八月札水提物对H22肝癌荷瘤鼠免疫功能的影响

目的探讨八月札水提物对H22肝癌荷瘤鼠免疫功能的影响及其对化疗药物环磷酰胺(CTX)的增效减毒作用。方法通过计算肿瘤抑制率和胸腺(脾)重量指数以及应用放射免疫法(RIA)检测H22荷瘤鼠血清中肿瘤坏死因子(TNF)-α和白细胞介素(IL)-2水平,观察八月札水提物对H22荷瘤鼠免疫功能的影响及其对化疗药物CTX的增效减毒效果。结果 CTX组、水提低组、水提高组、联合用药组与阴性对照组比较,荷瘤鼠肿瘤重量明显降低,肿瘤组织生长的抑制率分别为44.0%、36.4%、38.0%、58.4%和60.0%;而且八月札水提组及联合用药组小鼠存活数量明显高于CTX组;CTX组、水提低组、水提高组、联合用药组与阴性对照组比较,能够显著降低H22荷瘤鼠胸腺、脾重量指数;CTX组、水提低组、水提高组、联合用药组与阴性对照组比较,显著提高荷瘤鼠血清中IL-2和TNF-α水平。结论八月札水提物对H22荷瘤鼠肿瘤生长有显著抑制作用,能够显著提高荷瘤鼠血清中TNF-α和IL-2水平;同时,八月札水提物与CTX联合应用对荷瘤鼠血清中TNF-α和IL-2的提高效果更为明显,明显优于单独CTX组,推测八月札对CTX存在增效、减毒作用。     

华蟾素对H22荷瘤小鼠肝癌细胞Mg2+-ATP酶、葡萄糖-6-磷酸酶活性的影响

应用小鼠H22肝癌细胞悬液制作H22荷瘤小鼠腹水瘤模型,分别腹腔注射华蟾素、氟脲嘧啶(5-Fu)、生理盐水,计算肿瘤抑制率,观察肝癌细胞酶活性的变化。结果华蟾素组和5-Fu组的肿瘤抑制率分别是35.8%和40.7%,细胞质膜标志酶Mg2 -ATP酶(Mg2 -AT Pase)、内质网标志酶葡萄糖-6-磷酸酶(G-6-Pase)反应颗粒变小,数量减少,密度变低,酶活性明显下降。表明华蟾素可降低H22荷瘤小鼠肝癌细胞Mg2 -AT Pase及G-6-Pase的活性,抑制肿瘤细胞生长。     

八月札水提物对H22荷瘤小鼠突变型P53、Bcl-2和增殖细胞核抗原表达的影响

目的探讨八月札水提物对H22荷瘤小鼠肿瘤细胞增殖的抑制作用及其机制。方法健康昆明种小鼠90只制备为荷瘤小鼠并随机分成6组。通过苏木精-伊红(HE)染色观察各组肝脏、肾脏和肿瘤组织细胞的病理改变,免疫组织化学法检测各组肿瘤组织细胞中突变型(m)P53、Bcl-2和增殖细胞核抗原(PCNA)蛋白表达。结果对照组和八月札水提物组肝脏和肾脏未见明显病理学改变,CTX组和联合用药组可见轻微病理改变。与对照组比较,CTX组、水提低组、水提高组和水提低+CTX组、水提高+CTX组肿瘤组织重量明显降低(P<0.01),肿瘤抑制率分别为44.0%、36.4%、38.0%、58.4%和60.0%。与对照组比较,八月札水提物能够显著降低H22荷瘤小鼠肿瘤组织中mP53、Bcl-2和PCNA蛋白的表达(P<0.01)。其中,以八月札水提低+CTX组肿瘤组织中mP53、Bcl-2和PCNA蛋白阳性率最低,分别为(33.18±5.89)%,(22.11±5.28)%,(19.28±7.12)%。结论八月札水提物能够阻止H22荷瘤小鼠肿瘤组织mP53蛋白的生成,下调抑制凋亡基因Bcl-2的表达,抑制PCNA蛋白的表达,从而达到抑制肿瘤组织细胞增殖的作用,且对CTX表现出一定的增效减毒作用。     

五味子乙素联合顺铂诱导H22肝癌移植瘤细胞凋亡过程中caspase-3,8,9表达的研究

目的 观察五味子乙素(schisandrin B,SchB)联合顺铂诱导H22荷瘤小鼠细胞凋亡过程中caspase-3,8,9蛋白表达变化.方法 SchB和顺铂单独或联合作用于H22荷瘤小鼠,计算各组抑瘤率,用免疫组化法检测瘤组织中caspase-3,8,9蛋白表达.结果 顺铂组、SchB组及联合治疗组抑瘤率分别为42.00%、36.40%和68.80%;联合组caspase-3,8,9阳性表达明显高于对照组和单纯用药组.结论 联合组对H22荷瘤鼠实体瘤生长抑制作用较单独用药明显增强;联合组可能通过促进caspase-8和caspase-9表达,进而促进caspase-3表达诱导H22肿瘤细胞凋亡.     

