研究论文

异常黑胆质成熟剂合用5-氟尿嘧啶对移植性EAC肿瘤的增效减毒作用

  • 热娜古丽·艾则孜, 帕尔哈提·塔衣尔, 艾尼娃尔·艾克木, 艾山江·阿帕尔, 祖拉亚提, 陆明, 塔依尔江·吐尔逊, 哈木拉提·吾甫尔
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  • 1. 新疆医科大学附属中医医院, 乌鲁木齐 830000;
    2. 新疆医科大学第一附属医院, 乌鲁木齐 830054;
    3. 新疆医科大学药学院, 乌鲁木齐 830011;
    4. 喀什地区第一人民医院, 喀什 844000;
    5. 长春师范大学化学学院, 长春 130000;
    6. 新疆医科大学维吾尔医学院, 乌鲁木齐 830011
热娜古丽·艾则孜,副教授,研究方向为肿瘤的维吾尔医干预,电子信箱:rena727@sina.com

收稿日期: 2013-12-03

  修回日期: 2014-02-24

  网络出版日期: 2014-04-19

基金资助

国家重点基础研究发展计划(973计划)项目(2011CB512004);教育部长江学者和创新团队发展计划项目(IRT0977)

Synergistic Attenuation of Abnormal Savda Munziq Combination with 5-Fluorouracil on Transplantated EAC Tumor

  • AIZEZI Renaguli, TAYIR Parhat, AIKEMU Ainiwaer, APER Aishanjan, Zuliayati, LU Ming, TUERXUN Tayierjiang, UPUR Halmurat
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  • 1. The Affiliated Traditional Chinese Medicine Hospital, Xinjiang Medical University, Urumqi 830000, China;
    2. The First Affiliated Hospital, Xinjiang Medical University, Urumqi 830054, China;
    3. College of Pharmacy, Xinjiang Medical University, Urumqi 830011, China;
    4. The First People's Hospital of Kashgar, Kashgar 840000, China;
    5. College of Chemistry, Changchun Normal University, Changchun 130000, China;
    6. Faculty of Traditional Uighur Medicine, Xinjiang Medical University, Urumqi 830011, China

Received date: 2013-12-03

  Revised date: 2014-02-24

  Online published: 2014-04-19

摘要

为探讨异常黑胆质成熟剂对移植性EAC 肿瘤的抑制作用及异常黑胆质成熟剂对5-氟尿嘧啶致毒副作用的保护作用和增效减毒作用,建立了移植性EAC 肿瘤模型,60 只小鼠随机分为正常对照组、肿瘤模型组、5-氟尿嘧啶(5-Fu)对照组、5-FU 联合异黑高剂量组、5-FU 联合异黑中剂量组、5-FU 联合异黑低剂量组6 组,观察小鼠抑瘤率、脾指数、胸腺指数和肝脏指数,小鼠血清中的超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)含量的变化。研究结果表明,5-FU 联合异常黑胆质成熟剂高剂量组、5-FU 联合异常黑胆质成熟剂中剂量组、5-FU 联合异常黑胆质成熟剂低剂量组和氟尿嘧啶对照组的抑瘤率分别为42.41%、58.09%,41.58%和50.83%。正常对照组与肿瘤模型组小鼠胸腺质量比、脾脏质量比和肝脏质量比相比,差异有显著性(P<0.05)。与肿瘤模型组比较,5-FU 联合异常黑胆质成熟剂中剂量组、5-FU 联合异常黑胆质成熟剂低剂量组的胸腺质量比均明显降低;与氟尿嘧啶对照组比较,5-FU 联合异常黑胆质成熟剂高剂量组、5-FU 联合异常黑胆质成熟剂中剂量组、5-FU 联合异常黑胆质成熟剂低剂量组的脾脏质量比均明显升高,差异均有显著性(P<0.05)。与肿瘤模型组比较,5-FU 联合异常黑胆质成熟剂高剂量组、5-FU 联合异常黑胆质成熟剂低剂量组的肝脏质量比变化明显,差异均有显著性(P<0.05)。正常对照组与肿瘤模型组小鼠血清中SOD 活性,GSH-Px 活性,MDA 含量相比,差异有显著性(P<0.05)。与肿瘤模型组血清中SOD 活性、GSH-Px 活性比较,5-FU 联合异黑高低剂量组有显著升高,差异均有显著性(P<0.05),其中5-FU 联合异黑中剂量组最高,已接近正常值。与5-FU 对照组血清中SOD 活性、GSH-Px 活性比较,5-FU 联合异常黑胆质成熟剂各剂量组有显著升高,差异均有显著性(P<0.05),其中5-FU 联合异常黑胆质成熟剂中剂量组SOD、GSH-Px 活性最高,已接近正常值。MDA 含量在5-FU 联合异常黑胆质成熟剂中剂量最低,与肿瘤模型组比较有显著降低,差异均有显著性(P<0.05)。异常黑胆质成熟剂具有显著的免疫增强作用,表现在与5-氟尿嘧啶联合用药后对5-氟尿嘧啶所致的免疫功能损伤有保护作用,异常黑胆质成熟剂对移植性肿瘤EAC 肿瘤有较强的增效减毒作用。

