二甲双胍对肝癌荷瘤鼠抗肿瘤过程中AMPK、RAGE表达变化研究
发布时间:2019-05-29 00:25
【摘要】:目的:运用动物实验探讨二甲双胍对肝癌荷瘤鼠的抗肿瘤机制,并对传统观点的AMPK(adenosine monphosphate activated protein Kinase腺苷酸活化蛋白激酶)表达进行检测,同时检测AGEs/RAGE(advanced glycation end products/Receptor for advanced glycation end products糖基化终末产物/糖基化终末产物受体)通路的相关指标,研究两者之间可能的联系。方法:1、利用BALB/C裸鼠左侧腋下进行皮下HepG2肝癌细胞接种,制作裸鼠荷瘤模型,造模成功后随机分组进行空白对照,BSA,二甲双胍,AGEs-BSA,二甲双胍及AGEs-BSA两者联合等干预。2、定期测定裸鼠体重变化,测定空腹血糖,测量肿瘤体积的长短径a,b数值。3、经过4周的干预,取静脉血样本,静置过夜,离心1000转,20分钟后,取上清液-80℃保存,取血样本后,处死裸鼠,取肝细胞癌组织,正常肝组织,瘤旁组织于-80℃保存。4、运用ELISA法测定裸鼠血清中AGEs浓度,免疫组化法测定各组织中AMPK,RAGE等表达。结果:1、二甲双胍具有抑制肿瘤生长作用,能够减少荷瘤鼠体重(P0.05),对荷瘤鼠的空腹血糖无明显影响(P0.05)。2、ELISA测得注射AGEs的裸鼠,注射AGEs并联用二甲双胍的裸鼠血清中可测得含量较低的AGEs,其他组低于检测值下限。3、运用免疫组化法进行AMPK,RAGE检测,可发现二甲双胍可升高AMPK表达,降低RAGE表达。AGEs对于RAGE存在影响。结论:二甲双胍对于肝癌裸鼠荷瘤模型有抗肿瘤作用,可减轻裸鼠体重,对于空腹血糖无明显影响。可能通过激活AMPK途径,下调RAGE得以发挥抗肿瘤作用,长时间的干预下,AGEs可能存在降低RAGE表达,提高AMPK表达的作用,AMPK与RAGE可能存在一定联系,为二甲双胍抗肿瘤机制提供了新的思路。
[Abstract]:Objective: to investigate the anti-tumor mechanism of metformin in tumor-bearing mice with liver cancer and to detect the expression of AMPK (adenosine monphosphate activated protein Kinase adenylate activated protein kinase (adenylate activated protein kinase) from the traditional point of view. At the same time, the related indexes of AGEs/RAGE (advanced glycation end products/Receptor for advanced glycation end products glycosylation end product / glycosylation end product receptor pathway were detected, and the possible relationship between them was studied. Methods: 1. Subcutaneous HepG2 liver cancer cells were inoculated under the left armpit of BALB/C nude mice to establish tumor-bearing model in nude mice. After successful modeling, they were randomly divided into blank control, BSA, metformin, AGEs-BSA,. Metformin and AGEs-BSA combined intervention. 2. The body weight of nude mice was measured regularly, fasting blood glucose was measured, and the long and short diameter a, b value of tumor volume was measured. 3. After 4 weeks of intervention, venous blood samples were taken and put overnight. After 20 minutes of centrifugation, the culture medium was preserved at-80 鈩,
本文编号:2487494
[Abstract]:Objective: to investigate the anti-tumor mechanism of metformin in tumor-bearing mice with liver cancer and to detect the expression of AMPK (adenosine monphosphate activated protein Kinase adenylate activated protein kinase (adenylate activated protein kinase) from the traditional point of view. At the same time, the related indexes of AGEs/RAGE (advanced glycation end products/Receptor for advanced glycation end products glycosylation end product / glycosylation end product receptor pathway were detected, and the possible relationship between them was studied. Methods: 1. Subcutaneous HepG2 liver cancer cells were inoculated under the left armpit of BALB/C nude mice to establish tumor-bearing model in nude mice. After successful modeling, they were randomly divided into blank control, BSA, metformin, AGEs-BSA,. Metformin and AGEs-BSA combined intervention. 2. The body weight of nude mice was measured regularly, fasting blood glucose was measured, and the long and short diameter a, b value of tumor volume was measured. 3. After 4 weeks of intervention, venous blood samples were taken and put overnight. After 20 minutes of centrifugation, the culture medium was preserved at-80 鈩,
本文编号:2487494
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