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虫类攻毒法与草木解毒法对小鼠Lewis肺癌治疗作用的对比研究
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摘要
目的
     肺癌是临床最常见的恶性肿瘤之一,其发病率、死亡率均居癌症首位。导师邱幸凡教授结合多年临床经验提出“肺虚络痹毒结”为肺癌发病机制,其中“癌毒结聚”是发病的关键。临床常用虫类攻毒法、草木解毒法消除毒邪,取得了较好的疗效。本研究在此基础上,结合现代医学研究,探讨肺癌病因、病机及治法,并通过实验研究观察虫类攻毒方与草木解毒方在C57BL/6小鼠Lewis肺癌模型治疗中作用的异同,通过比较受试小鼠生存状态、体重变化、胸腺重量及胸腺指数,探讨虫类攻毒方、草木解毒方对受试小鼠免疫状态的影响;通过检测抑瘤率、小鼠Lewis肺癌肿瘤细胞增殖指数和组织形态,比较两方抑制肿瘤细胞增殖等方面作用,探讨虫类攻毒方、草木解毒方防治肺癌的机制。由于虫类攻毒药相对于草木解毒药有更强的通络作用,通过观察瘤组织血管形态,以及血管内皮生长因子相关蛋白C (VEGF-C)的表达,探讨虫类攻毒方与草木解毒方抗肺癌作用机制的异同;检测小鼠Lewis肺癌中P53蛋白表达和P53 mRNA表达、c-myc蛋白表达和c-myc mRNA表达的变化,探讨虫类攻毒方、草木解毒方防治肺癌的可能机制及作用异同,以指导临床治疗。
     方法
     1、理论研究采用文献整理结合临床实践的方法,探讨肺癌的病因病机及虫类攻毒法和草木解毒法防治肺癌作用机制的异同。2、本实验研究设5组:正常对照组、模型对照组、虫类攻毒组、草木解毒组、环磷酰胺组。通过复苏、接种、保种Lewis肺癌瘤株,选取生长良好的Lewis肺癌组织,剪碎匀浆,制成细胞悬液,接种于每只小鼠右腋皮下。复制C57BL/6小鼠Lewis肺癌模型。根据导师的临床经验选取蜈蚣、守宫、露蜂房组成虫类攻毒方,龙葵、白英、白蚤休组成草木解毒方。模型对照组、虫类攻毒组、草木解毒组、环磷酰胺组接种后第二天开始灌胃给药,连续12天。第13天颈椎脱臼处死小鼠。采取标本,进行以下检测:正常对照组、模型对照组、虫类攻毒组、草木解毒组、环磷酰胺组小鼠生存状态、体重的变化、胸腺重量、胸腺指数、抑瘤率、瘤组织细胞周期、瘤组织光镜和电镜下病理形态;以RT-PCR法观察模型对照组、虫类攻毒组、草木解毒组、环磷酰胺组小鼠瘤细胞VEGF-C mRNA、P53 mRNA和c-myc mRNA表达;以免疫组织化学法检测模型对照组、虫类攻毒组、草木解毒组、环磷酰胺组小鼠瘤细胞VEGF-C蛋白、P53蛋白和c-myc蛋白表达。
     结果
     1、通过对文献的整理,结合临床实践,提出肺癌主要病机为肺虚络痹毒结,其中“癌毒结聚”是发病的关键。临床常用虫类攻毒法、草木解毒法消除毒邪,结合现代中医学研究成果及我们在临床工作中治疗本病的体会,提出虫类攻毒药和草木解毒药在治疗肺癌过程中均起到不同治疗作用,其中以虫类攻毒药通络作用更为峻烈。临床当结合患者不同体质和不同病程相机而施。2、虫类攻毒方、草木解毒方可明显减少肿瘤细胞增殖指数,但作用要弱于环磷酰胺组;3、虫类攻毒方、草木解毒方对胸腺的抑制作用小于环磷酰胺组,并且能提高胸腺指数,从而起到提高机体免疫功能的作用;4、在抑制肿瘤重量方面,虫类攻毒方、草木解毒方的抑瘤率分别可达45.96%、26.68%,虫类攻毒方抑制肿瘤的作用优于草木解毒方;5、在改善生存质量方面,肿瘤重量过大直接影响了小鼠的生存质量,使得小鼠活动困难,功能衰竭,从而使中药改善小鼠生存质量的指标测定具有不确定性;6、在组织形态方面,电镜下观察可见虫类攻毒方、草木解毒方能导致肿瘤细胞线粒体肿胀,溶酶体和脂质小体增多,细胞核核仁消失、染色质边集于核膜下、染色质浓缩等,虫类攻毒方优于草木解毒方;HE染色后在光镜下观察,可见虫类攻毒组、草木解毒组瘤组织中微血管数量明显少于模型对照组和环磷酰胺组,并且虫类攻毒组中微血管数量明显少于草木解毒组;7、虫类攻毒方、草木解毒方具有抑制VEGF-C表达水平的作用,提示抑制VEGF-C表达水平可能是虫类攻毒方、草木解毒方防治肺癌的机制之一。在抑制小鼠Lewis肺癌血管生成方面虫类攻毒方效果优于草木解毒方,提示虫类攻毒方对Lewis肺癌移植瘤的抑瘤率优于草木解毒方,可能的机制是由于虫类攻毒方抑制Lewis肺癌VEGF-C表达方面优于草木解毒方;8、虫类攻毒方、草木解毒方具有提高P53的表达、抑制c-myc的表达的作用,提示提高P53的表达、抑制c-myc的表达可能是虫类攻毒方、草木解毒方防治肺癌的机制之一。
     结论
     1、肺癌主要病机为肺虚络痹毒结,其中“癌毒结聚”是发病的关键,虫类攻毒药和草木解毒药在治疗肺癌过程中均起到不同治疗作用,其中以虫类攻毒药通络作用更为峻烈。2、虫类攻毒方、草木解毒方的抗小鼠Lewis肺癌作用确切,并且虫类攻毒方在抑瘤率方面优于草木解毒方,两方均可以提高P53的表达、抑制c-myc的表达。虫类攻毒方抗肺癌作用优于草木解毒方,可能的机制是由于虫类攻毒方抑制Lewis肺癌VEGF-C表达方面优于草木解毒方,从而印证了导师邱幸凡教授提出的“络痹”是肺癌发生的重要病机的观点。虫类攻毒方、草木解毒方的作用机制主要为:1、调控肿瘤细胞G0/S位点,使肿瘤细胞阻滞于G0期,不再进入有丝分裂,从而达到抑制肿瘤的作用;2、虫类攻毒方、草木解毒方对Lewis肺癌模型小鼠胸腺的抑制作用弱于环磷酰胺,能激活胸腺功能,通过调节机体的免疫系统,促进肿瘤组织内淋巴细胞数量增加,从而达到增强免疫的作用;3、虫类攻毒方、草木解毒方具有提高P53表达、抑制VEGF-C、c-myc表达的作用,从而抑制瘤组织血管生成、肿瘤细胞增殖;4、本研究揭示了虫类攻毒方、草木解毒方的部分作用机制,但因中药复方作用的多靶点,提示应进一步思考和深入研究。
