麻雷汤治疗自身免疫性甲状腺炎的实验研究
|
摘要
目的麻雷汤是导师许芝银教授数十年治疗自身免疫性甲状腺炎临床有效方。本实验拟通过观察麻雷汤的急性毒性；观察麻雷汤对EAT小鼠脾淋巴细胞增殖的影响；观察麻雷汤对EAT小鼠外周血T淋巴细胞亚群的影响；观察麻雷汤对EAT小鼠甲状腺激素及自身抗体水平影响；观察麻雷汤对EAT小鼠甲状腺组织病理形态学的影响；观察麻雷汤对EAT小鼠甲状腺组织VEGF、Fas/Fas-L表达的影响。为临床应用该方提供充分的理论和准确的实验数据；探究麻雷汤治疗AT的可能作用机制；探讨AT的病因病机及治疗大法。
方法麻雷汤的制备：麻黄300g,雷公藤300g,桃仁300g,肉桂300g。1200g生药煎成500ml水溶液,每ml含生药2.4g。
取ICR小鼠50只,体重18.0-22.0g,随机分为5组,每组10只,雌雄各半,每组给药剂量分别为：26.88g/kg、33.6g/kg、42.Og/kg、53. Og/kg、67.Og/kg。实验前禁食(不禁水)12h,各组分别按上述剂量0.4ml／10g小鼠灌胃给药,1日1次,连续给药2周,观察记录实验小鼠活动、行为及死亡情况。
取雌性ICR小鼠80只,体重18.0-22.0g,随机分为8组,每组10只。模型组小鼠于皮下多点注射含PTg(0.25mg／ml)完全弗氏佐剂抗原共0.2ml,连续2周,每周一次,第3周起每只小鼠皮下注射PTg(0.25mg/ml)不完全弗氏佐剂抗原0.2ml,连续3周,每周一次。除正常对照组外,其余各组小鼠每天给予饮用高碘水(1升水中加入0.64克碘化钾配制而成)。正常对照组和模型组均给予等容量生理盐水,甲状腺片组：10mg／kg,强的松组：10mg／kg,雷公藤组：25μg／kg,麻雷汤大剂量组：20g／kg；麻雷汤中剂量组：10g／kg；麻雷汤小剂量组：5g／kg。各组均灌胃给药,0.1ml／10g。造模2周后开始给药,连续4周,1日1次。每组取3只小鼠于末次给药后,摘眼球取血,处死,剪开腹膜取脾脏,观察EAT小鼠脾淋巴细胞增殖情况,流式细胞术检测外周血T淋巴细胞亚群。
取雌性ICR小鼠160只,体重18.0-22.0g,随机分为8组,每组20只。处理如前。造模2周后开始给药,连续4周,1日1次。采用放射免疫法检测T3、T4、FT3、FT4、TSH、TGAb和TMAb;甲状腺组织作常规苏木素一伊红染色；观察小鼠甲状腺激素及自身抗体水平；免疫组化检测甲状腺组织VEGF、Fas/Fas-L蛋白的表达。
结果麻雷汤经口给药,20只小鼠按96g／kg给药后均无异常情况发生,2周内亦无死亡,该剂量为成人日口服剂量的143倍(等效剂量的13倍)；模型组小鼠血清中高滴度甲状腺自身抗体TGAb.TMAb的检出(与正常组相比较P＜0.01),小鼠甲状腺组织的淋巴细胞浸润等表明成功复制出小鼠EAT模型；麻雷汤能抑制EAT小鼠脾淋巴细胞增殖(加或不加conA):调节其外周血T淋巴细胞亚群CD4+／CD8+；降低EAT小鼠甲状腺激素(T3、T4)及甲状腺自身抗体水平；减轻其甲状腺腺体扩张、破坏及淋巴细胞浸润；使EAT小鼠甲状腺组织VEGF及Fas／Fas-L低表达。
结论麻雷汤是安全有效的治疗AT药物；麻雷汤抑制EAT小鼠脾淋巴细胞增殖；调节其外周血T淋巴细胞亚群CD4+／CD8+;降低其甲状腺激素(T3、T4)及甲状腺自身抗体水平；减轻其甲状腺腺体扩张、破坏及淋巴细胞浸润；降低其甲状腺组织VEGF及Fas／Fas-L表达。先天禀赋不足是本病的发病的基础和前提；脾肾阳虚是本病发生的主要病理阶段；气滞、痰凝、血瘀三者互结是本病发生的核心机制。脾肾阳虚、痰瘀互结是AT患者的主要病机；温阳破瘀化痰是本病的主要治疗大法。麻雷汤是脾肾阳虚、痰瘀互结型AT患者安全有效的经验方。
Purpose:Ma Lei Tang is Professor Xu Zhiyin decades clinically effective treatment of autoimmune thyroiditis. In this study, by looking at Ma Lei Tang to be the acute toxicity; observation of Ma Lei Tang on EAT mice spleen lymphocyte proliferation; observation of Ma Lei Tang on EAT in mice peripheral blood T lymphocyte subsets; observation of Ma Lei Tang on EAT thyroid hormone and antibody levels in mice affected; observation of EAT in mice Ma Lei Tang on the impact of pathological thyroid tissue; observation of EAT in mice Ma Lei Tang on thyroid VEGF, Fas\Fas-L expression. For clinical application of the theory provided by full and accurate experimental data; explore the possible role of treatment Ma Lei Tang in AT mechanisms and Etiology, Pathogenesis and treatment of Dafa in AT.
Methods:Preparation of Ma Lei Tang:Ephedra 300g, triptolide 300g, peach kernel 300g, cinnamon 300g.1200g crude drugs fry 500ml aqueous solution, each ml containing crude drugs 2.4g. ICR mice were obtained 50, weighing 18.0-22.Og, were randomly divided into five groups of 10 male and female in half, each dose were: 26.88g/kg,33.6 g/kg,42.0 g/kg,53.0 g/kg,67.0g/kg. Fasting before the experiment (can not help but water) 12h, respectively, in each group according to the above dose 0.4ml/10g mice gavage,1,1, continuous administration of 2 weeks, mice were observed and recorded activities, behavior and circumstances of death.
