| 徐加杰,葛明华,郑国湾,王林红,郭海魏,郑传铭.乌骨藤C21甾体苷对唾液腺腺样囊性癌荷瘤小鼠的抑制作用及机制研究[J].浙江中西医结合杂志,2019,29(5): |
| 乌骨藤C21甾体苷对唾液腺腺样囊性癌荷瘤小鼠的抑制作用及机制研究 |
| Inhibitory effect and mechanism of C21 steroidal glycosides on salivary adenoid cystic carcinoma in nude mice |
| 投稿时间：2019-01-14 修订日期：2019-04-01 |
| DOI： |
| 中文关键词: C21甾体苷 唾液腺腺样囊性癌 细胞凋亡 caspase-3 Bcl-2 |
| 英文关键词:C21 steroidal glycosides Salivary adenoid cystic carcinoma Apoptosis Caspase-3 Bcl-2 |
| 基金项目:浙江省中医药科技计划项目:乌骨藤中C21甾体苷抑制唾液腺腺样囊性癌的作用及机制研究(2018ZQ010) |
|
| 摘要点击次数: 663 |
| 全文下载次数: 1 |
| 中文摘要: |
| 目的 探讨乌骨藤C21甾体苷对唾液腺腺样囊性癌荷瘤小鼠的抗肿瘤作用及机制。方法 建立SACC-83细胞和SACC-LM细胞荷瘤裸鼠模型，给药组C21甾体苷(10 mg/kg/day)连续注射4周，模型组注射等量生理盐水，30天后取材。称瘤重，计算抑瘤率，各组裸鼠肿瘤、癌旁组织和肺组织HE染色观察病理改变，Western blot和qPCR分别检测C21甾体苷对各组瘤体组织caspase-3，Bcl-2，Bax的蛋白和mRNA的表达影响。结果 C21甾体苷给药4周后, SACC-83 C21甾体苷组的肿瘤体积与SACC-83模型组相比显著减小[(317.7±58.6)mm3比(232.6±32.8)mm3，P<0.05]，抑瘤率为26.8%；SACC-LM C21甾体苷组的肿瘤体积与SACC-LM模型组相比显著减小[(394.1±28.9)mm3比(296.5±38.8)mm3，P<0.05]，抑瘤率为24.8%。病理学结果显示C21甾体苷药物治疗后能抑制肿瘤的增殖和转移。Western blot结果显示，对于Bcl-2的蛋白水平，SACC-83 C21甾体苷组和SACC-LM C21甾体苷组相较于各自的模型组均显著下调且差异显著[(1.000 ± 0.069)比(0.563 ± 0.072)，P<0.01；(1.155 ± 0.071)比(0.664 ± 0.061)，P<0.01]；对于Bax和caspase-3的蛋白水平，SACC-83 C21甾体苷组和SACC-LM C21甾体苷组相较于各自的模型组均显著上调且差异显著[Bax: (1.000 ± 0.072)比(1.969 ± 0.181)，P<0.01；(0.844 ± 0.062)比(1.521 ± 0.120)，P<0.01；caspase-3:(1.000 ± 0.093)比(3.028 ± 0.256)，P<0.01；(0.890 ± 0.036)比(1.934 ± 0.188)，P<0.01]。qPCR结果同样表明C21甾体苷治疗后能显著抑制Bcl-2的mRNA表达水平[(1.002 ± 0.072)比(0.563 ± 0.014)，P<0.01；(1.172 ± 0.133)比(0.649 ± 0.065)，P<0.01]，上调Bax和caspase-3的mRNA表达水平[Bax: (1.005 ± 0.122)比(1.660 ± 0.227)，P<0.01；(0.817 ± 0.071)比(1.313 ± 0.115)，P<0.01；caspase-3: (1.001 ± 0.040)比(2.604 ± 0.174)，P<0.01；(0.886 ± 0.087)比(1.746 ± 0.080)，P<0.01]。结论 乌骨藤C21甾体苷可抑制唾液腺腺样囊性癌在裸鼠体内的增殖，其机制可能是通过促进细胞凋亡而发挥对肿瘤的抑制作用。 |
| 英文摘要: |
| Objective Our research aimed to investigate the inhibitory effect of C21 steroidal glycosides on salivary adenoid cystic carcinoma (SACC) in nude mice, and to explore the possible apoptosis mechanism. Methods After the SACC-83 and SACC-LM tumor cells were inoculated subcutaneously on the nude mice successfully, for C21 steroidal glycosides treated group, C21 steroidal glycosides with a dose of 10mg/kg/day was administrated for four weeks, model group were treated with saline. The nude mice were sacrificed at 30 days. Tumor inhibition rate were calculated, pathological changes were observed by HE staining, the effect of C21 steroidal glycosides on the expression of Bcl-2、Bax and caspase-3 in SACC tumor tissues were analyzed by Western blot and qPCR. Results After four weeks of administration with C21 steroidal glycosides, the tumor volume were decreased significantly [(317.7±58.6)mm3 versus (232.6±32.8mm)3 , P<0.05; (394.1±28.9) mm3 versus (296.5±38.8)mm3, P<0.05], and the inhibition rates of SACC-83 treated group and SACC-LM treated group were 26.8% and 24.8% compared with model group, respectively. Pathological results show that C21 steroidal glycosides can effectively inhibite the proliferation and metastasis of the tumor. Western blot results showed that C21 steroidal glycosides significantly down-regulatded the expression of Bcl-2 [(1.000 ± 0.069) versus (0.563 ± 0.072), P<0.01; (1.155 ± 0.071) versus (0.664 ± 0.061), P<0.01], activted the expression of caspase-3 and Bax in nude mice compared with model group [Bax: (1.000 ± 0.072) versus (1.969 ± 0.181), P<0.01; (0.844 ± 0.062) versus (1.521 ± 0.120), P<0.01; caspase-3: (1.000 ± 0.093) versus (3.028 ± 0.256), P<0.01; (0.890 ± 0.036) versus (1.934 ± 0.188), P<0.01]. qPCR also founded that the mRNA expression of Bcl-2 was significantly decreased [(1.002 ± 0.072) versus (0.563 ± 0.014), P<0.01; (1.172 ± 0.133) versus (0.649 ± 0.065), P<0.01], but mRNA expression of caspase-3 and Bax was increased with the administration of C21 steroidal glycosides [Bax: (1.005 ± 0.122) versus (1.660 ± 0.227), P<0.01; (0.817 ± 0.071) versus (1.313 ± 0.115), P<0.01; caspase-3: (1.001 ± 0.040) versus (2.604 ± 0.174), P<0.01; (0.886 ± 0.087) versus (1.746 ± 0.080), P<0.01]. Conclusion C21 steroidal glycosides can inhibit the proliferation of SACC in nude mice, and its mechanism may be promoting cell apoptosis in tumor. |
| 查看全文 查看/发表评论 下载PDF阅读器 |
| 关闭 |
|
|
|
