中华肿瘤杂志
中華腫瘤雜誌
중화종류잡지
CHINESE JOURNAL OF ONCOLOGY
2013年
1期
11-16
,共6页
胡永珍%王殿洪%栾彧%龚海东
鬍永珍%王殿洪%欒彧%龔海東
호영진%왕전홍%란욱%공해동
黄芩甙%脑胶质瘤%大鼠%p53%Bcl-2%细胞凋亡
黃芩甙%腦膠質瘤%大鼠%p53%Bcl-2%細胞凋亡
황금대%뇌효질류%대서%p53%Bcl-2%세포조망
Baicalin%Glioma,brain%Rats%p53%Bcl-2%Apoptosis
目的 研究黄芩甙对大鼠脑胶质瘤的作用机制.方法 建立Wistar大鼠脑深部胶质瘤模型.接种C6胶质瘤细胞后7d,将大鼠随机分为对照组(0.9％氯化钠注射液30 mg·kg-1·d-1,灌胃)、小剂量组(黄芩甙50mg·kg-1 ·d-1,灌胃)、中剂量组(黄芩甙100 mg·kg-1·d-1,灌胃)和大剂量组(黄芩甙200 mg·kg-1·d-1,灌胃).分析各组大鼠治疗后脑胶质瘤的病理学、MRI影像学和电镜检查结果,采用免疫组化染色检测p53和Bcl-2的表达,分析大鼠的平均生存时间和体重变化情况.结果 与对照组比较,大剂量组大鼠处死(濒死)前的肿瘤体积为(343.62±28.98)mm3,显著缩小(P＜0.01),生存时间为(42.83±4.77)d,显著延长(P＜0.01).对照组胶质瘤细胞p53蛋白强阳性细胞百分比为(84.47±3.74)％,中度阳性细胞百分比为(47.28±2.38)％,与阴性组[(12.91±1.07)％]比较,差异均有统计学意义(均P＜0.01)；大剂量组p53蛋白强阳性细胞百分比与对照组比较,差异有统计学意义(P＜0.01).对照组Bcl-2蛋白强阳性细胞百分比为(86.51±4.17)％,中度阳性细胞百分比为(48.19±2.11)％,与阴性组[(10.36±1.43)％]比较,差异均有统计学意义(均P＜0.01).电镜检查结果显示,黄芩甙可使胶质瘤细胞核和细胞器发生破坏.结论 黄芩甙对在体脑胶质瘤有明显抑制作用,其作用机制可能与下调突变型p53引发细胞凋亡有关,但与Bcl-2无关.
目的 研究黃芩甙對大鼠腦膠質瘤的作用機製.方法 建立Wistar大鼠腦深部膠質瘤模型.接種C6膠質瘤細胞後7d,將大鼠隨機分為對照組(0.9％氯化鈉註射液30 mg·kg-1·d-1,灌胃)、小劑量組(黃芩甙50mg·kg-1 ·d-1,灌胃)、中劑量組(黃芩甙100 mg·kg-1·d-1,灌胃)和大劑量組(黃芩甙200 mg·kg-1·d-1,灌胃).分析各組大鼠治療後腦膠質瘤的病理學、MRI影像學和電鏡檢查結果,採用免疫組化染色檢測p53和Bcl-2的錶達,分析大鼠的平均生存時間和體重變化情況.結果 與對照組比較,大劑量組大鼠處死(瀕死)前的腫瘤體積為(343.62±28.98)mm3,顯著縮小(P＜0.01),生存時間為(42.83±4.77)d,顯著延長(P＜0.01).對照組膠質瘤細胞p53蛋白彊暘性細胞百分比為(84.47±3.74)％,中度暘性細胞百分比為(47.28±2.38)％,與陰性組[(12.91±1.07)％]比較,差異均有統計學意義(均P＜0.01)；大劑量組p53蛋白彊暘性細胞百分比與對照組比較,差異有統計學意義(P＜0.01).對照組Bcl-2蛋白彊暘性細胞百分比為(86.51±4.17)％,中度暘性細胞百分比為(48.19±2.11)％,與陰性組[(10.36±1.43)％]比較,差異均有統計學意義(均P＜0.01).電鏡檢查結果顯示,黃芩甙可使膠質瘤細胞覈和細胞器髮生破壞.結論 黃芩甙對在體腦膠質瘤有明顯抑製作用,其作用機製可能與下調突變型p53引髮細胞凋亡有關,但與Bcl-2無關.
