中华地方病学杂志
中華地方病學雜誌
중화지방병학잡지
Chinese Journal of Endemiology
2015年
8期
573-577
,共5页
碘%甲状腺炎,自身免疫性,实验性%趋化因子类
碘%甲狀腺炎,自身免疫性,實驗性%趨化因子類
전%갑상선염,자신면역성,실험성%추화인자류
Iodine%Thyroiditis,autoimmune,experimental%Chemotactic factors
目的 观察碘对牛甲状腺球蛋白(bTg)诱导的实验性自身免疫性甲状腺炎(EAT)大鼠血清趋化因子IP-10及甲状腺组织IP-10 mRNA表达的影响.方法 选择4周龄雌性Lewis大鼠135只,采用随机数字表法按体质量分为对照组(NC,20只)、模型组(TG,25只)、高碘Ⅰ组(HⅠ,20只)、高碘模型Ⅰ组(HⅠ +TG,25只)、高碘Ⅱ组(HⅡ,20只)和高碘模型Ⅱ组(HⅡ+ TG,25只).HⅠ、HⅠ +TG组大鼠饮用含碘25.7 μg/L的去离子水,HⅡ、HⅡ+ TG组大鼠饮用含碘423.3 μg/L的去离子水,NC、rG组饮用蒸馏水.TG、HⅠ +TG和HⅡ+TG组大鼠皮下注射含8g/L bTg的不完全弗氏佐剂0.1 ml,每2周1次,共3次.15周末处死动物,采用砷-铈催化分光光度法(WS/T 107-2006)测定大鼠尿碘,光镜下观察甲状腺组织病理学改变,酶联免疫吸附试验(ELISA)检测大鼠血清IP-10含量,实时荧光定量PCR法检测甲状腺IP-10 mRNA表达.结果 各组大鼠尿碘中位数比较差异有统计学意义(x2=106.4,P＜0.05).其中TG、HⅠ、HⅠ +TG、HⅡ、HⅡ +TG组大鼠尿碘中位数(800.08、18 633.20、13 869.08、87 889.97、61 661.51 μg/L)均高于NC组(456.45 μg/L,P均＜0.05).各组大鼠病理改变等级随着碘摄入的提高逐渐加重,其中NC组大鼠甲状腺结构正常;TG组大鼠甲状腺滤泡间少量淋巴细胞浸润;HⅠ组大鼠甲状腺滤泡排列不整齐、部分滤泡组织破坏;HⅡ组大鼠甲状腺滤泡间大量炎性细胞浸润;HⅡ+ TG组大鼠甲状腺滤泡严重破坏、炎细胞弥漫性浸润.6组大鼠血清IP-10含量比较,差异无统计学意义(F=1.462,P＞ 0.05).HⅠ +TG组大鼠甲状腺IP-10 mRNA表达(2.80±1.73)高于NC组(1.65±1.62)和HⅠ组(1.07±1.00),HⅡ(0.64±0.64)、HⅡ +TG组(0.80±0.49)低于HⅠ +TG组(P均＜0.05).结论 过量碘摄入可增加EAT大鼠甲状腺组织中炎性程度,加重病理改变;这可能与过量碘影响甲状腺IP-10 mRNA表达有关.
目的 觀察碘對牛甲狀腺毬蛋白(bTg)誘導的實驗性自身免疫性甲狀腺炎(EAT)大鼠血清趨化因子IP-10及甲狀腺組織IP-10 mRNA錶達的影響.方法 選擇4週齡雌性Lewis大鼠135隻,採用隨機數字錶法按體質量分為對照組(NC,20隻)、模型組(TG,25隻)、高碘Ⅰ組(HⅠ,20隻)、高碘模型Ⅰ組(HⅠ +TG,25隻)、高碘Ⅱ組(HⅡ,20隻)和高碘模型Ⅱ組(HⅡ+ TG,25隻).HⅠ、HⅠ +TG組大鼠飲用含碘25.7 μg/L的去離子水,HⅡ、HⅡ+ TG組大鼠飲用含碘423.3 μg/L的去離子水,NC、rG組飲用蒸餾水.TG、HⅠ +TG和HⅡ+TG組大鼠皮下註射含8g/L bTg的不完全弗氏佐劑0.1 ml,每2週1次,共3次.15週末處死動物,採用砷-鈰催化分光光度法(WS/T 107-2006)測定大鼠尿碘,光鏡下觀察甲狀腺組織病理學改變,酶聯免疫吸附試驗(ELISA)檢測大鼠血清IP-10含量,實時熒光定量PCR法檢測甲狀腺IP-10 mRNA錶達.結果 各組大鼠尿碘中位數比較差異有統計學意義(x2=106.4,P＜0.05).其中TG、HⅠ、HⅠ +TG、HⅡ、HⅡ +TG組大鼠尿碘中位數(800.08、18 633.20、13 869.08、87 889.97、61 661.51 μg/L)均高于NC組(456.45 μg/L,P均＜0.05).各組大鼠病理改變等級隨著碘攝入的提高逐漸加重,其中NC組大鼠甲狀腺結構正常;TG組大鼠甲狀腺濾泡間少量淋巴細胞浸潤;HⅠ組大鼠甲狀腺濾泡排列不整齊、部分濾泡組織破壞;HⅡ組大鼠甲狀腺濾泡間大量炎性細胞浸潤;HⅡ+ TG組大鼠甲狀腺濾泡嚴重破壞、炎細胞瀰漫性浸潤.6組大鼠血清IP-10含量比較,差異無統計學意義(F=1.462,P＞ 0.05).HⅠ +TG組大鼠甲狀腺IP-10 mRNA錶達(2.80±1.73)高于NC組(1.65±1.62)和HⅠ組(1.07±1.00),HⅡ(0.64±0.64)、HⅡ +TG組(0.80±0.49)低于HⅠ +TG組(P均＜0.05).結論 過量碘攝入可增加EAT大鼠甲狀腺組織中炎性程度,加重病理改變;這可能與過量碘影響甲狀腺IP-10 mRNA錶達有關.
