富碘复方海藻玉壶汤对碘缺乏甲状腺细胞凋亡及凋亡调控基因表达的影响
摘要
目的观察富碘复方海藻玉壶汤对碘缺乏Wistar大鼠甲状腺滤泡上皮细胞凋亡及调控基因的影响。方法饲低碘饲料加1%高氯酸钠建立碘缺乏大鼠模型,将碘缺乏Wistar大鼠随机分为模型组、碘过量组、海藻玉壶汤Ⅰ组、海藻玉壶汤Ⅱ组。均饲低碘饲料,模型组饲等体积双蒸水;碘过量组饲含碘2000ug/L的高碘水;海藻玉壶汤Ⅰ组(碘含量1989.25ug/L),海藻玉壶汤Ⅱ组(碘含量46.89ug/L)常规剂量水煎,按人体表面积折算灌服剂量;正常组:正常饮食,每日灌服等体积双蒸水。脱氧核糖核苷酸末端转移酶介导原位缺口末端标记(TUNEL)确定细胞凋亡数。免疫组化方法观察Fas、FasL和bcl-2的表达,观察各组大鼠甲状腺细胞凋亡数及Fas/FasL,Bcl-2的表达。
结果予处理因素28天时:与正常组比较:模型组、碘过量组、海藻玉壶汤Ⅰ组、海藻玉壶汤Ⅱ组凋亡细胞数均明显增高,P分别<0.01、<0.05、<0.01和<0.05。Fas、Fasl的表达均明显增高,p均小于0.05,Bcl-2表达均明显降低,p均小于0.05。与模型组比较:碘过量组,海藻玉壶汤Ⅰ组、海藻玉壶汤Ⅱ组凋亡细胞数均明显降低,P均小于0.05。海藻玉壶汤Ⅰ组凋亡细胞数均明显低于海藻玉壶汤Ⅱ组,p<0.01。Fas、FasL表达均明显降低,p均<0.05,Bcl-2表达均有显著升高,p值均小于0.05。
结论细胞凋亡参与了碘缺乏致甲状腺肿的形成,富碘复方有效地降低了碘缺乏致甲状腺肿大鼠的细胞凋亡数量,去富碘中药复方对降低碘缺乏致甲状腺肿大鼠的细胞凋亡的数量疗效不如富碘中药复方;Fas/FasL、Bcl-2可能参与了碘缺乏致甲状腺肿大的细胞凋亡调控过程。
Objective To study the effect of Haizaoyuhutang with abundant iodine on apoptosis of follicular epithelial cells in goiter Wistar rats due to iodine deficiency.
Method Iodine deficiency rat model was m cade with sodium perchlorate and low iodine diet. and then divided the rats randomly into 4 groups:model control group, iodine excess group,HaizaoyuhutangⅠgroup,and HaizaoyuhutangⅡgroup.These rats were treated with low iodine diet, and model control group with Double Distilled Water(DDW). iodine excess group with liquid full of high iodine(2000ug/L). HaizaoyuhutangⅠgroup with Haizaoyuhutang (iodine contents is 1989.25ug/L ). HaizaoyuhutangⅡgroup with Haizaoyuhutang (iodine contents is 46.89ug/L ).But the normal group was made with common diet and DDW of the equal-volume. Deoxyribotide termina enzyme mediate with emarginationend in natural position end labeling to definite the number of apoptosis;observe the expression of Fas、FasL and bcL-2 with immunity.Observe the number of the apoptosis of thyroid cells and the expression of Fas/FasL BcL-2.
Results Giving the processing factor 28 days later, compared with the Nomal Group the number of apoptosis of Model group,Iodine excess group,HaizaoyuhutangⅠgroup and HaizaoyuhutangⅡgroup was obviously heighten.( p <0.01. p <0.05. p <0.01and p <0.05) The expression of Fas、FasL was obviously heighten .both P<0.05. The expression of Bcl-2 was obviously low both p <0.05。Compared with the modelcontral group . the number of apoptosis of Model group Iodine excess group HaizaoyuhutangⅠgroup and HaizaoyuhutangⅡgroup was obviously low. p <0.05。The number of apoptosis of HaizaoyuhutangⅠgroup was obviously lower than HaizaoyuhutangⅡgroup p<0.01。The expression of Fas/FasL got down obviously . both p <0.05. the expression of BcL-2 was significantly heighten. p <0.05.
Conclusion Apoptosis take part in the formation of the goiter due to iodine deficiency. Prescription with abundant iodine cut down the number of apoptosis of goiter due to iodine seficiency effectually.Prescription without abundant iodine was inferior to Prescription with abundant iodine. Fas/FasL、BcL-2 may take place in the process of the apoptosisof the goitor due to Iodine deficiency.