Objective
     Lung cancer was the most common malignant tumor of clinical, the incidence rate of cancer mortality in the first rank. Professor Qiu Xingfan mentor with many years experience in clinical treatment of lung cancer proposed the "dirty end virtual network paralysis virus" as the main pathogenesis of lung cancer, especially "cancer drug knot together" was the key to the incidence, clinical drug commonly used method of attack insects, vegetation detoxification method elimination of toxin, proved toxic method of attack insects, vegetation, detoxification method was effective, as the basis for this study, combined with modern medical research, in-depth study of lung cancer etiology, pathogenesis, and the experimental study drug law and observing insects attack vegetation Toxin on C57BL/6 mice with Lewis lung cancer xenograft model differences in the role of lung cancer, the survival status of mice by observing the subjects, body weight, thymus weight and thymus index of toxic side attack of insects, vegetation, toxic side immune function of mice tested; by detecting the inhibition rate of Lewis lung carcinoma mouse tumor cell proliferation index and morphology, drug side attack of insects, vegetation, toxic side effects of lung cancer prevention and control mechanism, and worms, virus attack detoxification side and vegetation between the two groups to improve immune function, inhibit tumor cell proliferation, the role of the comparison.The insects attack drug detoxification for vegetation Tongluo strong side effect, so by observing the tumor vascular morphology and vascular endothelial growth factor (VEGF-C) expression of virus attack insects and vegetation Toxin Act similarities and differences between the mechanism of anti-lung cancer. At the same time by detecting the mouse Lewis lung carcinoma tumor suppressor gene P53 protein expression and P53mRNA expression of oncogene c-myc protein expression and the expression of c-myc mRNA, and explore the toxic side attacking insects, vegetation, prevention and treatment of lung cancer may be toxic side mechanism, and the insects attacking side and the vegetation detoxification drug side P53, c-myc expression in comparison. Investigate the mechanism for the drug attack insects in the medical method, vegetation detoxification methods for the treatment of lung cancer provide the basis of experimental data and applications.