80 female ICR mice were randomly divided into 8 groups of 10 mouse. Model group mice at the subcutaneous injection of multi-point PTg (0.25mg/ml) complete Freund's adjuvant antigens were 0.2ml, for 2 weeks, once a week,3rd week of each mice were injected subcutaneously PTg (0.25mg/ml) incomplete Freund's adjuvant antigen 0.2ml,3 consecutive weeks, once a week. In addition to the normal control group, the remaining mice in each group given a daily drink iodine water (1 liter in the preparation made by adding 0.64 grams potassium iodide). The normal control group and model group were given same volume of normal saline, thyroxine group: lOmg/kg, prednisone group:10mg/kg, tripterygium Group:25μg/kg, Ma Lei Tang high-dose group:20g/kg; Ma Lei Tang middle dose group:10g/kg; Ma Lei Tang low-dose group:5g/kg. In each group were gavage,0.1 ml/10g. Making model 2 weeks after administration for 4 weeks, qd. To take three mice in each group after the last administration, picking eye blood, death, cut to take the spleen peritoneum was observed EAT proliferation of mouse spleen lymphocytes by flow cytometry of peripheral blood T-lymphocyte subsets.
160 female ICR mice were taken randomly divided into eight groups, each with 20. Treatment as before. Making model 2 weeks after administration for 4 weeks,1 day. Using radioimmunoassay T3, T4, FT3, FT4, TSH, TGAb and TMAb; thyroid tissue for routine hematoxylin-eosin stain; observation of thyroid hormone and antibody levels in mice; Immunohistochemical detection of thyroid tissue VEGF, Fas\ Fas-L protein expression.
Results:Ma Lei Tang after oral administration,20 mice after administration by 96g/kg no exception happens, there is no death within 2 weeks, the dose for an adult day oral doses of 143 times (equivalent dose of 13 times); model group of high serum titer of thyroid autoantibodies TGAb, TMAb detection (compared with normal group P<0.01), infiltration of lymphocytes in thyroid tissue in mice, suggests that to replicate the success of mouse EAT model; Ma EAT Ray Tang can inhibit the proliferation of mouse spleen lymphocytes (with or without conA); adjust their peripheral blood T-lymphocyte subsets CD4+/CD8+; reduce the EAT in mice of thyroid hormone (T3, T4) and thyroid antibody levels; mitigate its thyroid gland expansion, destruction and lymphocyte infiltration; to EAT mice thyroid tissue VEGF and Fas, Fas-L with low expression.
Conclusion:Ma Lei Tang is safe and effective treatment for AT drugs; Ma Lei Tang inhibited proliferation of mouse spleen lymphocytes EAT; adjust their peripheral blood T-lymphocyte subsets CD4+/CD8+; to reduce their thyroid hormone (T3, T4) and thyroid antibodies level; mitigate the thyroid gland expansion, destruction and lymphocyte infiltration; reduce their thyroid tissue VEGF and Fas, Fas-L expression. Congenital lack of disease incidence is the basis and prerequisite; spleen deficiency is Benbingfasheng The major pathological stage; Qi stagnation, Tanning, blood stasis three each node is the core mechanism Benbingfasheng. Spleen and kidney yang deficiency, phlegm and blood stasis is the main pathogenesis of patients with EAT; Onyang Po Yu phlegm is the main treatment of this disease Dafa. Ma Ray Tom is a spleen deficiency, phlegm and blood stasis type safe and effective in patients with AT experience side.
方法麻雷汤的制备：麻黄300g,雷公藤300g,桃仁300g,肉桂300g。1200g生药煎成500ml水溶液,每ml含生药2.4g。
取ICR小鼠50只,体重18.0-22.0g,随机分为5组,每组10只,雌雄各半,每组给药剂量分别为：26.88g/kg、33.6g/kg、42.Og/kg、53. Og/kg、67.Og/kg。实验前禁食(不禁水)12h,各组分别按上述剂量0.4ml／10g小鼠灌胃给药,1日1次,连续给药2周,观察记录实验小鼠活动、行为及死亡情况。
取雌性ICR小鼠80只,体重18.0-22.0g,随机分为8组,每组10只。模型组小鼠于皮下多点注射含PTg(0.25mg／ml)完全弗氏佐剂抗原共0.2ml,连续2周,每周一次,第3周起每只小鼠皮下注射PTg(0.25mg/ml)不完全弗氏佐剂抗原0.2ml,连续3周,每周一次。除正常对照组外,其余各组小鼠每天给予饮用高碘水(1升水中加入0.64克碘化钾配制而成)。正常对照组和模型组均给予等容量生理盐水,甲状腺片组：10mg／kg,强的松组：10mg／kg,雷公藤组：25μg／kg,麻雷汤大剂量组：20g／kg；麻雷汤中剂量组：10g／kg；麻雷汤小剂量组：5g／kg。各组均灌胃给药,0.1ml／10g。造模2周后开始给药,连续4周,1日1次。每组取3只小鼠于末次给药后,摘眼球取血,处死,剪开腹膜取脾脏,观察EAT小鼠脾淋巴细胞增殖情况,流式细胞术检测外周血T淋巴细胞亚群。
取雌性ICR小鼠160只,体重18.0-22.0g,随机分为8组,每组20只。处理如前。造模2周后开始给药,连续4周,1日1次。采用放射免疫法检测T3、T4、FT3、FT4、TSH、TGAb和TMAb;甲状腺组织作常规苏木素一伊红染色；观察小鼠甲状腺激素及自身抗体水平；免疫组化检测甲状腺组织VEGF、Fas/Fas-L蛋白的表达。
结果麻雷汤经口给药,20只小鼠按96g／kg给药后均无异常情况发生,2周内亦无死亡,该剂量为成人日口服剂量的143倍(等效剂量的13倍)；模型组小鼠血清中高滴度甲状腺自身抗体TGAb.TMAb的检出(与正常组相比较P＜0.01),小鼠甲状腺组织的淋巴细胞浸润等表明成功复制出小鼠EAT模型；麻雷汤能抑制EAT小鼠脾淋巴细胞增殖(加或不加conA):调节其外周血T淋巴细胞亚群CD4+／CD8+；降低EAT小鼠甲状腺激素(T3、T4)及甲状腺自身抗体水平；减轻其甲状腺腺体扩张、破坏及淋巴细胞浸润；使EAT小鼠甲状腺组织VEGF及Fas／Fas-L低表达。
结论麻雷汤是安全有效的治疗AT药物；麻雷汤抑制EAT小鼠脾淋巴细胞增殖；调节其外周血T淋巴细胞亚群CD4+／CD8+;降低其甲状腺激素(T3、T4)及甲状腺自身抗体水平；减轻其甲状腺腺体扩张、破坏及淋巴细胞浸润；降低其甲状腺组织VEGF及Fas／Fas-L表达。先天禀赋不足是本病的发病的基础和前提；脾肾阳虚是本病发生的主要病理阶段；气滞、痰凝、血瘀三者互结是本病发生的核心机制。脾肾阳虚、痰瘀互结是AT患者的主要病机；温阳破瘀化痰是本病的主要治疗大法。麻雷汤是脾肾阳虚、痰瘀互结型AT患者安全有效的经验方。
Purpose:Ma Lei Tang is Professor Xu Zhiyin decades clinically effective treatment of autoimmune thyroiditis. In this study, by looking at Ma Lei Tang to be the acute toxicity; observation of Ma Lei Tang on EAT mice spleen lymphocyte proliferation; observation of Ma Lei Tang on EAT in mice peripheral blood T lymphocyte subsets; observation of Ma Lei Tang on EAT thyroid hormone and antibody levels in mice affected; observation of EAT in mice Ma Lei Tang on the impact of pathological thyroid tissue; observation of EAT in mice Ma Lei Tang on thyroid VEGF, Fas\Fas-L expression. For clinical application of the theory provided by full and accurate experimental data; explore the possible role of treatment Ma Lei Tang in AT mechanisms and Etiology, Pathogenesis and treatment of Dafa in AT.
