江西中医药大学学报
江西中醫藥大學學報
강서중의약대학학보
Journal of Jiangxi University of Traditional Chinese Medicine
2015年
4期
72-75
,共4页
谢斌%余功%饶斌%刘红宁
謝斌%餘功%饒斌%劉紅寧
사빈%여공%요빈%류홍저
肝癌%六味地黄汤%环磷酰胺%VEGF%VEGFR2
肝癌%六味地黃湯%環燐酰胺%VEGF%VEGFR2
간암%륙미지황탕%배린선알%VEGF%VEGFR2
Cancer of the Liver%Liuwei Dihuang Decoction%Cyclophosphamide%VEGF%VEGFR2
目的:观察六味地黄汤辅助环磷酰胺对荷H22肝癌小鼠肝癌组织VEGF及VEGFR2蛋白表达的影响。方法:雄性昆明小鼠40只,随机分为模型组、化疗组、六味组、六味化疗联合组,每组10只。腋下注射H22细胞建立H22荷瘤模型,六味组造模前两周开始用药[剂量为22 g/(kg· d)],化疗组[剂量为50mg/(kg· d),隔日1次]及六味化疗组造模后用药,造模14 d后处死小鼠称重,取瘤组织称重计算抑瘤率,取脾组织称重计算脾指数,免疫组化检测VEGF与VEGFR2蛋白的表达。结果:化疗组与六味化疗联合组有良好的抑瘤作用;六味组脾指数增大,与模型组比较差异具有统计学意义(P<0.05),六味化疗联合组VEGF蛋白表达明显减少,与化疗组比较,差异有统计学意义(P<0.05),与六味组相比较,差异有统计学意义(P<0.05);六味化疗联合组VEGFR2蛋白表达减少,与模型组比较,差异有统计学意义(P<0.05);与六味组比较,有显著性差异(P<0.01)。结论:六味地黄汤辅助环磷酰胺可抑制荷H22肝癌小鼠组织VEGF与VEGFR2蛋白表达,减少肝癌组织血管增殖,从而发挥辅助化疗作用。
目的:觀察六味地黃湯輔助環燐酰胺對荷H22肝癌小鼠肝癌組織VEGF及VEGFR2蛋白錶達的影響。方法:雄性昆明小鼠40隻,隨機分為模型組、化療組、六味組、六味化療聯閤組,每組10隻。腋下註射H22細胞建立H22荷瘤模型,六味組造模前兩週開始用藥[劑量為22 g/(kg· d)],化療組[劑量為50mg/(kg· d),隔日1次]及六味化療組造模後用藥,造模14 d後處死小鼠稱重,取瘤組織稱重計算抑瘤率,取脾組織稱重計算脾指數,免疫組化檢測VEGF與VEGFR2蛋白的錶達。結果:化療組與六味化療聯閤組有良好的抑瘤作用;六味組脾指數增大,與模型組比較差異具有統計學意義(P<0.05),六味化療聯閤組VEGF蛋白錶達明顯減少,與化療組比較,差異有統計學意義(P<0.05),與六味組相比較,差異有統計學意義(P<0.05);六味化療聯閤組VEGFR2蛋白錶達減少,與模型組比較,差異有統計學意義(P<0.05);與六味組比較,有顯著性差異(P<0.01)。結論:六味地黃湯輔助環燐酰胺可抑製荷H22肝癌小鼠組織VEGF與VEGFR2蛋白錶達,減少肝癌組織血管增殖,從而髮揮輔助化療作用。
목적:관찰륙미지황탕보조배린선알대하H22간암소서간암조직VEGF급VEGFR2단백표체적영향。방법:웅성곤명소서40지,수궤분위모형조、화료조、륙미조、륙미화료연합조,매조10지。액하주사H22세포건립H22하류모형,륙미조조모전량주개시용약[제량위22 g/(kg· d)],화료조[제량위50mg/(kg· d),격일1차]급륙미화료조조모후용약,조모14 d후처사소서칭중,취류조직칭중계산억류솔,취비조직칭중계산비지수,면역조화검측VEGF여VEGFR2단백적표체。결과:화료조여륙미화료연합조유량호적억류작용;륙미조비지수증대,여모형조비교차이구유통계학의의(P<0.05),륙미화료연합조VEGF단백표체명현감소,여화료조비교,차이유통계학의의(P<0.05),여륙미조상비교,차이유통계학의의(P<0.05);륙미화료연합조VEGFR2단백표체감소,여모형조비교,차이유통계학의의(P<0.05);여륙미조비교,유현저성차이(P<0.01)。결론:륙미지황탕보조배린선알가억제하H22간암소서조직VEGF여VEGFR2단백표체,감소간암조직혈관증식,종이발휘보조화료작용。
Objective:To observe the effect of Liuwei Dihuang decoction ( LW) for assisting cyclophosphamide( CTX) on VEGF, VEG-FR2 expression in H22 tumor-bearing mice.Methods:40 male Kunming mice were randomly divided into model group, CTX group, LW group, the LW combined CTX group, 10 rats in each group.The establishment of H22 tumor model by axillary injection of H22 cells, LW group began to use medication of two weeks before molding [dose of 22 g/(kg· d)], CTX group [at a dose of 50mg/(kg · d) , every other day for 1 time] and LW group for drug after molding.Put the mice to death after 14 days of the group establishment, then take weighing, take tumor tissue weighing to calculate tumor-inhibition rate, spleen tissue weighing to calculate the spleen in-dex, make the protein expression after immunohistochemical detection of VEGF, VEGFR2.Results: the CTX group and combination group had a significant role in inhibiting tumor;LW group spleen index increased, the difference being statistically significant compared to the model group(P<0.05),combination group's VEGF protein expression decreased obviously,compared with CTX group,the differ-ence was statistically significant (P<0.05),compared with LW group,the difference was statistically significant (P<0.05);combina-tion group's VEGFR2 protein expression decreased obviously, compared with the model group, there was statistical significance differ-ence (P<0.05);compared with LW group,there was significant difference (P<0.01).Conclusion:The LW could enhance the antitu-mor effects of CTX.Its mechanism may be related to the combination which can reach the synergistic inhibitory effects of VEGF and VEGFR2 protein expression.