     Method
     1.The theoretical study, literature review, clinical practice, the method produced by lung cancer etiology, pathogenesis and drug characteristics for the cancer drug, respectively, and detoxification methods to attack a detailed discussion of modern medicine and our clinical research work experience in the treatment of the disease, poison attack insects and vegetation proposed antidote in the treatment of lung cancer treatment process plays a different role in both, in which the role of insects attack more poison Jun strong collaterals. When combined with clinical patients with different physical and cameras while the application of different courses.2.There were 5 groups in the experiment:control group, model control group, drug group attacking insects, vegetation detoxification group, cyclophosphamide group.By the recovery, vaccination, conservation Lewis lung tumor lines, select a good growth of Lewis lung cancer, cut and homogenized into cells were inoculated subcutaneously in each mouse in the right armpit. Copy C57BL/6 mice Lewis lung cancer xenograft model. Selected based on clinical experience instructors centipede, gecko, dew worm attack drug side honeycomb form, Solanum nigrum, white British, white composition of vegetation detoxification square off fleas. Model control group, drug group attacking insects, vegetation, the day after detoxification group received oral administration for 12 days, intraperitoneal injection of cyclophosphamide. On day 13 mice were sacrificed by cervical dislocation. To take samples, make the following test:the normal control group, model control group, drug group attacking insects, vegetation detoxification group, cyclophosphamide group were living condition, changes in body weight, thymus weight, thymus index, tumor inhibition rate of tumor cell cycle, tumor pathology light microscope and electron microscope morphology; RT-PCR method to observe the model control group, drug group attacking insects, vegetation detoxification group, cyclophosphamide group were tumor cells VEGF mRNA, P53 mRNA and the expression of c-myc mRNA situation; by immunohistochemical detection model control group, drug group attacking insects, vegetation detoxification group, cyclophosphamide group VEGF protein in tumor cells in mice, P53 protein and c-myc protein expression situation.
     Results
     1.The insects attack drug side vegetation detoxification only significantly reduce tumor cell proliferation index, but the effect was weaker than cyclophosphamide group; 2.Drug party worm attack, vegetation, toxic side effects on the thymus of cyclophosphamide inhibition of less than group, and can increase the thymus index, which play a role in enhancing immune; 3.Tumor weight in mice with tumor suppression, the drug party worm attack, the plants were toxic side can reach 45.96%,26.68%, worms attack toxic side effects than inhibition of tumor detoxification side vegetation; 4.In terms of improving the quality of life, excessive direct impact on tumor weight in mice quality of life, making the mouse has difficulties, failure to make traditional Chinese medicine to improve the quality of life in mice The index determination is uncertain; 5.In the morphology, the electron microscope shows toxic side attacking insects, vegetation, can only lead to tumor cell detoxification swelling of mitochondria, lysosomes and lipid bodies increase in nucleolus disappear chromatin margination at the nuclear membrane, the chromatin condensation, etc, worms attacking side than vegetation detoxification drug side; HE staining and observed under light microscope, showing that drug groups attack insects, vegetation, detoxification group was significantly the number of tumor microvessel less than the model control group and the cyclophosphamide group, and the insects attack the number of drug group was significantly less than the Microvascular vegetation detoxification group; 6.Drug party worm attack, the plants can inhibit the toxic side expression of VEGF-C role, suggesting that inhibition of VEGF-C expression levels may be toxic side attacking insects, vegetation, toxic side one of the mechanisms of lung cancer prevention. Lewis lung carcinoma in mice aspects of tumor angiogenesis drug party worm attack detoxification side was better than grass, suggesting that we attack drug party worm Lewis lung carcinoma on the inhibition rate than detoxification side vegetation, the possible mechanism was due to drug party worm attack Lewis lung carcinoma inhibited VEGF-C expression was better than that of vegetation Jiedu; 7.Drug side attacking insects, vegetation, toxic side has increased the level of P53 expression, inhibit the expression of c-myc effect, suggesting improve the level of P53 expression, inhibit the expression of c-myc may be drug side attacking insects, vegetation, toxic side one of the mechanisms of lung cancer prevention.