Methods:Preparation of Ma Lei Tang:Ephedra 300g, triptolide 300g, peach kernel 300g, cinnamon 300g.1200g crude drugs fry 500ml aqueous solution, each ml containing crude drugs 2.4g. ICR mice were obtained 50, weighing 18.0-22.Og, were randomly divided into five groups of 10 male and female in half, each dose were: 26.88g/kg,33.6 g/kg,42.0 g/kg,53.0 g/kg,67.0g/kg. Fasting before the experiment (can not help but water) 12h, respectively, in each group according to the above dose 0.4ml/10g mice gavage,1,1, continuous administration of 2 weeks, mice were observed and recorded activities, behavior and circumstances of death.
80 female ICR mice were randomly divided into 8 groups of 10 mouse. Model group mice at the subcutaneous injection of multi-point PTg (0.25mg/ml) complete Freund's adjuvant antigens were 0.2ml, for 2 weeks, once a week,3rd week of each mice were injected subcutaneously PTg (0.25mg/ml) incomplete Freund's adjuvant antigen 0.2ml,3 consecutive weeks, once a week. In addition to the normal control group, the remaining mice in each group given a daily drink iodine water (1 liter in the preparation made by adding 0.64 grams potassium iodide). The normal control group and model group were given same volume of normal saline, thyroxine group: lOmg/kg, prednisone group:10mg/kg, tripterygium Group:25μg/kg, Ma Lei Tang high-dose group:20g/kg; Ma Lei Tang middle dose group:10g/kg; Ma Lei Tang low-dose group:5g/kg. In each group were gavage,0.1 ml/10g. Making model 2 weeks after administration for 4 weeks, qd. To take three mice in each group after the last administration, picking eye blood, death, cut to take the spleen peritoneum was observed EAT proliferation of mouse spleen lymphocytes by flow cytometry of peripheral blood T-lymphocyte subsets.
160 female ICR mice were taken randomly divided into eight groups, each with 20. Treatment as before. Making model 2 weeks after administration for 4 weeks,1 day. Using radioimmunoassay T3, T4, FT3, FT4, TSH, TGAb and TMAb; thyroid tissue for routine hematoxylin-eosin stain; observation of thyroid hormone and antibody levels in mice; Immunohistochemical detection of thyroid tissue VEGF, Fas\ Fas-L protein expression.
Results:Ma Lei Tang after oral administration,20 mice after administration by 96g/kg no exception happens, there is no death within 2 weeks, the dose for an adult day oral doses of 143 times (equivalent dose of 13 times); model group of high serum titer of thyroid autoantibodies TGAb, TMAb detection (compared with normal group P<0.01), infiltration of lymphocytes in thyroid tissue in mice, suggests that to replicate the success of mouse EAT model; Ma EAT Ray Tang can inhibit the proliferation of mouse spleen lymphocytes (with or without conA); adjust their peripheral blood T-lymphocyte subsets CD4+/CD8+; reduce the EAT in mice of thyroid hormone (T3, T4) and thyroid antibody levels; mitigate its thyroid gland expansion, destruction and lymphocyte infiltration; to EAT mice thyroid tissue VEGF and Fas, Fas-L with low expression.
Conclusion:Ma Lei Tang is safe and effective treatment for AT drugs; Ma Lei Tang inhibited proliferation of mouse spleen lymphocytes EAT; adjust their peripheral blood T-lymphocyte subsets CD4+/CD8+; to reduce their thyroid hormone (T3, T4) and thyroid antibodies level; mitigate the thyroid gland expansion, destruction and lymphocyte infiltration; reduce their thyroid tissue VEGF and Fas, Fas-L expression. Congenital lack of disease incidence is the basis and prerequisite; spleen deficiency is Benbingfasheng The major pathological stage; Qi stagnation, Tanning, blood stasis three each node is the core mechanism Benbingfasheng. Spleen and kidney yang deficiency, phlegm and blood stasis is the main pathogenesis of patients with EAT; Onyang Po Yu phlegm is the main treatment of this disease Dafa. Ma Ray Tom is a spleen deficiency, phlegm and blood stasis type safe and effective in patients with AT experience side.
引文
[1]穆耕林.温阳化痰法治疗小鼠自身免疫性甲状腺炎的实验研究[D].南京：南京中医学院,1992
[2]魏友松.益气养阴法治疗自身免疫性甲状腺炎的实验研究[D].南京：南京中医学院,1994.
[3]魏友松,许芝银.麻黄、雷公藤、黄蜀葵花对自身免疫性甲状腺炎小鼠模型的影响[J].南京中医药大学学报,1997,(4)：25.
[4]朱云华,许芝银,孙景军,等.中药治疗实验性自身免疫性甲状腺炎中甲状腺球蛋白的免疫组化观察[J].南京中医药大学学报,1996,12(3)：31-32.
[5]孙景军,朱云华,穆耕林,等.中药治疗EAT的病理组织学和超微结构变化的观察[J].南京中医药大学学报,1999,15(3)：155-156.
[6]陈荣明等.麻黄中不同提取物对细胞免疫的影响[J].南京中医药大学学报(自然科学版)2001,17(4)：234-236.
[7]华川,许芝银。雷公藤治疗桥本氏甲状腺炎实验研究[J].实用中医药杂志,2003,(8)：397-399.
[8]华川,许芝银.温瘿消治疗桥本氏甲状腺炎的实验研究[J].江苏中医药,2003,(8)：52-54.