本文引用格式

热娜古丽·艾则孜, 帕尔哈提·塔衣尔, 艾尼娃尔·艾克木, 艾山江·阿帕尔, 祖拉亚提, 陆明, 塔依尔江·吐尔逊, 哈木拉提·吾甫尔 . 异常黑胆质成熟剂合用5-氟尿嘧啶对移植性EAC肿瘤的增效减毒作用[J]. 科技导报, 2014 , 32(10) : 68 -73 . DOI: 10.3981/j.issn.1000-7857.2014.10.012

Abstract

This paper studies the inhibitive effect of the abnormal savda munziq on the transplanted EAC tumor and the protective effect of the abnormal savda munziq on 5-fluorouracil-induced toxicity. The 60 transplantated EAC tumor model mice were randomly divided into 6 groups: The normal control group, the tumor control group, the 5-fluorouracil (5-FU) group, the high dose 5-FU ASMq group, the middle dose 5-FU ASMq group, and the low dose 5-FU ASMq group. The content changes of the mouse tumor inhibition rate, the spleen index, the thymus index, and the indices of liver, mouse serum SOD, MDA, GSH-Px were observed. In the 5-FU high-dose ASMq group, the 5-FU medium-dose ASMq group, the 5-FU low-dose ASMq group and the 5-FU group, the values of the tumor inhibition rate were found to be 42.41%, 58.09%, 41.58% and 50.83%, respectively, showing that the tumor function is weakened. Compared with the model group, the thymus/body weight ratio is clearly reduced in the 5-FU medium-dose ASMq group and the 5-FU low-dose ASMq group. Compared with the 5-FU group, the spleen/body weight ratio is clearly increased in the 5-FU high-dose ASMq group, the 5-FU medium-dose ASMq group, and the 5-FU low-dose ASMq group, and the difference was significant (P<0.05). In the 5-FU ASMq dose groups, the levels of SOD and GSH-Px are reduced compared with that in the 5-FU control group, and the difference is significant (P<0.05). In the 5-FU medium-dose ASMq group, the SOD and GSH-Px levels are high. With respect to the MDA values, the 5-FU medium-dose ASMq group has the lowest values and in comparison with the model control group, the difference is significant (P<0.05). With respect to the SOD and GSH-Px levels, compared with the model group, the 5-FU high dose ASMq group has lower levels, and the difference is significant (P<0.05). For the synergy and the attenuation of the abnormal savda munziq combined 5-fluorouracil to the transplanted EAC tumor, abnormal savda munziq dose group, the SOD, GSHPx levels are up to close to normal. The lowest MDA values of the abnormal savda munziq dose group indicate that the combination of the abnormal savda munziq can reduce the toxicity of the 5-fluorouracil portability EAC tumor significantly.