     Conclusion
     Drug party worm attack, the anti-side vegetation detoxification Lewis lung carcinoma in mice the exact role and drug party worm attack rate in the tumor than detoxification side vegetation, which both parties can improve the level of P53 expression, inhibition of c-myc expression. Insects attacking anti-cancer drug side effects side detoxification better than grass, the mechanism may be due to toxic side worm attack Lewis lung carcinoma inhibited VEGF-C expression was better than grass detoxification side, which confirms the mentor Professor Qiu Xingfan's "network Bi" was an important pathogenesis of lung cancer point of view. Insects attacking drug side effects side detoxification mechanisms of vegetation mainly:1. Control tumor cell Go /S locus, the tumor cells were arrested in Go phase, no entry into mitosis, and thus inhibit tumor effect; 2.Worms attack drug class side, the vegetation on the Lewis lung cancer model detoxification side thymus weaker than the inhibitory effect of cyclophosphamide, thymic function can be activated, by regulating the body's immune system, promote the increase in the number of lymphocytes in tumor tissue, so as to achieve enhanced immunity effect; 3.Drug side attacking insects, vegetation, toxic side has increased the level of P53 expression, inhibition of VEGF-C, c-myc expression level of the role, thereby inhibiting tumor angiogenesis, tumor cell proliferation; 4.This study reveals a worm attack drug class side, the vegetation part of the mechanism of detoxification side, but the role of traditional Chinese medicine research in multi-target and the objective existence of complex, suggesting that we should further thinking and further study.
引文
[1]吴一龙,张明和,廖美琳,等.肺癌的诊断和分期临床指导[J].中国肺癌杂志,2003,6(5):330-334.
    [2]隋·巢元方.诸病源候论·卷三十一·恶核肿候[M].北京:人民军医出版社,2006:327.
    [3]清·冯兆张.冯氏锦囊秘录·杂症大小合参卷十二·方脉·咳嗽[M].北京:中国中医药出版社,1996:341.
    [4]清·吴仪洛.成方切用·卷八上·润燥门[M].天津:天津科学技术出版社,2001:321.
    [5]明·李中梓.医宗必读·卷之七·积聚[M].北京:人民卫生出版社,1995:378.
    [6]中藏经·卷上.积聚癥瘕杂虫论第十八[M].北京:人民卫生出版社,2007年:15.
    [7]明·吴有性.温疫论·上卷·原病[M].北京:人民卫生出版社,1990:2.
    [8]杨士瀛医学全书·仁斋直指方论·癌[M].北京:中国中医药出版社,2006:279.
    [9]赵智强,李嘉.略论周仲瑛教授的癌毒学说及临床用应[J].新中医,1998,30(10):6-8.
    [10]明·李中梓.医宗必读·卷之七·积聚[M].北京:人民卫生出版社,1995:378.
    [11]黄杰熙.本草问答评注[M].山西:山西科学教育出版社,1991:83.
    [12]田静,丁金芳.施志明教授用虫类药治疗肺癌经验介绍[J].新中医,2004,36(3):12-13.
    [13]高静东,陈嘉璐,张蕾.清热解毒法对小鼠Lewis肺癌瘤组织MMP-9及TIMP-1表达的影响[J].江苏中医药,2010,42(10):76-77.
    [14]王惟恒.以毒攻毒治癌症[J].中国中医药报,2007,6(15):6.