毛尖蘑子实体粗多糖对肿瘤生长及免疫器官的影响

目的 探讨毛尖蘑子实体粗多糖(MJMP)对H22荷瘤小鼠的抗肿瘤作用以及对免疫器官的影响.方法 将不同浓度的MJMP作用于H22荷瘤小鼠,计算胸腺指数、脾指数、抑瘤率,观察H22荷瘤小鼠免疫器官的变化及肿瘤生长情况.结果 多糖作用组与空白对照组及阴性对照组脾指数比较无统计学意义(P＞0.05),胸腺指数有差异(P＜0.05).小鼠体内实验显示MJMP可明显抑制肿瘤生长.结论 MJMP对小鼠免疫功能有增强的作用,对肿瘤的生长具有抑制作用.     

冬凌草甲素抑制H22小鼠移植性实体瘤增殖的作用

目的 探讨不同浓度的冬凌草甲素对小鼠H22肿瘤细胞生长影响及其抑瘤作用机制.方法 将H22肿瘤细胞接种到小鼠皮下,建立肝癌H22移植瘤模型.用高、中、低三个剂量的冬凌草甲素灌胃2 w后,检测抑瘤率,并用TUNEL法和免疫组化方法检测H22肿瘤细胞的凋亡率和对bcl-2、p53、caspase3基因表达的影响. 结果 小鼠H22肿瘤细胞对冬凌草甲素敏感,明显抑制肿瘤细胞的增殖(P<0.01),高剂量组肿瘤抑制率达52.33%,与丝裂霉素结果相近(P>0.05);实验后小鼠体重没有明显下降,小鼠肿瘤抑制率随剂量升高而增加,高剂量组达(48.31±1.74) %;高剂量组bcl-2和p53基因表达下调,阳性率分别为(18.32±0.32)%、(27.57±0.51)%,caspase3阳性率上调为(62.59±0.57)%.结论 冬凌草甲素可抑制小鼠H22肿瘤细胞的增殖,并下调bcl-2和p53基因表达,而激活caspase3基因表达引起肿瘤细胞的凋亡有关.     

芝麻素对H22荷瘤小鼠的抑瘤作用及其机制

目的 观察芝麻提取物芝麻素对H22荷瘤小鼠的抑瘤作用,并探讨其作用机制.方法 将移植H22肝癌瘤株的64只昆明种小鼠随机分成4组:模型组、环磷酰胺组、芝麻素高浓度组及芝麻素低浓度组,连续用药10 d.比较各组抑瘤率、胸腺指数、脾指数及增殖细胞核抗原(PCNA)表达水平.结果 低浓度的芝麻素在体内对H22肿瘤细胞的生长有明显的抑制作用,使动物的免疫器官重量增加,并对肿瘤组织PCNA的表达有显著的抑制作用.结论 芝麻素抑制H22细胞的机制可能是通过促进宿主免疫功能、抑制肿瘤细胞内PCNA表达来实现的.     