参考文献

[1] Schottenfeld D, Beebe-Dimmer J L. Advances in cancer epidemiology: Understanding causal mechanisms and the evidence for implementing interventions[J]. Annual Review of Public Health, 2005, 26(1): 37-60.
[2] Parkin D M, Bray F, Ferlay J, et al. Global cancer statistics, 2002[J]. A Cancer Journal for Clinicians, 2005, 55(2): 74-108.
[3] Jemal A, Murray T, Ward E, et al. Cancer statistics, 2005[J]. A Cancer Journal for Clinicians, 2005, 55(1): 10-30.
[4] Yang L, Parkin D M, Li L D, et al. Estimation and projection of the national profile of cancer mortality in China:1991-2005[J]. British Journal of Cancer, 2004, 90(11): 2157-66.
[5] Yang L, Parkin D M, Ferlay J, et al. Estimates of cancer incidence in China for 2000 and projections for 2005[J]. Cancer Epidemiology, Biomarkers & Prevention, 2005, 14(1): 243-50.
[6] Yang L, Parkin D M, Li L, et al. A comparison of the sources of cancer mortality in China[J]. Cancer Causes & Control, 2004, 15(7): 681-687.
[7] Pao W, Wang T Y, Riely G J, et al. KRAS mutation and primary resistance of lung adenocarcinoma to gefitinib or erlotinib[J]. PLOS, 2005, 2(1): 57-61.
[8] Camp E R, Summy J, Bauer T, et al. Molecular mechanisms of resistance to therapies targeting the epidermal growth factor receptor[J]. Clinical Cancer Research, 2005, 11(1): 397-405.
[9] Learn C A, Hartzell T L, Wikstrand C J, et al. Resistance to tyrosine kinase inhibition by mutant epidermal growth factor receptor variant III contributes to the neoplastic phenotype of glioblastoma multiforme[J]. Clinical Cancer Research, 2004, 10(9): 3216-3224.
[10] Kokubo Y, Gemma A, Noro R, et al. Reduction of PTEN protein and loss of epidermal growth factor receptor gene mutation in lung cancer with natural resistance to gefitinib(Iressa)[J]. British Journal of Cancer, 2005, 92(9): 1711-1719.
[11] 甄永苏. 抗肿瘤新药研发的机遇与挑战[J]. 科技导报. 2008, 26 (19): 3. Zhen Yongsu. Opportunities and challenges in research and development of new anticancer drugs[J]. Science & Technology Review, 2008, 26(19): 3.
[12] 易沙克江·马合穆德. 中国医学百科全书维吾尔医学分卷[M]. 乌鲁 木齐: 新疆人民卫生出版社, 1988. Mahmud Ishakjan. Chinese medical encyclopedia uighur medicine volume[M]. Urumqi: Xinjiang People's Medical Publishing House, 1988.
[13] 阿布都克力木·吐尔逊. 肿瘤发病机制的维医理论探讨[J]. 维吾尔医 专科学校学报, 2003(2): 36-38. Tursun Abdukerim. To discuss the pathogenesis of tumor in uighur medicine theory[J]. Journal of Uighur Medicine College, 2003(2): 36-38.
[14] 木拉提·克扎衣别克,Brigitte Kopp, Sonja Prinz, 等. 异常黑胆质成熟 剂中各单味药对HL-60细胞增殖的抑制作用[J]. 科技导报, 2009, 27 (19): 94-98. Kizaibek Murat, Kopp Prinz, et al. Antiproliferative activity of individual herbs of abnormal savda munziq on HL-60 cells[J]. Science & Technology Review, 2009, 27(19): 94-98.
[15] 艾来提·米吉提, 阿地里江·阿不力米提, 尼加提·热合木, 等. 维医异 常黑胆质成熟剂对异常黑胆质载体动物模型下丘脑-垂体-肾上 腺轴形态学的影响[J]. 国际病理科学与临床杂志, 2008, 28(1): 6-9. Mijit Hairat, Abilmit Adiljan,Rahman Nijat, et al. Effect of abnormal savda munziq on morphological structure of hypothalamus-pituitaryadrenal axis cells in abnormal savda syndrome animal model[J]. Journal of International Pathology and Clinical Medicine,2008, 28(1): 6-9.