[9]孟达理,严士海,许芝银.麻黄多糖对绵羊红细胞所致小鼠溶血素生成的影响[J].江苏大学学报2007,17(5)：379-380.
[1]张伯臾主编.中医内科学[M].上海：海科学技术出版社,1989：218.
[2]陈如泉.慢性林巴细胞性甲状腺炎30例临床分析及辨证治疗[J].现代中医杂志,1993,7：1-3.
[3]陈志才,许芝银.扶正消瘿法治疗自身免疫性甲状腺炎38例临床观察[J].中国中西医结合杂志,1992,12(10)：611.
[4]卑其新.试论桥本氏病的辨证论治.全国第三界中医甲状腺病学术交流余论文集[C],1993,69-70.
[5]梁德进.从肝论治桥本氏病12例临床分析[J].内部资料.
[6]程如林,高寅香,叶正宝,等.雷公藤多甙片和甲状腺片冶疗慢性淋巴细胞性甲状腺炎疗效观察[J].中西医结合杂志,1988,8(11)：676.
[7]卞卫和,许芝银.扶正法在治疗甲状腺疾病中的应用[J].山西中医,1997,13(3)：54.
[8]伍锐敏,徐蒙,郎琳娜,等.桥本氏病56例临床治疗报告[J].中医杂志,1992,5：33.
[9]王孜优,张海发.理气滋肾法治疗慢性淋巴细胞性甲状腺炎133例[J].辽宁中医杂志,1989,11：617-618.
[10]肖秋生,王孜优.复方香附散治疗漫性淋巴性甲状腺炎265例[J].吉林中医药,1994,1：18-19.
[11]邝安堃,丁霆,陈家伦,等.中医辨证论治对原发性甲状腺功能减退的疗效与淋巴细胞核T3受体的关系[J].中西医结合杂志,1988,8(11)：650.
[12]卞卫和,许芝银.治疗自身免疫性甲状腺炎65例临床小结[J].河南中医,1997,17(2)：100-101.
[13]刘晓鹄,唐汉钧.益气养阴消瘿法治疗桥本氏甲状腺炎22例[J].新中医,1999,31(10)：33-34.
[14]吕月婵,王浩然.甲状腺免疫合剂对桥本氏甲状腺炎红细胞免疫功能的调节作用[J].中国中西医结合杂志,1995,15(7)：414-415
[15]黄庆仪.五加双参片对自身免疫性甲状腺TGA、TMA的影响[J].甘肃中医,2001,(3)：86-88.
[16]方德龄,傅冬芹.雷公藤和甲状腺片治疗桥本氏甲状腺炎[J].实用中西医结合杂志,1998,11(3)：281.
[17]张闿珍.80例甲状腺结节的中西医结合治疗[J].福建中医药,1988,1：19.
[18]林益川,张闿珍,方志平,等.48例桥本氏甲状腺炎的中西医结合治疗[J].福建中医药, 1996,27(4)：1-2.
[19]孔德明,刑玫,詹继红,等.中西医结合治疗桥本氏甲状腺炎的疗效观察[J].中国医药学报,1998,13(3)：35-37.
[20]孙燕,吴葆莹.中西医结合诊治桥本氏甲状腺炎[J].天津医科大学学报,1999,5(3)：74-75.
[21]牟丽平.雷公藤片佐治慢性淋巴细胞性甲状腺炎25例[J].蚌埠医学院学报,2000,25(4)：254-255.
[22]桂金水,严华,徐明海,等.不同灸法对人体免疫功能的影响[J].上海针灸杂志,1983,4： 21.
[23]胡国盛,陈汉平,侯永健,等.隔药灸治疗桥本氏甲状腺炎临床观察[J],中医杂志,1992,5： 30.
[24]卞卫和,许芝银.蜂毒治疗桥本氏病32例[J],南京中医药大学学报,1995,11(5)：45-46.
[25]孟凡江,冯莉.昆明山海棠降低桥本氏甲状腺炎患者血清TMAb和TGAb水平的研究[J].陕西医学杂志,1992,5：261.
[26]沈鸣,姚国英,方林钧.雷公藤多甙片治疗慢性淋巴细胞性甲状腺炎[J].上海医药,1996,(10)：21-22.
[27]周惠民.黄药子治疗桥本氏甲状腺炎引起中毒性肝炎3例报告[J].山东中医杂志,1989,13(2)：29.
[28]Estienne V, DuthoitC, CostanzoVD, et al.Multicenter study on TGPOautoantibody prevalence in various thyroid and non-thyroid diseases:relationships with thyroglobul in and thyroperoxidase autoant ibody parameters[J]. Eur J Endocrinol.1999 Dec,141(6):563～569.
[29]Cohen SB, Weetman AP. Antithyroid drugs ameliorate thymectomy-induced experimental autoimmunethyroiditis[J]. Autoiillmunity,1988,1(1):51-58.
[30]Fournier c, GepnerP, sadoukM, et al. In Vivo beneficial effects of cyclosporin A and 1,25-dihydroxyvitamin D3 On the induction of experimental autoimmune thyroiditis[J]. Clin Immunol Immunopathol 1990,54(1):53-63.
[31]Ansar Ahmeds, Young PR, Penhale WJ. Beneficial effect of testosterone in the treatment of chronic autoimmune thyroiditis in rats[J].J Immunol 1986 Jan, 136(1):143-147.
[32]Barbesino G, Chiovato L. The genetics of Hashimoto's disease[J]. Endocrinol Metab C1 in North Am 2000 Jun,29(2):357-374.
[33]seissler J, Wagners, schott M, et al. Low frequency of autoantibodies to the human Na(+)/I (-)symporter in patients with autoimmune thyroid disease[J], J clin Endocrinol Metab 2000 Dec,85(12):4630-4634.
[34]陈慎仁,黄焕坚,林延德.Fas-L/Fas与自身免疫性甲状腺炎[J].国外医学·内分泌学分册,2000,20(4)：175-178.
[35]Muller-Hocker J. Expression of bcl-2, Bax and Fas in oxyphil cells of Hashimoto thyroiditis[J].Virch OWS Arch 2000 Jun,436(6):602-607.
[36]KongYC, David CS. New revelations insusceptibility to autoimmune thyroiditis by the use of H2 and HLA class II transgenic models[J].Int Rev Immunol 2000.19(6): 573-585.
[37]Carayanniotis G, Kongy C. Pathogenic thyroglobulin peptides as model antigens: insights On the induction and maintenance Of autoimmune thyroiditis[J]. Int Rev Immunel 2000,19(6):557-572.
