNA was significantly lower in rat gastric carcinoma of rosiglitazone treated group when compared with the MNNG group. Similarly, COX - 2 immunoreactivity was mainly detected in the perinuclear and cytoplasm of carci-noma cells. Expression of COX - 2 was also observed in vascular endothelial cells, fibroblasts and inflam-matory mononuclear cells in the tumor stroma. Cytoplasmic staining for VEGF was mainly seen in the tumor cells and vascular endothelial ceils, whereas COX - 2 immunostain was lower and loss of VEGF ex-pression in vascular endothelial cell was observed in rat gastric carcinoma of rosiglitazonetreated group by immunohistochemistry. Conclusions Downregulation of COX -2 and VEGF may be one of the mecha-nisms underlying the chemopreventive effect of rosighizaone in gastric cancer.