鸦胆子油注射液对 H22细胞增殖的抑制作用及其机制探讨

目的：探讨鸦胆子油注射液在体内外对 H22细胞增殖的抑制作用及其作用机制。方法取 H22细胞培养,采用 MTT 法检测鸦胆子油对细胞增殖的影响;应用 H22细胞建立小鼠荷瘤模型,给予鸦胆子油治疗,计算抑瘤率、脾脏指数和胸腺指数,采用 MTT 法检测鸦胆子油对荷瘤小鼠脾细胞增殖的影响,采用双抗体夹心ABC-ELISA 法检测荷瘤鼠血清 TNF-α水平,采用放射免疫分析法检测转化生长因子（TGF）-α水平。结果鸦胆子油在（10~160）μg/ml 浓度范围内对 H22细胞的增殖抑制率为34.1%~52.31%,与对照组比有统计学意义;给予鸦胆子油25和50 mg＆#183;kg-1灌胃后,荷瘤小鼠瘤质量分别为（1.095±0.301） g 和（0.920±0.250） g,血清 TGF-α分别为（11.172±0.639） pg/ml 和（14.438±0.587） pg/ml,均较未治疗荷瘤动物显著下降[分别为（1.867±0.554） g 和（16.354±0.762） pg/ml],TNF-α水平分别为（28.132±2.456） pg/ml 和（26.521±3.267） pg/ml,较未治疗荷瘤动物显著升高[（20.231±2.614） pg/ml,P〈0.05];与对照组比,无论是 Con A 还是 LPS 刺激,荷瘤动物脾细胞增殖受到抑制（P〈0.05）。与荷瘤动物比,鸦胆子油体内给药则可促进脾细胞增殖,但对脾脏指数和胸腺指数无明显影响。结论鸦胆子油体内外均能抑制肝癌 H22细胞的生长,其抗肿瘤作用可能与改善荷瘤小鼠的脾细胞功能有关。     

干、鲜壁虎冻干粉对小鼠H22肝癌体内外抑制作用

目的:研究干、鲜壁虎冻干粉对荷H22实体型移植瘤小鼠体内抑瘤作用及其含药血清体外对H22肝癌细胞的增殖抑制作用.方法:采用昆明小鼠H22移植瘤模型观察干、鲜壁虎冻干粉体内抑瘤活性及小鼠胸腺、脾脏指数变化:MTT法检测不同浓度干、鲜壁虎冻干粉含药血清对H22肝癌细胞体外杀伤作用.结果:干、鲜壁虎低、中、高3个剂量组的抑瘤率分别为25.6%,40.0%,48.5%和20.7%,28.1%,51.1%.各壁虎组与西药5-FU组相比,不同程度提高了荷瘤小鼠的胸腺质量(P<0.01)、胸腺指数(P<0.05或P<0.01)和脾脏质量(P<0.05或P<0.01)、脾脏指数(P<0.05).含药血清在体外能够明显抑制H22细胞的增殖,干、鲜壁虎低、中、高含药血清组的增殖抑制率为17.4%,21.0%,34.5%和16.4%,26.3%,43.2%.结论:干、鲜壁虎冻干粉均具有良好的抗肿瘤作用.     

微米中药胰腺康对H22肿瘤小鼠抑瘤作用的实验研究

目的探讨微米中药胰腺康对H22小鼠的抑瘤作用及其对p53和caspase-3表达的影响。方法将H22肿瘤细胞接种到小鼠皮下,建立小鼠H22实体瘤模型,并对小鼠H22实体瘤模型进行微米中药及其提取液的处理,采用免疫组化方法检测实体瘤组织中p53和caspase-3蛋白的表达。结果小鼠体内实验显示微米中药可明显抑制肿瘤生长。p53蛋白表达率为31.73%,caspase-3蛋白表达率为41.16%,肿瘤抑制率为50.00%。结论胰腺康对H22肿瘤具有明显抑制作用,微米中药胰腺康与其提取液相比,能更有效地抑制肿瘤增殖,其抗瘤作用与诱导细胞凋亡有关。     

熊果酸对肝星状细胞增殖与凋亡的影响

目的 体外观察熊果酸对肝星状细胞增殖与凋亡的影响,探讨熊果酸诱导肝星状细胞凋亡的可能作用机制. 方法 将不同浓度熊果酸作用于肝星状细胞HSC-T6及肝细胞L02,分别在药物作用24、48、72 h后用四甲基偶氮唑盐法检测熊果酸对HSC-T6及L02细胞增殖的影响;流式细胞仪检测熊果酸对HSC-T6凋亡的影响;光学显微镜观察熊果酸作用后细胞形态学变化情况;免疫细胞化学法检测HSC-T6中Bcl-2、Bax和Caspase-3蛋白的表达情况. 结果 各种浓度的熊果酸均可抑制HSC-T6细胞的增殖,且呈剂量-时间依赖性;当熊果酸浓度为25、50、75μmol/L时可促进L02细胞增殖,浓度＞75μmol/L则表现为抑制L02细胞增殖.在病理形态学方面,熊果酸作用HSC-T6细胞48 h后,光学显微镜下可见细胞缩小变圆、核浓缩等.25、50、75 μmol/L熊果酸作用HSC-T6细胞48 h后,流式细胞仪检测显示细胞凋亡率分别为10.30%±3.85%、21.87%±4.46%、31.33%±6.18%,比对照组(2.93%±1.60%)明显升高(P＜0.01).免疫细胞化学显示Bax及Caspase-3蛋白表达较对照组升高(P＜0.05),且呈剂量依赖性,而Bcl-2蛋白表达水平与对照组无明显差异(P＞0.05).结论 在体外熊果酸可较明显地抑制HSC-T6细胞增殖,诱导其凋亡;对L02细胞的生长具有双向调节作用.熊果酸诱导HSC-T6细胞凋亡可能与降低Bcl-2/Bax比值、激活Caspase-3蛋白有关.     