목적 관찰전대우갑상선구단백(bTg)유도적실험성자신면역성갑상선염(EAT)대서혈청추화인자IP-10급갑상선조직IP-10 mRNA표체적영향.방법 선택4주령자성Lewis대서135지,채용수궤수자표법안체질량분위대조조(NC,20지)、모형조(TG,25지)、고전Ⅰ조(HⅠ,20지)、고전모형Ⅰ조(HⅠ +TG,25지)、고전Ⅱ조(HⅡ,20지)화고전모형Ⅱ조(HⅡ+ TG,25지).HⅠ、HⅠ +TG조대서음용함전25.7 μg/L적거리자수,HⅡ、HⅡ+ TG조대서음용함전423.3 μg/L적거리자수,NC、rG조음용증류수.TG、HⅠ +TG화HⅡ+TG조대서피하주사함8g/L bTg적불완전불씨좌제0.1 ml,매2주1차,공3차.15주말처사동물,채용신-시최화분광광도법(WS/T 107-2006)측정대서뇨전,광경하관찰갑상선조직병이학개변,매련면역흡부시험(ELISA)검측대서혈청IP-10함량,실시형광정량PCR법검측갑상선IP-10 mRNA표체.결과 각조대서뇨전중위수비교차이유통계학의의(x2=106.4,P＜0.05).기중TG、HⅠ、HⅠ +TG、HⅡ、HⅡ +TG조대서뇨전중위수(800.08、18 633.20、13 869.08、87 889.97、61 661.51 μg/L)균고우NC조(456.45 μg/L,P균＜0.05).각조대서병리개변등급수착전섭입적제고축점가중,기중NC조대서갑상선결구정상;TG조대서갑상선려포간소량림파세포침윤;HⅠ조대서갑상선려포배렬불정제、부분려포조직파배;HⅡ조대서갑상선려포간대량염성세포침윤;HⅡ+ TG조대서갑상선려포엄중파배、염세포미만성침윤.6조대서혈청IP-10함량비교,차이무통계학의의(F=1.462,P＞ 0.05).HⅠ +TG조대서갑상선IP-10 mRNA표체(2.80±1.73)고우NC조(1.65±1.62)화HⅠ조(1.07±1.00),HⅡ(0.64±0.64)、HⅡ +TG조(0.80±0.49)저우HⅠ +TG조(P균＜0.05).결론 과량전섭입가증가EAT대서갑상선조직중염성정도,가중병리개변;저가능여과량전영향갑상선IP-10 mRNA표체유관.
Objective To establish experimental autoimmune thyroiditis (EAT) rat model induced by bovine thyroglobulin (bTg) and to observe the effect of iodine on IP-10 in rat serum and IP-10 mRNA expression in rat thyroid tissue.Methods One hundred and thirty-five four-week old female Lewis rats were divided into normal control (NC,20 rats) group;TG group,25 rats;H Ⅰ group,20 rats;H Ⅰ + TG group,25 rats;H Ⅱ group,20 rats and H Ⅱ + TG group,25 rats according to a random number table.The water iodine concentration was 25.7 μg/L given to rats of HⅠ and H I + TG groups,and 423.3 μg/L of H Ⅱ and H Ⅱ + TG groups.Rats of NC and TG groups drank distilled water.Rats of TG,H Ⅰ + TG,H Ⅱ + TG groups were immunized with 0.1 ml bTg (8 g/L) in IFA.All rats were killed at the end of 15 weeks.Urinary iodine was determined by As3+-Ce4+ catalytic spectrophotometry (WS/T 107-2006).Pathological changes in thyroid tissue were observed by light microscope.Serum IP-10 was determined by enzyme-linked immunosorbent assay (ELISA),and IP-10 mRNA expression in thyroid was detected by real-time PCR.Results The differences of urinary iodine between groups were statistically significant (x2 =106.4,P ＜ 0.05).Compared with NC group (456.45 μg/L) urinary iodine in other groups increased significantly (TG,H Ⅰ,H Ⅰ + TG,HⅡ,HⅡ + TG:800.08,18 633.20,13 869.08,87 889.97,61 661.51 μg/L,all P ＜ 0.05).The pathological changes of rats in each group aggravated following increased iodine intake,NC group had normal thyroid structure;thyroid of TG group had a small amount of lymphocytes;thyroid of H Ⅰ group showed irregular follicular,part of the follicular was destroyed;a large number of lymphocytes infiltrated between follicular of H Ⅱ group;in H Ⅱ + TG group,the follicular was destroyed severely,diffuse inflammatory cell infiltration.The difference of serum IP-10 between groups no were statistically significant (F =1.462,P ＞ 0.05).The expression of IP-10 mRNA of H Ⅰ + TG (2.80 ± 1.73) rats thyroid was higher than that in NC (1.65 ± 1.62) and H Ⅰ (1.07 ± 1.00) groups,H Ⅱ (0.64 ± 0.64),H Ⅱ + TG (0.80 ± 0.49) were lower than H Ⅰ + TG group (all P ＜ 0.05).Conclusions Excessive iodine intake could have increased inflammatory cells in EAT rat and rats have showed more serious pathologic changes.These phenomena may be ralated with changed expression of IP-10 mRNA in EAT rat thyroid.