    [15]潘磊,陈培丰.清热解毒中药抗肿瘤作用机制研究进展[J].中华中医药学刊,2007,25(3):569.
    [16]陈锐深.现代中医肿瘤学[M].北京:人民卫生出版社,2003:117.
    [17]王一泉.中国药理学会中药药理第二届全国学术会议论文摘要.
    [18]赵玉芝,刘东义.蜈蚣糊治疗带状疱疹16例[J].辽宁中医杂志,1999,16(1):36.
    [19]宋萍.鲜壁虎冻干粉抑制H22肿瘤血管生成机制的实验研究[J].中国中西医结合杂志,2006,1(26):58-63.
    [20]张霄岳,常树春,刘叶青.参龙金灵丸对肺癌的临床疗效观察[J].中成药,2002,24:902-904.
    [21]陈熙.金龙胶囊合并化疗治疗晚期非小细胞肺癌的临床观察[J].实用肿瘤杂志,2006,21:267-268.
    [22]李琳.露蜂房的研究和应用[J].中草药,1998,29(4):277.
    [23]小原隆造.露蜂房的有毒成分露蜂房油的研究[J].日本药物学杂志,1928,7(2):254-257.
    [24]曾元璋.一种有毒中草药抗肿瘤作用浅析[J].湖南中医药导报,1998,4(5):8-9
    [25]谢远明,张长富.加味一贯煎治疗肺癌症106例[J].陕西中医,2002,23(4):302-303.
    [26]卜样兆,赵保民.中西医结合治疗老年人中晚期肺癌临床观察[J].2004,18(4):303-304.
    [27]赵晓琴,曾祥法.龙葵片对原发性肝癌治疗作用的临床研究[J].辽宁中医杂志,2002,29(11):671-672.
    [28]马安柱,赵红,张福林,等.腹腔化疗同参储培气汤治疗晚期肝癌36例[J].陕西中医,2004,25(1):41-42.
    [29]刘国良,李钟瑞,郭宏欣.中药体表外贴加化疗治疗肝癌61例临床观察[J].现代肿瘤医学,1997,5(4):225-226.
    [30]杜洪彬,宋慧.扶正消瘤汤合并MAF治疗晚期胃癌31例[J].黑龙江中医药,2004,3:13-14.
    [31]Nadkarni, M. K. Nadkarni, A. K. Indian Materia Medica,1954,1:1152
    [32]Chopra, R. N., Chopra, I. C., Handa, K. L. [J] Indigenous drugs of India,1958,885 and 524.
    [33]张锦燕.中药“龙葵”有助抗乳癌[J].新加坡联合早报,2005,2(28)
    [34]季宇彬,王胜惠,高世勇,等.龙葵碱对H22荷瘤小鼠细胞膜流动性和膜蛋白水平的影响[J].中草药,2005,36(2):239-241.
    [35]季宇彬,王胜惠,高世勇,等.龙葵碱对H2荷瘤小鼠肿瘤细胞膜唾液酸和封闭度的影响[J].中草药,2005,36(Ⅰ):79-80.
    [36]季宇彬,王宏亮,高世勇.龙葵碱对荷瘤小鼠肿瘤细胞DNA和RNA的影响[J].中草药,2005,36(8):1200-1202.
    [37]季宇彬,王宏亮,高世勇.龙葵碱对肿瘤细胞膜ATP酶活性的影响[J].哈尔滨商业大学学报(自然科学版),2005,21(2):127-129.
    [38]赖亚辉,刘良,董莉萍.龙葵浓缩果汁对S180荷瘤小鼠的抑瘤效应[J].中国预防医学杂志,2005,6(1):28-29.
    [39]王胜惠,从云峰,梁明,等.龙葵90%醇提取物对荷瘤肝癌小鼠生存时间及肉瘤瘤重影响[J].黑龙江医学,2005,29(6):421-422.
    [40]赵晓琴.复方龙葵糖浆诱导小鼠Hzz肝癌细胞凋亡作用机制研究[J].辽宁中医杂志,2005,32(9):974-975.
    [41]Ushio R,et al. Indian Materia Medica, CA,1989,110:141525b.
