中国地方病学杂志
中國地方病學雜誌
중국지방병학잡지
CHINESE JOURNAL OF ENDEMIOLOGY
2009年
3期
263-267
,共5页
于秀杰%李庆欣%刘泽兵%臧晓怡%李兰英
于秀傑%李慶訢%劉澤兵%臧曉怡%李蘭英
우수걸%리경흔%류택병%장효이%리란영
碘%甲状腺炎%细胞凋亡%细胞增殖
碘%甲狀腺炎%細胞凋亡%細胞增殖
전%갑상선염%세포조망%세포증식
Iodine%Thyroiditis%Apoptosis%Cell proliferation
目的 观察碘过量对不同遗传背景小鼠甲状腺炎诱发作用的异同.方法 选用NOD和Balb/c小鼠各14只,每个品系小鼠均分为对照组、碘化钠(NaI)组,分别饮用纯净水和0.05%NaI水8周.放射免疫法(RIA)和ELISA法分别检测血清中总T4(TT4)、甲状腺球蛋白抗体(TgAb)、甲状腺过氧化物酶抗体(TPOAb)和促甲状腺激素(TSH)水平,光镜下观察甲状腺形态学改变和免疫组化染色的甲状腺细胞凋亡情况,四甲基偶氮唑兰(MTT)法检测颈部淋巴结和脾淋巴细胞对甲状腺球蛋白刺激的增殖反应.结果 饮碘水8周后,NOD和Balb/c小鼠甲状腺相对质量,NaI组[(104.83±14.52)、(155.79±20.77)mg/kg]较对照组[(71.80±20.42)、(105.15±21.98)mg/kg]明显增加(t值分别为-3.293、-4.429,P均<0.01),甲状腺组织表现为滤泡扩张、胶质潴留;NOD、Balb/c小鼠血清TT4水平,NaI组[(29.52±4.42)、(19.53±2.35)nmol/L]较对照组[(33.40±5.38)、(23.47±6.22)nmol/L]呈下降趋势(t值分别为1.374、1.567,P>0.05);血清TSH水平,与对照组[(3.55±1.41)、(5.55±0.56)μg/L]比较,Balb/c小鼠NaI组[(4.14±1.71)μg/L]呈升高趋势(t=-0.705,P>0.05),NOD小鼠NaI组[(6.98±0.66)μg/L]明显升高(t=-3.562,P<0.01);NOD、Balb/c小鼠NaI组TgAb(1281、1364 cpm)和TPOAb水平(2.50×103、0.14×103U/L)与对照组(1297、1220 cpm,3.17×103、0.03×103 U/L)比较没有明显变化(Z值分别为-0.081、-0.703,-0.244、-1.293,P均>0.05).NOD小鼠NaI组甲状腺细胞凋亡数量较BMb/c小鼠增加,并且甲状腺内可见大量淋巴细胞浸润,组织结构破坏和纤维化的灶性病变;NOD小鼠淋巴结和脾淋巴细胞数量,NaI组(1.100±0.014、1.076±0.033)较对照组(0.993±0.011、1.005±0.003)增加(t值分别为-11.672、-4.314,P均<0.01).结论 碘可致Balb/c鼠甲状腺肿大,功能下降;NOD鼠除七述病变外,甲状腺发生明显炎症反应,并且针对Tg产生了致敏的淋巴细胞.碘过量可诱发NOD鼠发生自身免疫性甲状腺炎.
目的 觀察碘過量對不同遺傳揹景小鼠甲狀腺炎誘髮作用的異同.方法 選用NOD和Balb/c小鼠各14隻,每箇品繫小鼠均分為對照組、碘化鈉(NaI)組,分彆飲用純淨水和0.05%NaI水8週.放射免疫法(RIA)和ELISA法分彆檢測血清中總T4(TT4)、甲狀腺毬蛋白抗體(TgAb)、甲狀腺過氧化物酶抗體(TPOAb)和促甲狀腺激素(TSH)水平,光鏡下觀察甲狀腺形態學改變和免疫組化染色的甲狀腺細胞凋亡情況,四甲基偶氮唑蘭(MTT)法檢測頸部淋巴結和脾淋巴細胞對甲狀腺毬蛋白刺激的增殖反應.結果 飲碘水8週後,NOD和Balb/c小鼠甲狀腺相對質量,NaI組[(104.83±14.52)、(155.79±20.77)mg/kg]較對照組[(71.80±20.42)、(105.15±21.98)mg/kg]明顯增加(t值分彆為-3.293、-4.429,P均<0.01),甲狀腺組織錶現為濾泡擴張、膠質潴留;NOD、Balb/c小鼠血清TT4水平,NaI組[(29.52±4.42)、(19.53±2.35)nmol/L]較對照組[(33.40±5.38)、(23.47±6.22)nmol/L]呈下降趨勢(t值分彆為1.374、1.567,P>0.05);血清TSH水平,與對照組[(3.55±1.41)、(5.55±0.56)μg/L]比較,Balb/c小鼠NaI組[(4.14±1.71)μg/L]呈升高趨勢(t=-0.705,P>0.05),NOD小鼠NaI組[(6.98±0.66)μg/L]明顯升高(t=-3.562,P<0.01);NOD、Balb/c小鼠NaI組TgAb(1281、1364 cpm)和TPOAb水平(2.50×103、0.14×103U/L)與對照組(1297、1220 cpm,3.17×103、0.03×103 U/L)比較沒有明顯變化(Z值分彆為-0.081、-0.703,-0.244、-1.293,P均>0.05).NOD小鼠NaI組甲狀腺細胞凋亡數量較BMb/c小鼠增加,併且甲狀腺內可見大量淋巴細胞浸潤,組織結構破壞和纖維化的竈性病變;NOD小鼠淋巴結和脾淋巴細胞數量,NaI組(1.100±0.014、1.076±0.033)較對照組(0.993±0.011、1.005±0.003)增加(t值分彆為-11.672、-4.314,P均<0.01).結論 碘可緻Balb/c鼠甲狀腺腫大,功能下降;NOD鼠除七述病變外,甲狀腺髮生明顯炎癥反應,併且針對Tg產生瞭緻敏的淋巴細胞.碘過量可誘髮NOD鼠髮生自身免疫性甲狀腺炎.
