中华地方病学杂志
中華地方病學雜誌
중화지방병학잡지
Chinese Journal of Endemiology
2014年
5期
511-516
,共6页
边建朝%温玉学%蔺新英%杨群%高杰
邊建朝%溫玉學%藺新英%楊群%高傑
변건조%온옥학%린신영%양군%고걸
蛋白质类%碘%甲状腺%大鼠
蛋白質類%碘%甲狀腺%大鼠
단백질류%전%갑상선%대서
Protein%Iodine%Thyroid%Rats
目的 建立大鼠高碘低蛋白动物模型,观察高碘低蛋白对大鼠生长代谢的影响及甲状腺的病理形态学变化.方法 192只断乳1个月Wistar大鼠,雌雄各半,按体质量[(110±10)g]及性别采用随机数字表法分为①对照组(NI):正常饲料+自来水;②正常饲料+ 10倍碘组(10HI);③正常饲料+50倍碘组(50HI);④正常饲料+ 100倍碘组(100HI);⑤低蛋白对照组(LC):低蛋白饲料+自来水;;⑥低蛋白饲料+10倍碘组(L10HI);⑦低蛋白饲料+ 50倍碘组(L50HI);⑧低蛋白饲料+100倍碘组(L100HI).每组24只大鼠.NI、LC组大鼠每日摄碘量为4.65 μg/d,10倍、50倍、100倍碘组大鼠每日摄碘量分别为46.50、232.50、465.00μg/d.实验期为6个月,每周称大鼠体质量、记录饮水及饲料消耗情况;分别于实验第60、120、180天,每组取8只大鼠,收集尿液,砷铈催化分光光度法检测尿碘,并取血清,氯酸法检测血清碘.实验终末,取各组大鼠甲状腺组织,HE染色及透射电子显微镜观察病理及超微结构变化情况;末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)法检测甲状腺细胞凋亡情况.结果 实验第4、8、16、18、22、24周时,各组大鼠体质量组间比较差异有统计学意义(F值分别4.26、3.75、4.98、4.09、3.28、3.95,P均＜0.05).实验第60、120、180天时,各组大鼠尿碘、血清碘组间比较差异有统计学意义(H值分别为5.37、6.03,P均＜0.05).HE染色后光镜下观察,各组大鼠随着碘含量的增加甲状腺滤泡增大、上皮细胞呈扁平状、滤泡腔内充满丰富浓染胶质.透射电镜观察,各组大鼠随着碘含量的增加甲状腺滤泡上皮细胞内胶质小泡增多、内质网线粒体出现空泡样变、染色质浓缩、核膜不完整、核碎裂.各组大鼠甲状腺细胞凋亡指数组间比较差异有统计学意义(F=4.59,P＜0.01),其中L50HI、L100HI组[(21.50±5.20)‰、(26.70±6.40)‰]分别高于50HI、100HI组[(11.20±4.30)‰、(19.40±4.80)‰,P＜ 0.01或＜ 0.05].结论 高碘低蛋白可导致大鼠体格发育迟滞,碘代谢异常,并对甲状腺滤泡上皮细胞造成损伤.
目的 建立大鼠高碘低蛋白動物模型,觀察高碘低蛋白對大鼠生長代謝的影響及甲狀腺的病理形態學變化.方法 192隻斷乳1箇月Wistar大鼠,雌雄各半,按體質量[(110±10)g]及性彆採用隨機數字錶法分為①對照組(NI):正常飼料+自來水;②正常飼料+ 10倍碘組(10HI);③正常飼料+50倍碘組(50HI);④正常飼料+ 100倍碘組(100HI);⑤低蛋白對照組(LC):低蛋白飼料+自來水;;⑥低蛋白飼料+10倍碘組(L10HI);⑦低蛋白飼料+ 50倍碘組(L50HI);⑧低蛋白飼料+100倍碘組(L100HI).每組24隻大鼠.NI、LC組大鼠每日攝碘量為4.65 μg/d,10倍、50倍、100倍碘組大鼠每日攝碘量分彆為46.50、232.50、465.00μg/d.實驗期為6箇月,每週稱大鼠體質量、記錄飲水及飼料消耗情況;分彆于實驗第60、120、180天,每組取8隻大鼠,收集尿液,砷鈰催化分光光度法檢測尿碘,併取血清,氯痠法檢測血清碘.實驗終末,取各組大鼠甲狀腺組織,HE染色及透射電子顯微鏡觀察病理及超微結構變化情況;末耑脫氧覈苷痠轉移酶介導的dUTP缺口末耑標記(TUNEL)法檢測甲狀腺細胞凋亡情況.結果 實驗第4、8、16、18、22、24週時,各組大鼠體質量組間比較差異有統計學意義(F值分彆4.26、3.75、4.98、4.09、3.28、3.95,P均＜0.05).實驗第60、120、180天時,各組大鼠尿碘、血清碘組間比較差異有統計學意義(H值分彆為5.37、6.03,P均＜0.05).HE染色後光鏡下觀察,各組大鼠隨著碘含量的增加甲狀腺濾泡增大、上皮細胞呈扁平狀、濾泡腔內充滿豐富濃染膠質.透射電鏡觀察,各組大鼠隨著碘含量的增加甲狀腺濾泡上皮細胞內膠質小泡增多、內質網線粒體齣現空泡樣變、染色質濃縮、覈膜不完整、覈碎裂.各組大鼠甲狀腺細胞凋亡指數組間比較差異有統計學意義(F=4.59,P＜0.01),其中L50HI、L100HI組[(21.50±5.20)‰、(26.70±6.40)‰]分彆高于50HI、100HI組[(11.20±4.30)‰、(19.40±4.80)‰,P＜ 0.01或＜ 0.05].結論 高碘低蛋白可導緻大鼠體格髮育遲滯,碘代謝異常,併對甲狀腺濾泡上皮細胞造成損傷.