Effect of complex amino acid imbalance on growth of tumor in tumor-bearing rats

AIM: To investigate the effect of complex amino acid imbalance on the growth of tumor in tumor-bearing (TB) rats.METHODS: Sprague-Dawlley (SD) rats underwent jejunostomy for nutritional support. A suspension of Walker256 carcinosarcoma cells was subcutaneously inoculated.TB rats were randomly divided into groups A, B, C and D according to the formula of amino acids in enteral nutritional solutions, respectively. TB rats received jejunal feedings supplemented with balanced amino acids (group A),methionine-depleted amino acids (group B), valine-depleted amino acids (group C) and methionine- and valine-depleted complex amino acid imbalance (group D) for 10 days. Tumor volume, inhibitory rates of tumor, cell cycle and life span of TB rats were investigated.RESULTS: The G0/G1 ratio of tumor cells in group D (80.5±9.0) % was higher than that in groups A, B and C which was 67.0±5.1 %, 78.9±8.5 %, 69.2±6.2 %, respectively (P＜0.05). The ratio of S/G2M and PI in group D were lower than those in groups A, B and C. The inhibitory rate of tumor in groups B, C and D was 37.2 %, 33.3 % and 43.9 %,respectively (P＜0.05). The life span of TB rats in group D was significantly longer than that in groups B, C, and A.CONCLUSION: Methionine/valine-depleted amino acid imbalance can inhibit tumor growth. Complex amino acids of methionine and valine depleted imbalance have stronger inhibitory effects on tumor growth.     

Differential effects of chenodeoxycholic and ursodeoxycholic acids on interleukin 1, interleukin 6 and tumor necrosis factor-alpha production by monocytes.

Cell-mediated immunity and macrophage activity, especially that of Kupffer cells, are impaired during cholestasis. Some evidence exists that bile acids play a role in these immune defects. The purpose of this study was to evaluate the effects of individual bile acids on immunity and to determine whether monocytes could be a target. We assessed the effects of chenodeoxycholic acid, an endogenous bile acid, ursodeoxycholic acid, which has been shown to partially correct the immunological abnormalities observed in primary biliary cirrhosis, and their tauroconjugates on the production of interleukin-1, interleukin-6 and tumor necrosis factor-alpha. Chenodeoxycholic acid had a dose-dependent inhibitory effect on interleukin-1 (inhibitory concentration 50% = 60 mumol/L), interleukin-6 (inhibitory concentration 50% = 80 mumol/L) and tumor necrosis factor-alpha (inhibitory concentration 50% = 80 mumol/L) production; inhibition was almost complete at 250 mumol/L. In contrast, ursodeoxycholic acid had lesser or minimal inhibitory effects (inhibitory concentration 50% = 100 mumol/L for interleukin-1 and above 200 mumol/L for interleukin-6 and tumor necrosis factor-alpha). The inhibitory effects of taurochenodeoxy-cholic acid and tauroursodeoxycholic acid were similar to those of chenodeoxycholic acid and ursodeoxycholic acid, respectively. Ursodeoxycholic acid did not reverse the chenodeoxycholic acid-induced inhibition of interleukin-6 or tumor necrosis factor-alpha production. In conclusion, chenodeoxycholic acid exerts strong inhibitory effects on monocyte activity in vitro, whereas the effects of ursodeoxycholic acid are minor.     