结果予处理因素28天时:与正常组比较:模型组、碘过量组、海藻玉壶汤Ⅰ组、海藻玉壶汤Ⅱ组凋亡细胞数均明显增高,P分别<0.01、<0.05、<0.01和<0.05。Fas、Fasl的表达均明显增高,p均小于0.05,Bcl-2表达均明显降低,p均小于0.05。与模型组比较:碘过量组,海藻玉壶汤Ⅰ组、海藻玉壶汤Ⅱ组凋亡细胞数均明显降低,P均小于0.05。海藻玉壶汤Ⅰ组凋亡细胞数均明显低于海藻玉壶汤Ⅱ组,p<0.01。Fas、FasL表达均明显降低,p均<0.05,Bcl-2表达均有显著升高,p值均小于0.05。
结论细胞凋亡参与了碘缺乏致甲状腺肿的形成,富碘复方有效地降低了碘缺乏致甲状腺肿大鼠的细胞凋亡数量,去富碘中药复方对降低碘缺乏致甲状腺肿大鼠的细胞凋亡的数量疗效不如富碘中药复方;Fas/FasL、Bcl-2可能参与了碘缺乏致甲状腺肿大的细胞凋亡调控过程。
Objective To study the effect of Haizaoyuhutang with abundant iodine on apoptosis of follicular epithelial cells in goiter Wistar rats due to iodine deficiency.
Method Iodine deficiency rat model was m cade with sodium perchlorate and low iodine diet. and then divided the rats randomly into 4 groups:model control group, iodine excess group,HaizaoyuhutangⅠgroup,and HaizaoyuhutangⅡgroup.These rats were treated with low iodine diet, and model control group with Double Distilled Water(DDW). iodine excess group with liquid full of high iodine(2000ug/L). HaizaoyuhutangⅠgroup with Haizaoyuhutang (iodine contents is 1989.25ug/L ). HaizaoyuhutangⅡgroup with Haizaoyuhutang (iodine contents is 46.89ug/L ).But the normal group was made with common diet and DDW of the equal-volume. Deoxyribotide termina enzyme mediate with emarginationend in natural position end labeling to definite the number of apoptosis;observe the expression of Fas、FasL and bcL-2 with immunity.Observe the number of the apoptosis of thyroid cells and the expression of Fas/FasL BcL-2.
Results Giving the processing factor 28 days later, compared with the Nomal Group the number of apoptosis of Model group,Iodine excess group,HaizaoyuhutangⅠgroup and HaizaoyuhutangⅡgroup was obviously heighten.( p <0.01. p <0.05. p <0.01and p <0.05) The expression of Fas、FasL was obviously heighten .both P<0.05. The expression of Bcl-2 was obviously low both p <0.05。Compared with the modelcontral group . the number of apoptosis of Model group Iodine excess group HaizaoyuhutangⅠgroup and HaizaoyuhutangⅡgroup was obviously low. p <0.05。The number of apoptosis of HaizaoyuhutangⅠgroup was obviously lower than HaizaoyuhutangⅡgroup p<0.01。The expression of Fas/FasL got down obviously . both p <0.05. the expression of BcL-2 was significantly heighten. p <0.05.
Conclusion Apoptosis take part in the formation of the goiter due to iodine deficiency. Prescription with abundant iodine cut down the number of apoptosis of goiter due to iodine seficiency effectually.Prescription without abundant iodine was inferior to Prescription with abundant iodine. Fas/FasL、BcL-2 may take place in the process of the apoptosisof the goitor due to Iodine deficiency.
引文
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[2].申红梅,全球碘缺乏病流行现状中国地方病学杂志[J] 2005,24(5):587.
[3]Ruwhof C ,Drexhage HA. Iodine and thyroid autoimmune disease in animal models. Thyroid ,2001 ,11(5) :427-436.
[4]Feldt-Rasmussen U. Iodine and cancer. Thyroid ,2001 ,11 :483-486.
[5]陈祖培,当前碘缺乏病防治应当注意的问题,中国地方病学杂志[J]2004, 23(3):193-194.
[6]吴民义等,食盐加碘对轻度碘缺乏地区住院甲状腺疾病谱的影响中华内分泌代谢杂志[J]2004,20(2):2.
[7] WHO. Assessment of iodine deficiency disorders and monitoring their elimination. A guide for programme managers (secondedition) , 2001.
[8]藤卫平,防治碘缺乏病与碘过量,中华内分泌代谢杂志[J]2002 ,18(3):237-240.
[9].Suzuki H.Endemic coast goiter in Hokkad.Acta Endocrinology,1965(5):165.
[10].张晓平等,承德市1999年消除碘缺乏病阶段目标评估结果,中国地方病防治杂志[J] 2000,15(5):314.
[11].Kolaja KL,Petrick JS,Klaassen CD.Inhibition of gap-junctional-interllular commun ication in thyroid-follicular cells by propylthiou-racil and low iodine diet.Toxicology,2000,143:195-202.
[12]林来祥等,碘对甲状腺细胞凋亡bax、bcl-2基因mRNA表达的影响,中国地方病学杂志[J] 2005,24(3):245-247.
[13]李颖王丹娜,低碘和高碘对大鼠甲状腺细胞凋亡的影响,中国地方病学杂志[J] 2004 23(3):201-203.
[14]高天舒,膝卫平,细胞凋亡和自身免疫甲状腺疾病,中国预防医学杂志[J]2O02, 3(1):75.
[15] Hockenbery DM ,O ltvai ZN , Yin XM ,et al. Bcl22 functions in anantioxidantpathway to p revent apop to sis [J].Cell, 1993; 75: 241-251.
[16]Kase S.Osaki M,Adachi H,et a1.Expression of Fas and Fasligand in esophageal tissue mucosa and carcinomas[J].Int J Oncol,2002,2O:291-297.
[17]Liu C ,Derwahl M. The effect of iodide on thyroid gland[J] . Am J Compreh Med ,1999 ,1:191.
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