[38]WatanabeH, InabaM, Adachi Y, et al. Experimental autoimmune thyroiditis induced by thyroglobulin-pulsed dendritic cells[J]. Autoimmunity 1999,31(4):273-282.
[39]Nakashima M, Kong, Davies TF. The role of T cells expressing TcR V beta 13 in autoimmune thyroiditis induced by transfer of mouse thyroglobul in-act ivated lymphocytes:identification of two common CDR3 motifs[J].Clin Immuno Immunopathel 1996 Aug,80(2):204-210.
[40]Wnliams WV, Kyriakos M, Sharp GC, et al. The role of cellular proliferation in the induction of experimental autoimmune thyroiditis(EAT)in mice[J].Cell Immunol 1986 Nov,103(1):96-104.
[41]ChenK, Wei Y, SharpGC, et al. Characterization of thyroid fibrosis in a murine model of granulomatous experimental autoimmune thyroiditis[J].J Leukoc Biol 2000 Dec,68(6):828-835.
[42]陆凤先,戴承凯,王伟,等.甲状腺抗原诱导大鼠实验性自身免疫性甲状腺炎的研究[J].中华内分泌代谢杂志,1998,14(4)：252-256.
[43]王胜军,许化溪,刘恭植,等.树突状细胞对小鼠实验性自身免疫性甲状腺炎的作用[J].中国免疫学杂志,1999,15(7)：294-295.298.
1.张波.慢性淋巴细胞甲状腺炎的研究进展[J].国外医学外科学分册,1996,23(6)：331-335.
2.Feltkamp TEW, Aarden LA, Lucas CJ, et al. Genetic risk factor for autoimmune disease[J]. Immunol Today,1999,20(1):10.
3.边杰,王广回,王智慧.甲状腺疾病的诊断与冶疗.北京：人民卫生出版社出版,1984：306-320.
4.陈晓城.麻黄的药理作用研究进展[J],实用中医药杂志,2005,21(1)：58.
5.魏友松,许芝银.麻黄、雷公藤、黄蜀葵花对自身免疫性甲状腺炎小鼠模型的影响[J],南京中医药大学学报,1996,12(4)：25.
6.陈荣明,朱耕新,许芝银.麻黄中不同提取物对细胞免疫的影响[J],南京中医药大学学报(自然科学版),2001,17(4)：234.
7.杨康,刘维永,白云.草麻黄中补体抑制成分的纯化和活性[J],四军医大学学报,2000,21(12)：1558.
8. Gu WZ, Brandwein SR. Inhibition of typeⅡcollageninduced arthritis in rats by triptolide[J].Int Immunopharmacol,1998,20(8):389.
9.李瑞林,舒达夫主编.雷公藤的研究与临床应用[M].北京：中国科学技术出版社,1989：193-195
10.秦风华,谢蜀生,龙振洲.雷公藤总甙免疫抑制作用的机制[J].中国药理学通报,1991,7(6)：433.
11.曹敏,孙荣奇,吴达俊.中药雷公藤的研究进展[J],中成药,1996,18(4)：41.
12.田荻,辛红,秦建中.雷公藤甲素对人外周血白细胞分泌促炎症性细胞因子的影响[J],上海免疫学杂志,1997,17(1)：55.
13.吴俊,梁晓燕,杨奕,等.雷公藤Ly-22.2+细胞的激活作用[J].中国病理生理杂志,1996,12(1)：30-31.
14.范祖森,曹荣华,张庆殷,等.雷公藤多甙对大鼠佐剂性关节炎治疗作用和免疫机制研究[J].中国药理学通报,1996(6)：527.
15.林小明.桃仁化学成分和药理作用研究进展[J],蛇志,2007,19(2)：130-132.
16.赵素莲,戴兆雄.苦杏仁甙对小鼠脾脏NK细胞活性的影响[J],山西医学院学报,1993,(1)：14.
17.赵素莲,刘桂芬.苦杏仁甙对小鼠免疫功能的影响[J],山西医药杂志,1993,(3)166.
18.刘英,张伟刚,王雅贤,等.炒桃仁总蛋白对小鼠B细胞功能影响的实验研究[J].中医药学报,2001,29(2)：55-56.
19.许惠玉,运晨霞,王雅贤.桃仁总蛋白对荷瘤鼠T淋巴细胞亚群及细胞凋亡的影响[J].齐齐哈尔医学院学报,2004,25(5)：485-487.
20.昌跃山,王雅贤,运晨霞,等.桃仁总蛋白对荷瘤鼠1L-2、IL-4水平的影响[J].中医药信息,2004,21(4)：60-61.
21.刘英,张伟兵,张鹏宇,等.炒桃仁总蛋白对TNF-α、 IL-2产生水平的影响[J].中医药学 报,2001,29(4)；51-52.
22.张明发,沈雅琴.肉桂的药理作用及温里功效[J].陕西中医,1995,16(1)：39-42.
23.田端守.桂皮的药理和药效[J].国外医药植物药分册,1994,9(1)：15.
24.曾雪瑜,陈雪芬,韦宝伟,等.肉桂提取物对免疫功能影响的研究[J].广西医学,1984,6(2)：62.
25. Lee HS, Kim BS, Kim MK. Suppression effect of Cinnamomum cassia bark-derived component on nitric oxide synthase[J]. J Agile Food Chem,2002,50(26):7700-7703.
26. Lee SH,Lee SY, Son DJ, et al. Inhibitory effect of 2-hydroxycin namaldehyde on nitric oxide production through inhibition of NF-kappa B activation in RAW 264.7 cells[J]. Biochem Pharmaeol,2005,69(5):791-799.
[1]国家药品监督管理局.中药天然药物研究技术指导原则[M].2005,85
[2]陈奇主编.中药药理研究方法学[M].北京：人民卫生出版社,第1版,2000,112-118
[3]徐淑云主编.药理学实验方法学[M].北京：人民卫生出版社,2002,227-228
1.朱立平,陈学清.免疫学常用实验方法[M].北京：人民军医出版社,2000.26-28.
2.罗敏.分子内分泌学(基础与临床)[M].北京：人民军医出版社.2003.197-198.
3.王云峰,魏枫.桥本甲状腺炎治疗前后淋巴细胞亚群及细胞学的变化[J].内蒙古医学 杂志,2007,39(4)：426-428.
4.钟述猷,董晖,张宝泉,等.自身免疫性甲状腺疾病患者淋巴细胞亚群和自身抗体的检测及其临床意义[J].天津医药,1994,22(7)：391.
1.朱立平,陈学清.免疫学常用实验方法[M].北京：人民军医出版社,2000.26-28.