    [42]张永健,王耐勤,许树旭,等.复方中药注射液对人癌细胞体外杀伤效应及其对细胞周期的影响[J].中西医结合杂志,1989,7:416.
    [43]周金黄,王筠默.中药药理学[M].上海:上海科学技术出版社,1986:323.
    [44]王强,徐国钧.中药七叶一枝花类对L-929细胞的细胞毒活性研究[J].中草药,1987,18(11):526.
    [1]徐叔云,卞如濂,陈修主编.药理实验方法学[M].北京:人民卫生出版社,2002:1767,169,1764.
    [2]王洪图.黄帝内经研究大成[M].北京:北京出版社,1997,85.
    [3]徐光福.络病的内涵及其外延释义[J].中医药学刊,2005,23(1):96-98.
    [4]杨万里.浅谈“久病入络”的病机及临床意义[J].长治医学院学报,2003,17(1):45.
    [5]吴以岭.络病病因探析[J].疑难病杂志,2004,3(4):215.
    [6]Toh Y, Pencil SD, Nicolson GL. A novel candidatemetastasis-associated gene, Mtal, differentially expressed in highly metastatic mammary adenocarcinomacell lines. cDNA cloning, expression, and protein analyses. J Biol Chem.1994 Sep 16; 269 (37) 22958-63.
    [7]J Eskelinen MJ, Haglund UH. Prognosis of human pancreatic adenocarcinoma:review of clinical and histopathologieal variable and possible use of nowmolecularmethods [J]. Eur J Surg, 1999,165(4):292-306.
    [8]Neel BG, JhanWaR SC, Chaganti RS, et al. Two human. C-onc genes are located on the long arnl of chromosome. Proc Nail Acad Sci USA,1982; 79(24):7842-7846.
    [9]北川知行.(日文)早期癌的鉴别诊断与癌基因[J].癌临床,1988;34:1259.
    [10]谷文生,姜莉,张学,等.用聚合酶链反应检测小细胞肺癌myc族癌基因扩增的研究[J].中国医科大学学报,1994,23(3):203-206.
    [11]Zajac-Kaye M. C-myc oncogene:a key component in cell cycle regulation its implication for lung cancer [J]. Lung Cancer.2001 Dec,34 Suppl 2:S43-46.
    [12]陈杰.端粒酶逆转录酶和C-myc基因在肺癌中表达的研究[J].临床内科杂志.2003,(11):580-581.
    [13]李奇志,张胜名,毛永荣,等.非小细胞肺癌中c-myc蛋白表达及意义[J].Jounlal of Mathematjcal Medicime,2003,16(2):120-121.
    [14]马锴,沈毅.Survivin、p53及c-myc在食管鳞癌中的表达及临床意义[J].齐鲁医学杂志.2004,19(3):244-245.
    [15]刘乃国,马云,冯锐,等.p53、c-myc在口腔鳞癌中基因扩增和mRNA[J].滨州医学院学报,2003,26(3):401-404.
    [16]Flesher DW, Zetterberg A, Zhu JY, et al. Over expression of myc causes p53-dendent G2 arrest of nonnal fibroblasts [J]. Proc Nat-1 Acad Sci USA,2000,97 (19):10544-10547.
    [17]方志文,牟召霞,王新艳,等.p53与c-myc和cyclin B1在卵巢上皮性癌组织中的表达及意义[J].中华肿瘤防治杂志,2007,14(4):284-286.
    [1]程士德主编.内经[M].北京:人民卫生出版社,2006:289.
    [2]清·陈梦雷.古今图书集成·医部全录·诸疾·卷三百十六·积聚门[M].北京:人民卫生出版社,1962:2065.
    [3]丁光迪主编.诸病源候论校注[M].北京:人民卫生出版社,1991:578,610,564.
    [4]清·陈梦雷.古今图书集成·医部全录·诸疾·卷三百十六·积聚门[M].北京:人民卫生出版社,1962:2070.
    [5]明·张景岳.景岳全书.卷二十三[M].山西:山西科学技术出版社.2006:266.
    [6]明·李中梓.医宗必读[M].北京:人民卫生出版社.1995:378.
    [7]清·沈金鳘.杂病源流犀烛[M].北京:中国中医药出版社.1994:367.
