浙江中医药大学学报
浙江中醫藥大學學報
절강중의약대학학보
JOURNAL OF ZHEJIANG UNIVERSITY OF TRADITIONAL CHINESE MEDICINE
2014年
3期
243-249
,共7页
龙葵%抑瘤率%PCNA%p53%p21%凋亡%Bax/Bcl-2
龍葵%抑瘤率%PCNA%p53%p21%凋亡%Bax/Bcl-2
룡규%억류솔%PCNA%p53%p21%조망%Bax/Bcl-2
Solanum nigrum L%tumor inhibition rate%PCNA%p53%p21%apoptosis%Bax/Bcl-2
[目的]观察龙葵氯仿及正丁醇提取物对荷lewis肺癌小鼠肿瘤组织细胞周期调控相关蛋白、细胞凋亡及相关凋亡蛋白表达的影响。[方法]建立lewis肺癌模型,64只C57BL/6J小鼠随机分成模型组、环磷酰胺组、龙葵氯仿和正丁醇提取物高、中、低剂量组,给药15d后处死,剥离肿瘤组织,称重,计算肿瘤生长抑制率;TUNEL染色法检测细胞凋亡;免疫组织化学法检测PCNA、p53、p21和Bax、Bcl-2。[结果]龙葵氯仿及正丁醇提取物对荷瘤小鼠肿瘤增殖有一定抑制作用,其中氯仿提取物中剂量组和正丁醇提取物高剂量组的抑瘤率分别为38.93%和32.14%(P<0.01或P<0.05)。龙葵氯仿及正丁醇提取物可降低荷瘤小鼠肿瘤组织PCNA和P53阳性细胞表达率,分别为29.7%~58%和32%~56%,并提高P21阳性细胞表达率(20%~32%)(P<0.01或P<0.05)。荷瘤小鼠肿瘤组织细胞的凋亡率均不同程度升高(15%~38%)(P<0.01或P<0.05)。Bax阳性细胞表达率均有不同程度升高(11%~41%),Bcl-2阳性细胞表达率则均有不同程度降低(23%~37%)(P<0.01或P<0.05),并可不同程度上调荷瘤小鼠肿瘤组织Bax/Bcl-2的比值。[结论]龙葵正丁醇及氯仿提取物有一定抑制lewis肺癌的生长作用,其作用机制可能与对荷瘤小鼠肿瘤组织细胞周期调控相关蛋白(PCNA、p53、p21)表达的影响、上调肿瘤组织Bax蛋白的表达、下调Bcl-2蛋白的表达,上调Bax/Bcl-2的比值;促进肿瘤组织的细胞凋亡等相关。
[目的]觀察龍葵氯倣及正丁醇提取物對荷lewis肺癌小鼠腫瘤組織細胞週期調控相關蛋白、細胞凋亡及相關凋亡蛋白錶達的影響。[方法]建立lewis肺癌模型,64隻C57BL/6J小鼠隨機分成模型組、環燐酰胺組、龍葵氯倣和正丁醇提取物高、中、低劑量組,給藥15d後處死,剝離腫瘤組織,稱重,計算腫瘤生長抑製率;TUNEL染色法檢測細胞凋亡;免疫組織化學法檢測PCNA、p53、p21和Bax、Bcl-2。[結果]龍葵氯倣及正丁醇提取物對荷瘤小鼠腫瘤增殖有一定抑製作用,其中氯倣提取物中劑量組和正丁醇提取物高劑量組的抑瘤率分彆為38.93%和32.14%(P<0.01或P<0.05)。龍葵氯倣及正丁醇提取物可降低荷瘤小鼠腫瘤組織PCNA和P53暘性細胞錶達率,分彆為29.7%~58%和32%~56%,併提高P21暘性細胞錶達率(20%~32%)(P<0.01或P<0.05)。荷瘤小鼠腫瘤組織細胞的凋亡率均不同程度升高(15%~38%)(P<0.01或P<0.05)。Bax暘性細胞錶達率均有不同程度升高(11%~41%),Bcl-2暘性細胞錶達率則均有不同程度降低(23%~37%)(P<0.01或P<0.05),併可不同程度上調荷瘤小鼠腫瘤組織Bax/Bcl-2的比值。[結論]龍葵正丁醇及氯倣提取物有一定抑製lewis肺癌的生長作用,其作用機製可能與對荷瘤小鼠腫瘤組織細胞週期調控相關蛋白(PCNA、p53、p21)錶達的影響、上調腫瘤組織Bax蛋白的錶達、下調Bcl-2蛋白的錶達,上調Bax/Bcl-2的比值;促進腫瘤組織的細胞凋亡等相關。
[목적]관찰룡규록방급정정순제취물대하lewis폐암소서종류조직세포주기조공상관단백、세포조망급상관조망단백표체적영향。[방법]건립lewis폐암모형,64지C57BL/6J소서수궤분성모형조、배린선알조、룡규록방화정정순제취물고、중、저제량조,급약15d후처사,박리종류조직,칭중,계산종류생장억제솔;TUNEL염색법검측세포조망;면역조직화학법검측PCNA、p53、p21화Bax、Bcl-2。[결과]룡규록방급정정순제취물대하류소서종류증식유일정억제작용,기중록방제취물중제량조화정정순제취물고제량조적억류솔분별위38.93%화32.14%(P<0.01혹P<0.05)。룡규록방급정정순제취물가강저하류소서종류조직PCNA화P53양성세포표체솔,분별위29.7%~58%화32%~56%,병제고P21양성세포표체솔(20%~32%)(P<0.01혹P<0.05)。하류소서종류조직세포적조망솔균불동정도승고(15%~38%)(P<0.01혹P<0.05)。Bax양성세포표체솔균유불동정도승고(11%~41%),Bcl-2양성세포표체솔칙균유불동정도강저(23%~37%)(P<0.01혹P<0.05),병가불동정도상조하류소서종류조직Bax/Bcl-2적비치。[결론]룡규정정순급록방제취물유일정억제lewis폐암적생장작용,기작용궤제가능여대하류소서종류조직세포주기조공상관단백(PCNA、p53、p21)표체적영향、상조종류조직Bax단백적표체、하조Bcl-2단백적표체,상조Bax/Bcl-2적비치;촉진종류조직적세포조망등상관。