2.罗敏.分子内分泌学(基础与临床)[M].北京：人民军医出版社.2003.197-198.
3.张志远,郑武飞.Graves病和桥本氏甲状腺炎患者的T淋巴细胞亚群异常[J].国外医学·内分泌学分册,1984,9(3)：134.
4.王云峰,魏枫.桥本甲状腺炎治疗前后淋巴细胞亚群及细胞学的变化[J].内蒙古医学杂志,2007,39(4)：426-428.
5.钟述猷,董晖,张宝泉,等.自身免疫性甲状腺疾病患者淋巴细胞亚群和自身抗体的检测及其临床意义[J].天津医药,1994,22(7)：391.
1.张均田.现代药理实验方法[M].北京：北京医科大学中国协和医科大学联合出版社,1999：680-688.
2.朱立平,陈学清.免疫学常用实验方法[M].北京：人民军医出版社,2000.26-28
3.白耀.甲状腺病学[M].北京：科学技术文献出版社,145-161
4.孙葳,宋光华,贺斌.碘和甲状腺球蛋白诱导大鼠实验性自身免疫性甲状腺炎的研究[J].中华内科杂志,2000,39(12)：841-842.
5.吴拥军,许芝银,高国宇,等.麻黄桃仁颗粒对实验性自身免疫性甲状腺炎体液免疫作用的研究[J].辽宁中医杂志,2006,33(11)：1506
1.张均田.现代药理实验方法[M].北京：北京医科大学中国协和医科大学联合出版社,1999：680-688.
2.朱立平,陈学清.免疫学常用实验方法[M].北京：人民军医出版社,2000.26-28.
1.张均田.现代药理实验方法[M].北京：北京医科大学中国协和医科大学联合出版社,1999：680-688.
2.朱立平,陈学清.免疫学常用实验方法[M].北京：人民军医出版社,2000.26-28.
3. FavaRA, OlsenNJ, SppencerGreeng, etal. Vascualar permeability factor endothelial growth factor(VPF VEGF). accumulation and expression in human synovial fluids and rheumatoid syovial tissue[J].J Exp Med.1994,180:341.
1.张均田.现代药理实验方法[M].北京：北京医科大学中国协和医科大学联合出版社,1999：680-688.
2.朱立平,陈学清.免疫学常用实验方法[M].北京：人民军医出版社,2000.26-28.
3.张雅萍,姬秋如,张万会,等.桥本甲状腺炎中Fas和Fas-L的表达[J].第四军医大学学报,2000；21(2)：223-225.
4.高福智,陈晓梅,赵文革,等.Fas系统介导的细胞凋亡与大鼠自体免疫性甲状腺炎的研究[J].内分泌外科杂志,2008,3(2)：76-78.
[2]魏友松.益气养阴法治疗自身免疫性甲状腺炎的实验研究[D].南京：南京中医学院,1994.
[3]魏友松,许芝银.麻黄、雷公藤、黄蜀葵花对自身免疫性甲状腺炎小鼠模型的影响[J].南京中医药大学学报,1997,(4)：25.
[4]朱云华,许芝银,孙景军,等.中药治疗实验性自身免疫性甲状腺炎中甲状腺球蛋白的免疫组化观察[J].南京中医药大学学报,1996,12(3)：31-32.
[5]孙景军,朱云华,穆耕林,等.中药治疗EAT的病理组织学和超微结构变化的观察[J].南京中医药大学学报,1999,15(3)：155-156.
[6]陈荣明等.麻黄中不同提取物对细胞免疫的影响[J].南京中医药大学学报(自然科学版)2001,17(4)：234-236.
[7]华川,许芝银。雷公藤治疗桥本氏甲状腺炎实验研究[J].实用中医药杂志,2003,(8)：397-399.
[8]华川,许芝银.温瘿消治疗桥本氏甲状腺炎的实验研究[J].江苏中医药,2003,(8)：52-54.
[9]孟达理,严士海,许芝银.麻黄多糖对绵羊红细胞所致小鼠溶血素生成的影响[J].江苏大学学报2007,17(5)：379-380.
[1]张伯臾主编.中医内科学[M].上海：海科学技术出版社,1989：218.
[2]陈如泉.慢性林巴细胞性甲状腺炎30例临床分析及辨证治疗[J].现代中医杂志,1993,7：1-3.
[3]陈志才,许芝银.扶正消瘿法治疗自身免疫性甲状腺炎38例临床观察[J].中国中西医结合杂志,1992,12(10)：611.
[4]卑其新.试论桥本氏病的辨证论治.全国第三界中医甲状腺病学术交流余论文集[C],1993,69-70.
[5]梁德进.从肝论治桥本氏病12例临床分析[J].内部资料.
[6]程如林,高寅香,叶正宝,等.雷公藤多甙片和甲状腺片冶疗慢性淋巴细胞性甲状腺炎疗效观察[J].中西医结合杂志,1988,8(11)：676.
[7]卞卫和,许芝银.扶正法在治疗甲状腺疾病中的应用[J].山西中医,1997,13(3)：54.
[8]伍锐敏,徐蒙,郎琳娜,等.桥本氏病56例临床治疗报告[J].中医杂志,1992,5：33.
[9]王孜优,张海发.理气滋肾法治疗慢性淋巴细胞性甲状腺炎133例[J].辽宁中医杂志,1989,11：617-618.
[10]肖秋生,王孜优.复方香附散治疗漫性淋巴性甲状腺炎265例[J].吉林中医药,1994,1：18-19.
[11]邝安堃,丁霆,陈家伦,等.中医辨证论治对原发性甲状腺功能减退的疗效与淋巴细胞核T3受体的关系[J].中西医结合杂志,1988,8(11)：650.
[12]卞卫和,许芝银.治疗自身免疫性甲状腺炎65例临床小结[J].河南中医,1997,17(2)：100-101.
[13]刘晓鹄,唐汉钧.益气养阴消瘿法治疗桥本氏甲状腺炎22例[J].新中医,1999,31(10)：33-34.
[14]吕月婵,王浩然.甲状腺免疫合剂对桥本氏甲状腺炎红细胞免疫功能的调节作用[J].中国中西医结合杂志,1995,15(7)：414-415
[15]黄庆仪.五加双参片对自身免疫性甲状腺TGA、TMA的影响[J].甘肃中医,2001,(3)：86-88.
[16]方德龄,傅冬芹.雷公藤和甲状腺片治疗桥本氏甲状腺炎[J].实用中西医结合杂志,1998,11(3)：281.
[17]张闿珍.80例甲状腺结节的中西医结合治疗[J].福建中医药,1988,1：19.
