中华微生物学和免疫学杂志
中華微生物學和免疫學雜誌
중화미생물학화면역학잡지
CHINESE JOURNAL OF MICROBIOLOGY AND IMMUNOLOGY
2014年
2期
128-132
,共5页
张占东%徐静%李计来%李树香%周亚%王欣怡%刘敬%张云涛
張佔東%徐靜%李計來%李樹香%週亞%王訢怡%劉敬%張雲濤
장점동%서정%리계래%리수향%주아%왕흔이%류경%장운도
融合蛋白%免疫应答%抗血管生成%肿瘤治疗
融閤蛋白%免疫應答%抗血管生成%腫瘤治療
융합단백%면역응답%항혈관생성%종류치료
Fusion protein%Immune response%Anti-angiogenesis%Oncotherapy
目的 通过BALB/c小鼠肿瘤模型观察HBcAg-VEGF1(血管内皮生长因子)抗原表位融合蛋白的抗肿瘤作用.方法 将接种了106个CT-26结肠癌细胞的BALB/c肿瘤小鼠随机分为HBcAg-VEGF1组、HBcAg组和生理盐水(NS)组,每组10只.HBcAg-VEGF1组、HBcAg组分别肌肉注射含铝佐剂的HBcAg-VEGF1、HBcAg蛋白各20μg/100μl每只;NS组注射生理盐水,每周1次共免疫4次.检测小鼠血清中抗VEGF抗体和VEGF浓度的变化趋势、肿瘤体积、生存率、肿瘤重量及微血管密度等指标,分析其抗肿瘤效果.结果 在其抗肿瘤实验中,HBcAg-VEGF1组血清中产生了较高滴度的抗VEGF抗体,其VEGF浓度显著低于HBcAg组和NS组;肿瘤体积、生存率等指标与HBcAg组和NS组比较,差异有统计学意义(P<0.05);HBcAg-VEGF1组、HBcAg组和NS组的肿瘤组织微血管密度分别为(18.6±2.7)、(39.8±4.9)和(38.4±6.1),肿瘤重量分别为(3.937±0.370)g、(6.039±1.016)g和(6.363±0.941)g,HBcAg-VEGF1组与其他两组比较,差异均有统计学意义(P<0.01).结论 HBcAg-VEGF1抗原表位融合蛋白能够刺激肿瘤小鼠机体产生免疫应答,产生特异性的抗VEGF抗体,并且能够通过减少血管新生来抑制CT-26肿瘤组织的生长.
目的 通過BALB/c小鼠腫瘤模型觀察HBcAg-VEGF1(血管內皮生長因子)抗原錶位融閤蛋白的抗腫瘤作用.方法 將接種瞭106箇CT-26結腸癌細胞的BALB/c腫瘤小鼠隨機分為HBcAg-VEGF1組、HBcAg組和生理鹽水(NS)組,每組10隻.HBcAg-VEGF1組、HBcAg組分彆肌肉註射含鋁佐劑的HBcAg-VEGF1、HBcAg蛋白各20μg/100μl每隻;NS組註射生理鹽水,每週1次共免疫4次.檢測小鼠血清中抗VEGF抗體和VEGF濃度的變化趨勢、腫瘤體積、生存率、腫瘤重量及微血管密度等指標,分析其抗腫瘤效果.結果 在其抗腫瘤實驗中,HBcAg-VEGF1組血清中產生瞭較高滴度的抗VEGF抗體,其VEGF濃度顯著低于HBcAg組和NS組;腫瘤體積、生存率等指標與HBcAg組和NS組比較,差異有統計學意義(P<0.05);HBcAg-VEGF1組、HBcAg組和NS組的腫瘤組織微血管密度分彆為(18.6±2.7)、(39.8±4.9)和(38.4±6.1),腫瘤重量分彆為(3.937±0.370)g、(6.039±1.016)g和(6.363±0.941)g,HBcAg-VEGF1組與其他兩組比較,差異均有統計學意義(P<0.01).結論 HBcAg-VEGF1抗原錶位融閤蛋白能夠刺激腫瘤小鼠機體產生免疫應答,產生特異性的抗VEGF抗體,併且能夠通過減少血管新生來抑製CT-26腫瘤組織的生長.
목적 통과BALB/c소서종류모형관찰HBcAg-VEGF1(혈관내피생장인자)항원표위융합단백적항종류작용.방법 장접충료106개CT-26결장암세포적BALB/c종류소서수궤분위HBcAg-VEGF1조、HBcAg조화생리염수(NS)조,매조10지.HBcAg-VEGF1조、HBcAg조분별기육주사함려좌제적HBcAg-VEGF1、HBcAg단백각20μg/100μl매지;NS조주사생리염수,매주1차공면역4차.검측소서혈청중항VEGF항체화VEGF농도적변화추세、종류체적、생존솔、종류중량급미혈관밀도등지표,분석기항종류효과.결과 재기항종류실험중,HBcAg-VEGF1조혈청중산생료교고적도적항VEGF항체,기VEGF농도현저저우HBcAg조화NS조;종류체적、생존솔등지표여HBcAg조화NS조비교,차이유통계학의의(P<0.05);HBcAg-VEGF1조、HBcAg조화NS조적종류조직미혈관밀도분별위(18.6±2.7)、(39.8±4.9)화(38.4±6.1),종류중량분별위(3.937±0.370)g、(6.039±1.016)g화(6.363±0.941)g,HBcAg-VEGF1조여기타량조비교,차이균유통계학의의(P<0.01).결론 HBcAg-VEGF1항원표위융합단백능구자격종류소서궤체산생면역응답,산생특이성적항VEGF항체,병차능구통과감소혈관신생래억제CT-26종류조직적생장.
Objective To evaluate the antitumor effects of the recombinant fusion protein Hepatitis B Core Antigen-Vascular Endothelial Growth Factor 1 (HBcAg-VEGF1) in a CT-26 colon carcinoma-bearing mouse model.Methods BALB/c mice were subcutaneously inoculated with CT-26 colon cancer cells,and then randomly divided into three groups including HBcAg-VEGF1 group (n=10),HBcAg group (n=10) and NS group (n=10).The mice in HBcAg-VEGF1 group and HBcAg group were respectively injected with 20 μg/100 μl HBcAg-VEGF1 and HBcAg mixed with aluminum adjuvant once a week for 4 weeks,while mice in NS group were injected with normal saline accordingly.Six parameters including serum concentrations of anti-VEGF antibody and VEGF,tumor volume,survival rates,tumor weight and microvessel density were analyzed.Results Compared with HBcAg group and NS group,high titers of anti-VEGF antibody and low concentration of VEGF were detected in serum from mice in HBcAg-VEGF1 group (P<0.05).The mice in HBcAg-VEGF1 group showed smaller tumor volume and longer survival time than those in HBcAg group and NS group (P<0.05).The microvessel density of the HBcAg-VEGF1 group (18.6 ±2.7) was significantly lower than that of HBcAg group (39.8 ±4.9) and NS group (38.4±6.1) (P<0.01).Moreover,the tumor weight [(3.937±0.370) g] was significantly lighter than that of HBcAg group [(6.039±1.016) g] and NS group [(6.363±0.941) g] (P<0.01).Conclusion HBcAg-VEGF1 epitope fusion protein could induce the expression of specific anti-VEGF antibody to inhibit the growth of CT-26 colon carcinoma cells in mice.