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目的:观察癌痛平胶囊对H22荷瘤小鼠肿瘤生长转移的抑制作用,探讨其作用机制。方法:ICR小鼠接种H22肝癌细胞株,建立H22荷瘤小鼠模型。将H22荷瘤小鼠随机分为模型组、顺铂组、癌痛平高、低剂量组,模型组每日ig等容积生理盐水,癌痛平高、低剂量组每日ig癌痛平(36,18 g·kg~(-1)),顺铂组每日ip顺铂(2 mg·kg~(-1))。各组连续给药7 d,处死荷瘤小鼠,剥离瘤体称重,按公式计算抑瘤率。采用免疫组化检测肿瘤组织中血管内皮生长因子(VEGF)蛋白表达,使用实时荧光定量PCR(Real-time PCR)以及免疫印迹法(Western blot)检测肿瘤组织中C-X-C趋化因子配体12(CXCL12)及C-X-C趋化因子受体4(CXCR4)基因以及蛋白表达的改变。结果:癌痛平高、低剂量显著抑制小鼠H22荷瘤小鼠肿瘤的生长,癌痛平高剂量显著降低肿瘤组织中VEGF蛋白表达,并抑制CXCL12和受体CXCR4的基因及蛋白表达(P<0.01)。结论:癌痛平胶囊对H22荷瘤小鼠肿瘤生长转移具有一定的抑制作用,其作用机制可能是通过降低肿瘤组织VEGF蛋白表达以及干预CXCL12/CXCR4生物轴抑制肿瘤转移。
Objective: To observe the inhibitory effect of GuTongPing capsule on tumor growth and metastasis of H22 tumor-bearing mice and to explore its mechanism. Methods: ICR mice were inoculated with H22 hepatocarcinoma cell lines to establish H22 tumor-bearing mice model. H22 tumor-bearing mice were randomly divided into model group, cisplatin group, cancer pain level high and low dose group, model group daily ig volume of saline, flat cancer pain, low-dose group daily ig cancer pain level 36,18 g · kg -1), cisplatin group daily ip cisplatin (2 mg · kg -1)). The rats in each group were given continuous administration for 7 days, and the tumor-bearing mice were sacrificed and the tumors were weighed. The tumor inhibition rate was calculated according to the formula. The expression of vascular endothelial growth factor (VEGF) protein in tumor tissue was detected by immunohistochemistry. Real-time PCR and Western blot were used to detect the expression of CXC chemokine ligand 12 (CXCL12 ) And CXC chemokine receptor 4 (CXCR4) gene and protein expression changes. Results: The high and low dose of cancer pain can significantly inhibit the tumor growth of H22 tumor-bearing mice. The high dose of cancer pain can significantly decrease the expression of VEGF protein and the expression of CXCL12 and CXCR4 (P <0.01). CONCLUSION: GuTongPing Capsule can inhibit tumor growth and metastasis in H22 tumor-bearing mice. Its mechanism may be through inhibiting the expression of VEGF protein in tumor tissue and interfering with the biological axis of CXCL12 / CXCR4 in tumor metastasis.