목적 관찰전과량대불동유전배경소서갑상선염유발작용적이동.방법 선용NOD화Balb/c소서각14지,매개품계소서균분위대조조、전화납(NaI)조,분별음용순정수화0.05%NaI수8주.방사면역법(RIA)화ELISA법분별검측혈청중총T4(TT4)、갑상선구단백항체(TgAb)、갑상선과양화물매항체(TPOAb)화촉갑상선격소(TSH)수평,광경하관찰갑상선형태학개변화면역조화염색적갑상선세포조망정황,사갑기우담서란(MTT)법검측경부림파결화비림파세포대갑상선구단백자격적증식반응.결과 음전수8주후,NOD화Balb/c소서갑상선상대질량,NaI조[(104.83±14.52)、(155.79±20.77)mg/kg]교대조조[(71.80±20.42)、(105.15±21.98)mg/kg]명현증가(t치분별위-3.293、-4.429,P균<0.01),갑상선조직표현위려포확장、효질저류;NOD、Balb/c소서혈청TT4수평,NaI조[(29.52±4.42)、(19.53±2.35)nmol/L]교대조조[(33.40±5.38)、(23.47±6.22)nmol/L]정하강추세(t치분별위1.374、1.567,P>0.05);혈청TSH수평,여대조조[(3.55±1.41)、(5.55±0.56)μg/L]비교,Balb/c소서NaI조[(4.14±1.71)μg/L]정승고추세(t=-0.705,P>0.05),NOD소서NaI조[(6.98±0.66)μg/L]명현승고(t=-3.562,P<0.01);NOD、Balb/c소서NaI조TgAb(1281、1364 cpm)화TPOAb수평(2.50×103、0.14×103U/L)여대조조(1297、1220 cpm,3.17×103、0.03×103 U/L)비교몰유명현변화(Z치분별위-0.081、-0.703,-0.244、-1.293,P균>0.05).NOD소서NaI조갑상선세포조망수량교BMb/c소서증가,병차갑상선내가견대량림파세포침윤,조직결구파배화섬유화적조성병변;NOD소서림파결화비림파세포수량,NaI조(1.100±0.014、1.076±0.033)교대조조(0.993±0.011、1.005±0.003)증가(t치분별위-11.672、-4.314,P균<0.01).결론 전가치Balb/c서갑상선종대,공능하강;NOD서제칠술병변외,갑상선발생명현염증반응,병차침대Tg산생료치민적림파세포.전과량가유발NOD서발생자신면역성갑상선염.
Objective To observe the different effects of iodine excess on inducing two strain mice thyroiditis. Methods NOD and Balb/c mice, each having 14 mice, were divided into NaI and control group. The mice were given 0.05% NaI water for 8 weeks in NaI group. RIA and ELISA were used respectively to detect TT4, TgAb, TPOAb and TSH level in serum. Morphology changes of thyroid and apoptosis of thyrocytes stained by immunohistochemistry were observed under light microscope. Lymphocytic proliferation of cervical lymph node and spleen to responding to Tg were detected by MTr method. Results After intake of iodine water for 8 weeks, NOD and Balb/c mice showed relative quality of thyroid in Nal group[(104.83±14.52), (155.79±20.77)mg/kg]obviously increased compared with control group[(71.80±20.42), (105.15±21.98)mg/kg, t values:-3.293,-4.429, all P< 0.01)], enlarged follicular lumen with colloid accumulation were observed in thyroid. Serum level of TT4 in Nal group [(29.52±4.42), (19.53± 2.35)nmol/L]to control group[33.40±5.38), (23.47±6.22)nmol/L]of NOD and Balb/c mice showed a decreasing tendency(t values: 1.374,1.567, all P > 0.05). TSH of Nal group showed an increasing tendency in Balb/c mice[(4.14±1.71)μg/L, compared with control [(3.55±1.41)μg/L, t values:-0.705, P > 0.05]and obviously increased in NOD mice [(6.98±0.66)μg/L, compared with control[(555±056)μg/L, t values:-3.562, P< 0.01], but no change of TgAb and TPOAb level in Nal group(1281,1364 cpm, 2.50×103, 0.14×103U/L were observed, compared with control(1297,1220 cpm, 3.17×103,0.03×103 U/L; Zvalues:-0.081,-0.703, -0.244,-1.293, all P > 0.05). In NOD mice NaI group, apoptosis of thyrocytes was more intense than Balb/c mice, obvious infiltration of lymphoeytes, disorganization and focus fibrosis was seen in thyroid. The cell amount of NaI group increased in NOD mice lymph node and spleen cells[(1.100±0.014), (1.076±0.033)]were more than that in the control group [(0.993±0.011), (1.005±0.003), t value:-11.672,-4.314, P < 0.01). Conclusions Iodine leads to enlargement of thyroid and malfunction of thyroid in Balb/c mice. Besides, NOD mice have generate inflammatory reaction in thyroid and produced sensitized lymphocytes to Tg. Iodine excess can induce NOD mice to occur autoimmune thyroiditis.