[18]林益川,张闿珍,方志平,等.48例桥本氏甲状腺炎的中西医结合治疗[J].福建中医药, 1996,27(4)：1-2.
[19]孔德明,刑玫,詹继红,等.中西医结合治疗桥本氏甲状腺炎的疗效观察[J].中国医药学报,1998,13(3)：35-37.
[20]孙燕,吴葆莹.中西医结合诊治桥本氏甲状腺炎[J].天津医科大学学报,1999,5(3)：74-75.
[21]牟丽平.雷公藤片佐治慢性淋巴细胞性甲状腺炎25例[J].蚌埠医学院学报,2000,25(4)：254-255.
[22]桂金水,严华,徐明海,等.不同灸法对人体免疫功能的影响[J].上海针灸杂志,1983,4： 21.
[23]胡国盛,陈汉平,侯永健,等.隔药灸治疗桥本氏甲状腺炎临床观察[J],中医杂志,1992,5： 30.
[24]卞卫和,许芝银.蜂毒治疗桥本氏病32例[J],南京中医药大学学报,1995,11(5)：45-46.
[25]孟凡江,冯莉.昆明山海棠降低桥本氏甲状腺炎患者血清TMAb和TGAb水平的研究[J].陕西医学杂志,1992,5：261.
[26]沈鸣,姚国英,方林钧.雷公藤多甙片治疗慢性淋巴细胞性甲状腺炎[J].上海医药,1996,(10)：21-22.
[27]周惠民.黄药子治疗桥本氏甲状腺炎引起中毒性肝炎3例报告[J].山东中医杂志,1989,13(2)：29.
[28]Estienne V, DuthoitC, CostanzoVD, et al.Multicenter study on TGPOautoantibody prevalence in various thyroid and non-thyroid diseases:relationships with thyroglobul in and thyroperoxidase autoant ibody parameters[J]. Eur J Endocrinol.1999 Dec,141(6):563～569.
[29]Cohen SB, Weetman AP. Antithyroid drugs ameliorate thymectomy-induced experimental autoimmunethyroiditis[J]. Autoiillmunity,1988,1(1):51-58.
[30]Fournier c, GepnerP, sadoukM, et al. In Vivo beneficial effects of cyclosporin A and 1,25-dihydroxyvitamin D3 On the induction of experimental autoimmune thyroiditis[J]. Clin Immunol Immunopathol 1990,54(1):53-63.
[31]Ansar Ahmeds, Young PR, Penhale WJ. Beneficial effect of testosterone in the treatment of chronic autoimmune thyroiditis in rats[J].J Immunol 1986 Jan, 136(1):143-147.
[32]Barbesino G, Chiovato L. The genetics of Hashimoto's disease[J]. Endocrinol Metab C1 in North Am 2000 Jun,29(2):357-374.
[33]seissler J, Wagners, schott M, et al. Low frequency of autoantibodies to the human Na(+)/I (-)symporter in patients with autoimmune thyroid disease[J], J clin Endocrinol Metab 2000 Dec,85(12):4630-4634.
[34]陈慎仁,黄焕坚,林延德.Fas-L/Fas与自身免疫性甲状腺炎[J].国外医学·内分泌学分册,2000,20(4)：175-178.
[35]Muller-Hocker J. Expression of bcl-2, Bax and Fas in oxyphil cells of Hashimoto thyroiditis[J].Virch OWS Arch 2000 Jun,436(6):602-607.
[36]KongYC, David CS. New revelations insusceptibility to autoimmune thyroiditis by the use of H2 and HLA class II transgenic models[J].Int Rev Immunol 2000.19(6): 573-585.
[37]Carayanniotis G, Kongy C. Pathogenic thyroglobulin peptides as model antigens: insights On the induction and maintenance Of autoimmune thyroiditis[J]. Int Rev Immunel 2000,19(6):557-572.
[38]WatanabeH, InabaM, Adachi Y, et al. Experimental autoimmune thyroiditis induced by thyroglobulin-pulsed dendritic cells[J]. Autoimmunity 1999,31(4):273-282.
[39]Nakashima M, Kong, Davies TF. The role of T cells expressing TcR V beta 13 in autoimmune thyroiditis induced by transfer of mouse thyroglobul in-act ivated lymphocytes:identification of two common CDR3 motifs[J].Clin Immuno Immunopathel 1996 Aug,80(2):204-210.
[40]Wnliams WV, Kyriakos M, Sharp GC, et al. The role of cellular proliferation in the induction of experimental autoimmune thyroiditis(EAT)in mice[J].Cell Immunol 1986 Nov,103(1):96-104.
[41]ChenK, Wei Y, SharpGC, et al. Characterization of thyroid fibrosis in a murine model of granulomatous experimental autoimmune thyroiditis[J].J Leukoc Biol 2000 Dec,68(6):828-835.
[42]陆凤先,戴承凯,王伟,等.甲状腺抗原诱导大鼠实验性自身免疫性甲状腺炎的研究[J].中华内分泌代谢杂志,1998,14(4)：252-256.
[43]王胜军,许化溪,刘恭植,等.树突状细胞对小鼠实验性自身免疫性甲状腺炎的作用[J].中国免疫学杂志,1999,15(7)：294-295.298.
1.张波.慢性淋巴细胞甲状腺炎的研究进展[J].国外医学外科学分册,1996,23(6)：331-335.
2.Feltkamp TEW, Aarden LA, Lucas CJ, et al. Genetic risk factor for autoimmune disease[J]. Immunol Today,1999,20(1):10.
3.边杰,王广回,王智慧.甲状腺疾病的诊断与冶疗.北京：人民卫生出版社出版,1984：306-320.
4.陈晓城.麻黄的药理作用研究进展[J],实用中医药杂志,2005,21(1)：58.
5.魏友松,许芝银.麻黄、雷公藤、黄蜀葵花对自身免疫性甲状腺炎小鼠模型的影响[J],南京中医药大学学报,1996,12(4)：25.
6.陈荣明,朱耕新,许芝银.麻黄中不同提取物对细胞免疫的影响[J],南京中医药大学学报(自然科学版),2001,17(4)：234.
7.杨康,刘维永,白云.草麻黄中补体抑制成分的纯化和活性[J],四军医大学学报,2000,21(12)：1558.
8. Gu WZ, Brandwein SR. Inhibition of typeⅡcollageninduced arthritis in rats by triptolide[J].Int Immunopharmacol,1998,20(8):389.