목적 연구황금대대대서뇌효질류적작용궤제.방법 건립Wistar대서뇌심부효질류모형.접충C6효질류세포후7d,장대서수궤분위대조조(0.9％록화납주사액30 mg·kg-1·d-1,관위)、소제량조(황금대50mg·kg-1 ·d-1,관위)、중제량조(황금대100 mg·kg-1·d-1,관위)화대제량조(황금대200 mg·kg-1·d-1,관위).분석각조대서치료후뇌효질류적병이학、MRI영상학화전경검사결과,채용면역조화염색검측p53화Bcl-2적표체,분석대서적평균생존시간화체중변화정황.결과 여대조조비교,대제량조대서처사(빈사)전적종류체적위(343.62±28.98)mm3,현저축소(P＜0.01),생존시간위(42.83±4.77)d,현저연장(P＜0.01).대조조효질류세포p53단백강양성세포백분비위(84.47±3.74)％,중도양성세포백분비위(47.28±2.38)％,여음성조[(12.91±1.07)％]비교,차이균유통계학의의(균P＜0.01)；대제량조p53단백강양성세포백분비여대조조비교,차이유통계학의의(P＜0.01).대조조Bcl-2단백강양성세포백분비위(86.51±4.17)％,중도양성세포백분비위(48.19±2.11)％,여음성조[(10.36±1.43)％]비교,차이균유통계학의의(균P＜0.01).전경검사결과현시,황금대가사효질류세포핵화세포기발생파배.결론 황금대대재체뇌효질류유명현억제작용,기작용궤제가능여하조돌변형p53인발세포조망유관,단여Bcl-2무관.
Objective To investigate the therapeutic mechanism of baicalin on rat brain glioma.Methods Deep brain glioma models were established by injection of glioma cell line C6 cells into the brain of Wistar rats.The rats at 7 days after modeling were randomly divided into tumor control group(0.9％ NaCl solution 30 mg · kg-1 · d-1 garage)and experimental groups.The experimental rats was divided into 3 groups:low dose group (50 mg · kg-1 · d-1),middle dose group (100 mg · kg-1 · d-1) and high dose group (200 mg · kg-1 · d-1),given the baicalin by garage.Pathological and electron microscopic changes were observed.The expressions of p53 and Bcl-2 were determined by immunohistochemistry,and the changes of MRI,the average survival time and body weight of the rats in each group after treatments were analyzed.Results Compared with the control group,the tumor diameter and volume of high dose group rats before sacrifice were significantly reduced (P ＜ 0.01),and the survival time was significantly prolonged (P ＜ 0.01).Immunohistochemistry revealed strong positive expression rate of mutant p53 (84.47 ± 3.74) ％ and moderately positive rate (47.28 ±2.38)％ in the control group,significantly higher than that in the negative group (12.91 ± 1.07) ％ (P ＜ 0.01).The positive rate of mutant p53 of the high dose group was (46.42 ±2.19)％,significantly lower than that of the control group (84.47 ±3.74)％ (P ＜ 0.01).The expression rate of Bcl-2 in the control group was strongly positive (86.51 ± 4.17)％ and moderate positive (48.19 ± 2.11) ％,significantly higher than that of the negative group (10.36 ± 1.43) ％ (P ＜0.01).Electron microscopy revealed that baicalin caused damages of the cell nuclei and organelles in the gliomas.Conclusions Baicalin has significant inhibitory effect on glioma in vivo,and its mechanism may be related to cell apoptosis induced by down-regulated expression of mutant p53,but not related with Bcl-2 expression.