[Objective] To observe the effects of mice tumor tissue protein involved in cellcycle regulation, cellapoptosis and apoptosis related proteins expression on lewis lung tumor mice by chloroform extract and n-Butyl acrylate extract from Solanum nigrum L. [Methods] Set up Lewis lung tumor model, 64 mice were randomly divided into a tumor-burdened blank control group,cyclophosphamide group, chloroform and n-butanol extract high, medium and low dose groups, drug delivery 15 days then put them to death, stripping tumor tissue, weighing, calculating tumor growth inhibition rate;TUNEL staining method to detect apoptosis; Immune histochemical method detection of PCNA, p53, p21 and Bax, Bcl-2.[Results] Chloroform and n-butanol extracts from Solanum nigrum L had certain inhibitory effect on tumor proliferation in tumor-burdened mice, the inhibitory rate of chloroform extract medium dose group and n-butanol extract high dose group were respectively 38.93% and 32.14%, two extracts could reduce a tumor-burdened mice tumor tissue PCNA and P53 positive cells expression rate, increase the rate of P21 positive cells expression. The cellapoptosis rate and the Bax positive cells expression rate rose in different extent, the Bcl-2 positive cells expression rate was reduced in different extent, and the extracts could raise the ratio of Bax/Bcl-2 of mice tumor tissues.[Conclusion] The chloroform extract and n-Butyl acrylate extract from Solanum nigrum L has certain inhibition effect on lewis lung cancer growth, the mechanism may be related to a tumor-burdened mice tumor tissue protein involved in cellcycle regulation(PCNA, p53, p21) expression, increasing the influence of tumor tissue expression of Bax protein, cutting the Bcl-2 protein expression, raising the ratio of Bax/Bcl-2, promoting apoptosis of tumor tissue, etc.