9.李瑞林,舒达夫主编.雷公藤的研究与临床应用[M].北京：中国科学技术出版社,1989：193-195
10.秦风华,谢蜀生,龙振洲.雷公藤总甙免疫抑制作用的机制[J].中国药理学通报,1991,7(6)：433.
11.曹敏,孙荣奇,吴达俊.中药雷公藤的研究进展[J],中成药,1996,18(4)：41.
12.田荻,辛红,秦建中.雷公藤甲素对人外周血白细胞分泌促炎症性细胞因子的影响[J],上海免疫学杂志,1997,17(1)：55.
13.吴俊,梁晓燕,杨奕,等.雷公藤Ly-22.2+细胞的激活作用[J].中国病理生理杂志,1996,12(1)：30-31.
14.范祖森,曹荣华,张庆殷,等.雷公藤多甙对大鼠佐剂性关节炎治疗作用和免疫机制研究[J].中国药理学通报,1996(6)：527.
15.林小明.桃仁化学成分和药理作用研究进展[J],蛇志,2007,19(2)：130-132.
16.赵素莲,戴兆雄.苦杏仁甙对小鼠脾脏NK细胞活性的影响[J],山西医学院学报,1993,(1)：14.
17.赵素莲,刘桂芬.苦杏仁甙对小鼠免疫功能的影响[J],山西医药杂志,1993,(3)166.
18.刘英,张伟刚,王雅贤,等.炒桃仁总蛋白对小鼠B细胞功能影响的实验研究[J].中医药学报,2001,29(2)：55-56.
19.许惠玉,运晨霞,王雅贤.桃仁总蛋白对荷瘤鼠T淋巴细胞亚群及细胞凋亡的影响[J].齐齐哈尔医学院学报,2004,25(5)：485-487.
20.昌跃山,王雅贤,运晨霞,等.桃仁总蛋白对荷瘤鼠1L-2、IL-4水平的影响[J].中医药信息,2004,21(4)：60-61.
21.刘英,张伟兵,张鹏宇,等.炒桃仁总蛋白对TNF-α、 IL-2产生水平的影响[J].中医药学 报,2001,29(4)；51-52.
22.张明发,沈雅琴.肉桂的药理作用及温里功效[J].陕西中医,1995,16(1)：39-42.
23.田端守.桂皮的药理和药效[J].国外医药植物药分册,1994,9(1)：15.
24.曾雪瑜,陈雪芬,韦宝伟,等.肉桂提取物对免疫功能影响的研究[J].广西医学,1984,6(2)：62.
25. Lee HS, Kim BS, Kim MK. Suppression effect of Cinnamomum cassia bark-derived component on nitric oxide synthase[J]. J Agile Food Chem,2002,50(26):7700-7703.
26. Lee SH,Lee SY, Son DJ, et al. Inhibitory effect of 2-hydroxycin namaldehyde on nitric oxide production through inhibition of NF-kappa B activation in RAW 264.7 cells[J]. Biochem Pharmaeol,2005,69(5):791-799.
[1]国家药品监督管理局.中药天然药物研究技术指导原则[M].2005,85
[2]陈奇主编.中药药理研究方法学[M].北京：人民卫生出版社,第1版,2000,112-118
[3]徐淑云主编.药理学实验方法学[M].北京：人民卫生出版社,2002,227-228
1.朱立平,陈学清.免疫学常用实验方法[M].北京：人民军医出版社,2000.26-28.
2.罗敏.分子内分泌学(基础与临床)[M].北京：人民军医出版社.2003.197-198.
3.王云峰,魏枫.桥本甲状腺炎治疗前后淋巴细胞亚群及细胞学的变化[J].内蒙古医学 杂志,2007,39(4)：426-428.
4.钟述猷,董晖,张宝泉,等.自身免疫性甲状腺疾病患者淋巴细胞亚群和自身抗体的检测及其临床意义[J].天津医药,1994,22(7)：391.
1.朱立平,陈学清.免疫学常用实验方法[M].北京：人民军医出版社,2000.26-28.
2.罗敏.分子内分泌学(基础与临床)[M].北京：人民军医出版社.2003.197-198.
3.张志远,郑武飞.Graves病和桥本氏甲状腺炎患者的T淋巴细胞亚群异常[J].国外医学·内分泌学分册,1984,9(3)：134.
4.王云峰,魏枫.桥本甲状腺炎治疗前后淋巴细胞亚群及细胞学的变化[J].内蒙古医学杂志,2007,39(4)：426-428.
5.钟述猷,董晖,张宝泉,等.自身免疫性甲状腺疾病患者淋巴细胞亚群和自身抗体的检测及其临床意义[J].天津医药,1994,22(7)：391.
1.张均田.现代药理实验方法[M].北京：北京医科大学中国协和医科大学联合出版社,1999：680-688.
2.朱立平,陈学清.免疫学常用实验方法[M].北京：人民军医出版社,2000.26-28
3.白耀.甲状腺病学[M].北京：科学技术文献出版社,145-161
4.孙葳,宋光华,贺斌.碘和甲状腺球蛋白诱导大鼠实验性自身免疫性甲状腺炎的研究[J].中华内科杂志,2000,39(12)：841-842.
5.吴拥军,许芝银,高国宇,等.麻黄桃仁颗粒对实验性自身免疫性甲状腺炎体液免疫作用的研究[J].辽宁中医杂志,2006,33(11)：1506
1.张均田.现代药理实验方法[M].北京：北京医科大学中国协和医科大学联合出版社,1999：680-688.
2.朱立平,陈学清.免疫学常用实验方法[M].北京：人民军医出版社,2000.26-28.
1.张均田.现代药理实验方法[M].北京：北京医科大学中国协和医科大学联合出版社,1999：680-688.
2.朱立平,陈学清.免疫学常用实验方法[M].北京：人民军医出版社,2000.26-28.
3. FavaRA, OlsenNJ, SppencerGreeng, etal. Vascualar permeability factor endothelial growth factor(VPF VEGF). accumulation and expression in human synovial fluids and rheumatoid syovial tissue[J].J Exp Med.1994,180:341.
1.张均田.现代药理实验方法[M].北京：北京医科大学中国协和医科大学联合出版社,1999：680-688.
2.朱立平,陈学清.免疫学常用实验方法[M].北京：人民军医出版社,2000.26-28.
3.张雅萍,姬秋如,张万会,等.桥本甲状腺炎中Fas和Fas-L的表达[J].第四军医大学学报,2000；21(2)：223-225.
4.高福智,陈晓梅,赵文革,等.Fas系统介导的细胞凋亡与大鼠自体免疫性甲状腺炎的研究[J].内分泌外科杂志,2008,3(2)：76-78.