[16] 阿不都热依木, 哈木拉提. 异常黑胆质成熟剂和清除剂抗氧化作用 的ESR研究[J]. 中药新药与临床药理, 2001, 12(6): 420-422. Abudureyimu, Hamulati. ESR study on antioxidant effect of abnormal savda munziq and musil[J]. Traditional Chinese Medicine and clinical pharmacology, 2001, 12(6): 420-422.
[17] Halmurat U, Abdiryim Y, Anwar U, et al. Uighur traditional medicine syndrome of abnormal savda in men is associated with oxidative stress, which can be improved by Munziq and Mushil of abnormal savda[J]. Thérapie, 2004, 59(4): 483-484.
[18] Abdiryim Y, Halmurat U, Anwar U, et al. Protective effects of Munziq and Mushil of abnormal Savda to mitochondrial oxidative damage[J]. Fundamental & Clinical Pharmacology, 2004, 18(4): 471-476.
[19] 阿不都热依木·玉苏甫, 哈木拉提·吾甫尔, 吐尔洪·卡迪尔. 异常黑 胆质成熟剂醇提物诱导HepG2 细胞凋亡机制的研究[J]. 中成药, 2006, 28(7): 1008. Yusup Abdureyim, Upur Hulmrat, Kadir Turghun, Mechanism of Abnormal Savda Munziq ethanol extract on HepG2 cell apoptosis[J]. Chinese Traditional Patent Medicine, 2006, 28(7): 1008.
[20] 哈木拉提·吾甫尔, 艾斯卡尔·依米提, 伊里哈木江·沙比提. 异常黑 胆质成熟剂与清除剂对人Hela细胞凋亡基因表达的影响[J]. 细胞与 分子免疫学杂志, 2001, 17(2): 109-111. Upur Hulmrat, Yimit Askar, Sabit Ilhamjan. Abnormal savda munziq and mushil impact on human gene expression of apopotosis Hela[J]. Chinese Journal of Cellular and Molecular Immunology, 2001, 17(2): 109-111.
[21] 哈木拉提·吾甫尔, 李林, 陈艳. 异常黑胆质成熟剂与清除剂对氧化 损伤的淋巴细胞p53蛋白表达的影响[J]. 新疆医科大学学报, 2005, 28(4): 287-289. Upur Hulmrat, Li Lin, Chen Yan. Influence of abnormal savda munziq and mushil on p53 protein and gene expression oxidized of human lymphocytes in vitro[J]. Journal of Xinjiang Medical University, 2005, 28(4): 287-289.
[22] 姬艳丽, 李林, 武贵臻, 等. 异常黑胆质成熟剂与清除剂对H2O2诱导 的淋巴细胞凋亡的影响[J]. 新疆医科大学学报, 2005, 28(4): 293-296. Ji Yanli, Li Lin, Wu Guizhen, et al. The influence of abnormal savda munziq and Mushil on H2O2-induced lymphocyte apoptosis[J]. Journal of Xinjiang Medical University, 2005, 28(4): 293-296.
[23] 张莉, 哈木拉提·吾甫尔, 张仑. 异常黑胆质成熟剂提取物对小鼠辐 射的防护作用[J].中南大学学报: 医学版, 2007, 32(1): 69-73. Zhang Li, Upur Hulmrat, Zhang Lun. Protective effect of abnormal savda munzip on radiation-induced damage in mice[J]. Journal of Central South University: Medical Sciences Edition, 2007, 32(1): 69-73.
[24] 艾斯卡尔·依米提, 哈木拉提·吾甫尔, 布再娜甫·伊力哈木. 维吾尔 医成熟及清除剂诱导T淋巴瘤细胞凋亡的研究[J]. 中药药理与临 床, 2000, 16(2): 33-34. Yimit Askar, Upur Hulmrat, Yilihulm Buzainapu. Uighur herbal medicine Munziq and Mushil induced T lymphoma cells apoptosis research[J]. Pharmacology and Clinics of Chinese Materia Medica, 2000, 16(2): 33-34.
[25] 蔡红卫, 冯娟娟. 三氟拉嗪对癫痫大鼠NO、NOS、SOD、MDA的影响[J]. 世界中西医结合杂志, 2010(7): 14-15. Cai Hongwei, Feng Juanjuan. Impacts of Trifluoperazine on NO, NOS, SOD and MDA in the Rats with Epilepsy[J]. World Journal of Integrated Traditional and Western Medicine, 2010(7): 14-15.
[26] 胡汉华, 盛磊, 哈木拉提·吾甫尔. 维药异常黑胆质成熟剂的抗肿瘤 作用及其对细胞迁移的影响[J]. 科技导报, 2011, 29(3): 62-65. Hu Hanhua, Sheng Lei, Upur Halmurat. Anti-cancer effects of uighur medicine abnormal savda munzip and its influence on cell migration[J]. Science & Technology Review, 2011, 29(3): 62-65.
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