Inhibitory effects of ursolic acid on hepatic polyol pathway and glucose production in streptozotocin-induced diabetic mice

The effects of ursolic acid on the polyol pathway and glucose homeostasis-related metabolism were examined in the livers of streptozotocin (STZ)-induced diabetic mice fed a high-fat (37% calories from fat) diet for 4 weeks. Male mice were divided into nondiabetic, diabetic control, and diabetic-ursolic acid (0.05% wt/wt) groups. Diabetes was induced by the injection of STZ (200 mg/kg body weight, intraperitoneally). Although an ursolic acid supplement lowered the blood glucose level, it did not affect the plasma leptin and adiponectin levels. The present study shows that the blood glucose levels have a positive correlation with the hepatic sorbitol dehydrogenase activities (r = 0.39, P < .05). Ursolic acid significantly inhibited sorbitol dehydrogenase activity as well as aldose reductase activity in the liver. The supplementation of ursolic acid significantly increased glucokinase activity, while decreasing glucose-6-phosphatase activity in the livers of STZ-induced diabetic mice. Ursolic acid significantly elevated the hepatic glycogen content compared with the diabetic control group. Supplementation with ursolic acid significantly lowered the plasma total cholesterol, free fatty acid, and triglyceride concentrations compared with the diabetic control group, whereas it normalized hepatic triglyceride concentration. A negative correlation was found between the hepatic triglyceride concentration and blood glucose levels (r = −0.50, P < .01) in regard to insulin-dependent diabetic mice. The hepatic fatty acid synthase activity was significantly lower in the ursolic acid group than in the diabetic control group, whereas hepatic fatty acid β-oxidation and carnitine palmitoyltransferase activities were significantly higher. These results indicate that ursolic acid may be beneficial in preventing diabetic complications by improving the polyol pathway as well as the lipid metabolism and that it can function as a potential modulator of hepatic glucose production, which is partly mediated by up-regulating glucose utilization and glycogen storage and down-regulating glyconeogenesis in the liver.     

Ursolic acid inhibits neointima formation in the rat carotid artery injury model

Triterpenoids are natural compounds that are found in a large variety of plants and vegetarian foods, and are used for medicinal purposes in many Asian countries. Pentacyclic triterpenes, such as ursolic acid, have been reported to exhibit anticancer and anti-inflammatory properties. The present study was designed to assess the effects of ursolic acid in the migration and proliferation of vascular smooth muscle cells (VSMC), and in a vascular injury model. The exposure of VSMC to ursolic acid results in a chemotaxis inhibition, in a reduction of the expression of proliferating cell nuclear antigen (PCNA) and in a disorganization of beta-tubulin and vimentin cytoskeletal proteins. Administration of ursolic acid in the rat carotid balloon catheter injury model shows a significant inhibition of neointimal hyperplasia. Thus, we have demonstrated that daily doses of 6 mg/kg body weight for 10 days reduce both the ratio of intimal to medial areas and the degree of stenosis by 80%, and suppress the expression of PCNA in both neointima and media. These results suggest that pentacyclic triterpenes may be of potential therapeutic value in vascular injury, and a possible treatment strategy for the prevention of the progression of atherosclerosis and restenosis after angioplasty.     

Ursolic acid prevents endoplasmic reticulum stress-mediated apoptosis induced by heat stress in mouse cardiac myocytes

Heat stress causes serious physiological dysfunction of cardiac myocytes and is associated with several types of cardiovascular diseases. However, the underlying mechanisms and therapeutic strategies to alleviate heat stress-induced myocardial damage are not available. The objective of this study was to (1) investigate the functional role of endoplasmic reticulum (ER) stress-mediated apoptosis in heat exposure-induced myocardial damage, and (2) to evaluate the effects of ursolic acid on the myocardial apoptosis as well as the underlying mechanisms in mouse cardiac myocytes. We show here that heat stress-induced apoptosis is predominantly mediated by the activation of PERK-eIF2α-CHOP unfolded protein response which up-regulates the protein expression of Puma, and by the modulation of cellular redox state. Intriguingly, the myocardial apoptosis is markedly attenuated by ursolic acid treatment. Mechanistically, the protective effects of ursolic acid are mediated, at least partly, by reestablishing the intracellular redox state and inducing the expression of the anti-apoptotic protein Mcl-1, which, in turn, inactivating CHOP-induced Puma up-regulation. The striking finding that ursolic acid has both anti-apoptotic and antioxidative activities against ER stress-associated myocardial damage suggests that supplementation of ursolic acid might be a potential strategy to reduce the detrimental effects of heat stress in cardiomyocytes.     