    [8]清·唐容川.血证论[M].上海:上海人民出版社,1977:85.
    [9]明·罗周彦.医宗粹言[M].安徽:安徽科学技术出版社,2000:46.
    [10]李忠,陈信义.肺癌中医临床研究进展与用药思路[J].中国医药学报,2004,19(3):176-178.
    [11]朱华宇,周岱翰.益气解毒法治疗晚期肺癌的思路探讨[J].中华中医药杂志,2006,21(4):235-236.
    [12]刘嘉湘,刘苓霜.癌症的中医药治疗[J].抗癌,2006,12(3):20.
    [13]刘丽坤.肺癌的病机及治法探讨[J].中国中医基础医学杂志,2004,10(5):75.
    [14]崔永玲,李建生.治疗肺癌的经验[J].北京中医,2005,24(1):16.
    [15]刘嘉湘,施志明,李和根,等.益肺抗瘤饮治疗271例非小细胞肺癌临床观察.上海中医药杂志,2001,34(2):4-6.
    [16]王笑民,郁仁存,王禹堂,等.益气活血散结法配合化疗治疗晚期非小细胞肺癌的临床研究[J].中国中西医结合杂志,1997,17(2):86-87.
    [17]孙书贤,王笑民,郁仁存.益气活血法治疗晚期非小细胞肺癌的疗效分 析[J].中国中医药信息杂志,2002,9(7):57-58.
    [18]柴可群,王德玉.化痰祛瘀解毒法在肺癌治疗中的运用探讨[J].浙江中医杂志,2003,38(2):254-256.
    [19]左明焕,胡凯文,陈信义.痰瘀:非小细胞肺癌的证候特征[J].中国医药学报,2002,17(11):2-4.
    [20]洪广祥.治疗晚期肺癌的经验[J].新中医,1996,28(3):3-5.
    [21]辛海,马琴.防治恶性肿瘤转移的理论探讨[J].中国中医基础医学杂志,2004,12(2):45-47.
    [22]张健,李忠.固摄法的提出与恶性肿瘤的中医治疗探讨[J].中国医药学报,1997,12(6):12-14.
    [23]林洪生.威麦宁胶囊治疗非小细胞肺癌的临床研究[J].肿瘤研究与临床,2003,15(6):368-370.
    [24]娄金丽,林洪生.威麦宁体外枕肿瘤作用的实验研究浅探[J].中医药学刊.2004,22(5):810-811.
    [25]刘嘉湘.中医药在肿瘤治疗中的优势[J].抗癌,2003,(1):16-17.
    [26]周岱翰.中医肿瘤疗效评价系统在晚期非小细胞肺癌中的应用[J].中国肿瘤,2005,14(10):654-657.
    [27]杨葆康,姜仁成.灵仙丹熏吸疗法治疗中晚期肺癌66例[J].辽宁中医杂志,1994,21(7):323.
    [28]宣丽华,徐福,刘鲁明.温经膏穴位外敷治疗肺癌疗效观察[J].浙江中西医结合杂志, 2000,10(10):596-597.
    [29]杨爱光,王兴双.安肺膏外贴治疗肺癌[J].中医外治杂志,1996,13(2):31.
    [30]孟勇.华蟾素在中晚期肺癌介入治疗中的应用[J].新乡医学院学报,2000,17(4):266-267.
    [31]李永光,赵泉林,张盂香,等.气至病所治疗肺癌的初步研究[J].中国针灸,1989,2(3):24.
    [32]左秀玲.孔最穴在肺癌止痛中的应用[J].河北中医,1991.13(3):4.
    [33]杨维泓,沈敏鹤,刘鲁明,等.穴位注射治疗肺癌咯血40例[J].辽宁中医杂志,1992,3(2):30.
    [34]张洪亮,曾永秀.试述中医药防治肿瘤中存在的六个问题[J].新疆中医药,2001,19(2):1-2.
    [35]陈炜,石娇,李晋川,等.中西医结合治疗非小细胞肺癌的Meta分析[J].实用预防医学,2010,17(7)1360-1363.
    [36]李凡.中西医结合治疗非小细胞肺癌临床观察[J].实用中医药杂志,2007,23(2):97.

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