| 王健伟,王 俊,刘 昉,戴 珂,王 超.蜂毒素通过下调F2RL1表达从而遏制胶质瘤细胞荷瘤小鼠肿瘤增殖的机制[J].现代生物医学进展英文版,2023,(5):830-834. |
| 蜂毒素通过下调F2RL1表达从而遏制胶质瘤细胞荷瘤小鼠肿瘤增殖的机制 |
| Melittin Inhibits Tumor Proliferation in Glioma-bearing Mice by Downregulating F2RL1 Expression |
| Received:July 07, 2022 Revised:July 30, 2022 |
| DOI：10.13241/j.cnki.pmb.2023.05.006 |
| 中文关键词: 蜂毒素 F2RL1 胶质瘤细胞 荷瘤小鼠 细胞凋亡 |
| 英文关键词: Mellittin F2RL1 Glioma cells Tumor-bearing mice Apoptosis |
| 基金项目:国家自然科学基金项目（81960454） |
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| 中文摘要: |
| 摘要 目的：探讨蜂毒素通过下调F2RL1表达从而遏制胶质瘤细胞荷瘤小鼠肿瘤增殖的机制。方法：40只雄性 NOD/SCID小鼠（5周龄，15-18 g）购自北京维塔河实验动物技术公司。实验前，让小鼠适应环境一周。NOD/SCID 小鼠在右侧海马体中注射了2×105 U87-MG细胞建立异种移植模型。当肿瘤体积增长到100 mm3时，将小鼠随机分为模型组（空腹注射生理盐水）和蜂毒素组（腹腔注射5 mg/kg 蜂毒素），每组20只小鼠。在第5天(注射的第5天)、第10天、第15天每次处死5只小鼠，通过实时PCR分析小鼠肿瘤组织中F2RL1、Bcl-2、Bax和Capase-3的mRNA表达。使用卡尺测量荷瘤小鼠肿瘤体积，使用电子天平对肿瘤组织进行称重测量。通过蛋白印迹分析肿瘤组织中p-PI3K、p-AKT 和p-mTOR的蛋白表达。通过TUNEL染色检测人脑肿瘤中凋亡细胞的百分比。结果：蜂毒素组F2RL1 mRNA表达较模型组降低（P<0.05），蜂毒素抑制F2RL1 mRNA表达。第5 d、10 d和15 d测得肿瘤体积发现蜂毒素肿瘤体积较模型组减小（P<0.05）。第5 d、10 d和15 d测得肿瘤体积发现蜂毒素肿瘤重量较模型组减轻（P<0.05）。蜂毒素组p-PI3K、p-AKT 和p-mTOR的蛋白表达较模型组降低（P<0.05）。蜂毒素组Bax和Capase-3的mRNA表达较模型组降低（P<0.05），蜂毒素组Bcl-2 mRNA表达较模型组升高（P<0.05）。蜂毒素组TUNEL阳性细胞的百分比较较模型组升高（P<0.05）。结论：蜂毒素通过下调肿瘤小鼠体内F2RL1表达抑制PI3K/AKT信号通路激活，促进了体内肿瘤细胞凋亡，从而有效抑制经胶质瘤细胞的生长、增殖。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the mechanism of melittin inhibiting tumor proliferation in glioma cell tumor-bearing mice by down-regulating the expression of F2RL1. Methods: Forty male NOD/SCID mice (5 weeks old, 15-18 g) were purchased from Beijing Weitahe Laboratory Animal Technology Company. Mice were acclimated to the environment for a week before the experiment. NOD/SCID mice were injected with 2×105 U87-MG cells in the right hippocampus to establish a xenograft model. When the tumor volume increased to 100 mm3, the mice were randomly divided into model group (injected with normal saline on an empty stomach) and melittin group (injected with 5 mg/kg melittin intraperitoneally), 20 mice in each group. Five mice were sacrificed each time on day 5 (day 5 of injection), day 10, and day 15. The mRNA expression of F2RL1, Bcl-2, Bax and Capase-3 in mouse tumor tissues was analyzed by real-time PCR. The tumor volume of the tumor-bearing mice was measured using calipers, and the tumor tissue was weighed using an electronic balance. The protein expression of p-PI3K, p-AKT and p-mTOR in tumor tissues was analyzed by Western blotting. The percentage of apoptotic cells in human brain tumors was detected by TUNEL staining. Results: The expression of F2RL1 mRNA in the melittin group was lower than that in the model group(P<0.05), and melittin inhibited the expression of F2RL1 mRNA. The tumor volume measured on the 5th, 10th and 15th days showed that the melittin tumor volume was reduced compared with the model group (P<0.05). The tumor volume was measured on the 5th, 10th and 15th days, and the melittin tumor weight was reduced compared with the model group(P<0.05). The protein expressions of p-PI3K, p-AKT and p-mTOR in the melittin group were lower than those in the model group(P<0.05). The mRNA expressions of Bax and Capase-3 in the melittin group were lower than those in the model group (P<0.05), and the mRNA expression of Bcl-2 in the melittin group was higher than that in the model group (P<0.05). The percentage of TUNEL positive cells in the melittin group was higher than that in the model group(P<0.05). Conclusion: Mellitin inhibits the activation of PI3K/AKT signaling pathway by down-regulating the expression of F2RL1 in tumor mice, and promotes tumor cell apoptosis in vivo, thereby effectively inhibiting the growth and proliferation of glioma cells. |
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