목적 건립대서고전저단백동물모형,관찰고전저단백대대서생장대사적영향급갑상선적병리형태학변화.방법 192지단유1개월Wistar대서,자웅각반,안체질량[(110±10)g]급성별채용수궤수자표법분위①대조조(NI):정상사료+자래수;②정상사료+ 10배전조(10HI);③정상사료+50배전조(50HI);④정상사료+ 100배전조(100HI);⑤저단백대조조(LC):저단백사료+자래수;;⑥저단백사료+10배전조(L10HI);⑦저단백사료+ 50배전조(L50HI);⑧저단백사료+100배전조(L100HI).매조24지대서.NI、LC조대서매일섭전량위4.65 μg/d,10배、50배、100배전조대서매일섭전량분별위46.50、232.50、465.00μg/d.실험기위6개월,매주칭대서체질량、기록음수급사료소모정황;분별우실험제60、120、180천,매조취8지대서,수집뇨액,신시최화분광광도법검측뇨전,병취혈청,록산법검측혈청전.실험종말,취각조대서갑상선조직,HE염색급투사전자현미경관찰병리급초미결구변화정황;말단탈양핵감산전이매개도적dUTP결구말단표기(TUNEL)법검측갑상선세포조망정황.결과 실험제4、8、16、18、22、24주시,각조대서체질량조간비교차이유통계학의의(F치분별4.26、3.75、4.98、4.09、3.28、3.95,P균＜0.05).실험제60、120、180천시,각조대서뇨전、혈청전조간비교차이유통계학의의(H치분별위5.37、6.03,P균＜0.05).HE염색후광경하관찰,각조대서수착전함량적증가갑상선려포증대、상피세포정편평상、려포강내충만봉부농염효질.투사전경관찰,각조대서수착전함량적증가갑상선려포상피세포내효질소포증다、내질망선립체출현공포양변、염색질농축、핵막불완정、핵쇄렬.각조대서갑상선세포조망지수조간비교차이유통계학의의(F=4.59,P＜0.01),기중L50HI、L100HI조[(21.50±5.20)‰、(26.70±6.40)‰]분별고우50HI、100HI조[(11.20±4.30)‰、(19.40±4.80)‰,P＜ 0.01혹＜ 0.05].결론 고전저단백가도치대서체격발육지체,전대사이상,병대갑상선려포상피세포조성손상.
Objective To establish an animal model of high-iodine and low-protein in Wistar rats,and to observe the effect of combined excess-iodine and low-protein diet on growth,metabolism and morphological changes in thyroid.Methods According to body weight[(110 ± 10)g] and sex(half male and half female),one hundred and ninety-two Wistar rats,1 month after weaning,were randomly divided into ① normal iodine control group (NI),② 10-fold excess-iodine group (10HI),③ 50-fold excess-iodine group (50HI),④ 100-fold excess-iodine group (100HI),⑤ low-protein control group (LC),⑥ low-protein and l 0-fold excess-iodine group (L10HI),⑦low-protein and 50-fold excess-iodine group (L50HI),⑧ low-protein and 100-fold excess-iodine group(L100HI).Twenty-four rats were in each group,with the experimental period of 6 months.The iodine content of NI and LC groups was 4.65 μg/d; 10HI,50HI and 100HI groups were 46.50,232.50 and 465.00 μg/d,respectively.The animal's body weight,water and feed consumption were recorded weekly.At the end of 60,120,180 days,urine and blood samples were collected from eight rats in each group.Urinary iodine was tested by arseni cerium catalytic spectrophotometry; serum iodine was tested by the method of chloric acid.Histological change of the thyroid gland was observed by transmission electron microscopy and hematoxylin-eosin (HE) staining at the end of 6 months; apoptosis of thyroid was tested by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) method.Results At the end of 4,8,16,18,22 and 24 weeks,the differences of body mass of rats among groups were statistically significant(F =4.26,3.75,4.98,4.09,3.28,3.95,all P ＜ 0.05).At the end of 60,120,180 days,the differences of iodine concentration in urine and blood among groups were statistically significantly (H =5.37,6.03,all P ＜ 0.05).Light microscopy showed that thyroid follicular epithelial cells became flattened,and follicles became distended with colloid following increasing of iodine concentration.Electron microscopy showed increased glial vesicles,condensation of nuclear chromatin,karyopyknosis,and karyolysis with increasing of iodine concentration.The differences of apoptotic indexes among groups were statistically significant (F =4.59,P ＜ 0.01).The apoptotic indexes of L50HI and L100HI groups [(21.50 ± 5.20)‰,(26.70 ± 6.40)‰] were higher than those of 50HI and 100HI groups [(11.20 ± 4.30)‰,(19.40 ± 4.80)‰,P ＜ 0.01 or ＜ 0.05].Conclusion Excessiodine and low-protein can cause growth retardation,abnormal iodine metabolism,and thyroid follicular epithelium damage in Wistar rats.