5-Aminosalicylic Acid and Olsalazine Inhibit Tumor Growth in a Rodent Model of Colorectal Cancer

The ability of 5-aminosalicylic acid and olsalazine to inhibit colonic aberrant crypts and tumors was investigated in 1,2-dimethylhydrazine-treated rats. The effect of these drugs on the rates of tumor apoptosis and proliferation was studied as potential mechanisms for their action. 5-Aminosalicylic acid reduced the number of aberrant crypt foci by over one third, while olsalazine had no effect on this parameter. However, both agents effectively reduced tumor number and load, increased the rate of tumor apoptosis, and reduced the rate of tumor cell proliferation. In conclusion, 5-aminosalicylic acid and olsalazine are both ultimately effective chemopreventive agents in this model; however, only 5-aminosalicylic acid inhibited the formation of aberrant crypt foci. The inhibitory effect of these agents in tumors is related to the inhibition of proliferation and the induction of apoptosis.     

超分子铂类药物西茜铂体内外对消化系肿瘤的抑制作用

目的:评价超分子药物西茜铂实验性治疗消化系肿瘤的效果.方法:用细胞培养方法测定西茜铂和卡铂对肝癌(BEL7402),胰腺癌(BXCP-3,JF305),胃癌(MG803,SG7901)和结肠癌(CX-1)6株消化系癌细胞株和一株人胚胎肺成纤维细胞的半数抑制浓度(IC_(50)).建立肝癌H22昆明鼠模型和人胰腺癌JF305裸鼠模型,腹腔注射高(20 mg/ kg)、中(15 mg/kg)、低(10 mg/kg)剂量西茜铂,测定其在动物体内的抑瘤作用,注射葡萄糖注射液作为阴性对照,注射20 mg/kg卡铂作为阳性对照.HE染色判断肿瘤组织的坏死.CD34抗体免疫组化染色观察肿瘤组织中微血管的生长状况.结果:西茜铂对6株肿瘤细胞的IC_(50)值明显低于卡铂,约为后者1/3至1/2.但2种药物对人胚胎肺成纤维细胞的半数抑制浓度(IC_(50))均大于240 mg/L.在肝癌H22荷瘤昆明小鼠,腹腔注射高、中、低剂量西茜铂的抑瘤率分别为56.1%-67.0%,46.9%-54.8%和42.4%-44.3%,卡铂的抑瘤率是50.3%-51.3%.西茜铂和卡铂治疗组的瘤质量与葡萄糖组相比,明显降低(t>2.91,P<0.01).20 mg/kg西茜铂的抑瘤率高于相同剂量卡铂的抑瘤率,瘤质量均值也明显轻于卡铂组(t=2.39,P<0.05).在接种人胰腺癌JF305裸鼠,高、中、低剂量西茜铂组的抑瘤率分别为61.4%-73.4%,51.4%-54.0%和17.6%-22.6%,卡铂的抑瘤率是37.1%-42.0%.中、高剂量的抑瘤率明显高于卡铂组,瘤质量明显低于葡萄糖组和卡铂组(t>2.28,P<0.05).经HE染色后,在接种人胰腺癌JF305裸鼠,西茜铂治疗组的瘤组织见大片出血性坏死.CD34抗体免疫组化染色在葡萄糖组可见有大量的微血管形成,而西茜铂治疗组仅有少数微血管生成,微血管生成受到抑制.结论:超分子药物西茜铂对消化系统肿瘤有明显的抑制作用,其作用明显高于卡铂.     

刚地弓形虫对荷瘤小鼠肿瘤组织微血管生成的抑制作用

摘 要：目的 观察刚地弓形虫感染对BALB/c小鼠ct26细胞皮下移植瘤血管生成的抑制作用及其作用机理。方法 建立刚地弓形虫感染的小鼠结肠癌ct26皮下移植瘤模型,观察弓形虫感染对小鼠的生存延长率、对肿瘤的质量抑制率,并采用免疫组化方法检测弓形虫感染对肿瘤组织MVD、VEGF、TSP-1表达的影响。结果 弓形虫感染的小鼠生存时间比对照组长（P<0.05）,生存延长率为57.45%,肿瘤质量抑制率为47.23%;弓形虫感染的小鼠肿瘤组织中MVD及VEGF表达水平低于对照组（P=0.005,P=0.03）,TSP-1表达高于对照组（P=0.005）。结论 弓形虫感染能抑制荷瘤小鼠肿瘤组织微血管生成;下调VEGF及上调TSP-1与弓形虫感染抗肿瘤血管生成有关。