中国地方病学杂志
中國地方病學雜誌
중국지방병학잡지
CHINESE JOURNAL OF ENDEMIOLOGY
2012年
3期
251-254
,共4页
卓小花%刘欣%胡志梅%臧晓怡%孙云%李兰英
卓小花%劉訢%鬍誌梅%臧曉怡%孫雲%李蘭英
탁소화%류흔%호지매%장효이%손운%리란영
碘%缺乏症%促甲状腺素β剪接变体%甲状腺素%内分泌系统%免疫系统
碘%缺乏癥%促甲狀腺素β剪接變體%甲狀腺素%內分泌繫統%免疫繫統
전%결핍증%촉갑상선소β전접변체%갑상선소%내분비계통%면역계통
Iodine%Deficiency diseases%Thyroid-stimulating hormone β splice variant%Thyroxin%Endocrine system%Immune system
目的 制备碘缺乏小鼠模型,检测促甲状腺激素(TSH)β剪接变体(TSHβ-Ⅴ)是否受循环中甲状腺激素的调节,探讨免疫系统来源的TSHβ-Ⅴ在维持甲状腺自稳态中的作用.方法 选用离乳BALB/c小鼠20只,雌雄各半.小鼠按体质量和性别随机分为2组,每组10只.对照组:饮去离子水,普通饲料喂养；低碘组:饮去离子水,低碘饲料(含碘量20 - 40μg /kg)喂养,每日碘摄入量约为0.25μg/d.3个月后处死小鼠,化学发光免疫分析法(CIA)检测小鼠血清中甲状腺激素和TSH水平,实时定量(RT)-PCR法测定小鼠骨髓、外周血、甲状腺、垂体TSHβ-Ⅴ的表达.结果 低碘组小鼠血清总甲状腺素(TT4)、游离甲状腺素(FT4)、总三碘甲腺原氨酸(TT3)、游离三碘甲腺原氨酸(FT3)[ (0.47±0.70)nmol/L、(2.41±0.28)pmol/L、(0.76±0.08 )nmol/L、(4.01±0.40) pmol/L]显著低于对照组[(55.2±3.68)nmol/L、(32.72±1.02) pmol/L、(1.10±0.06)nmol/L、(5.40±0.38 )pmol/L,t=43.81、86.04、9.81、7.51,P均＜0.01]；低碘组小鼠TSH[(35.67±17.39)mU/L]明显高于对照组[(0.24±0.10)mU/L,t =-6.11、,P＜0.001]；低碘组小鼠骨髓、外周血TSHβ-Ⅴ mRNA表达水平[(9.62±0.60)、(9.25±0.83)]均低于正常对照组(7.69±0.36、7.11±0.41,t=6.77、5.64,P均＜0.001)；低碘组小鼠甲状腺TSHβ-Ⅴ mRNA表达(9.32±0.91)与对照组(9.12±0.62)相比较,差异无统计学意义(t=0.45,P＞0.05)；在骨髓、外周血、甲状腺未检出天然型TSHβ;垂体中TSHβ-Ⅴ mRNA和天然型TSHβ表达水平(1.99±0.61、- 7.17±1.78)均高于对照组(5.75±0.98、-1.43±0.51,t=-8.02、- 7.60,P均＜0.01].结论 低碘饮食引发小鼠甲状腺功能低下,抑制骨髓和外周血TSHβ-Ⅴ mRNA的表达,提示免疫系统来源的TSHβ-Ⅴ可能具有比天然型TSHβ更重要的免疫-甲状腺调节作用.
目的 製備碘缺乏小鼠模型,檢測促甲狀腺激素(TSH)β剪接變體(TSHβ-Ⅴ)是否受循環中甲狀腺激素的調節,探討免疫繫統來源的TSHβ-Ⅴ在維持甲狀腺自穩態中的作用.方法 選用離乳BALB/c小鼠20隻,雌雄各半.小鼠按體質量和性彆隨機分為2組,每組10隻.對照組:飲去離子水,普通飼料餵養；低碘組:飲去離子水,低碘飼料(含碘量20 - 40μg /kg)餵養,每日碘攝入量約為0.25μg/d.3箇月後處死小鼠,化學髮光免疫分析法(CIA)檢測小鼠血清中甲狀腺激素和TSH水平,實時定量(RT)-PCR法測定小鼠骨髓、外週血、甲狀腺、垂體TSHβ-Ⅴ的錶達.結果 低碘組小鼠血清總甲狀腺素(TT4)、遊離甲狀腺素(FT4)、總三碘甲腺原氨痠(TT3)、遊離三碘甲腺原氨痠(FT3)[ (0.47±0.70)nmol/L、(2.41±0.28)pmol/L、(0.76±0.08 )nmol/L、(4.01±0.40) pmol/L]顯著低于對照組[(55.2±3.68)nmol/L、(32.72±1.02) pmol/L、(1.10±0.06)nmol/L、(5.40±0.38 )pmol/L,t=43.81、86.04、9.81、7.51,P均＜0.01]；低碘組小鼠TSH[(35.67±17.39)mU/L]明顯高于對照組[(0.24±0.10)mU/L,t =-6.11、,P＜0.001]；低碘組小鼠骨髓、外週血TSHβ-Ⅴ mRNA錶達水平[(9.62±0.60)、(9.25±0.83)]均低于正常對照組(7.69±0.36、7.11±0.41,t=6.77、5.64,P均＜0.001)；低碘組小鼠甲狀腺TSHβ-Ⅴ mRNA錶達(9.32±0.91)與對照組(9.12±0.62)相比較,差異無統計學意義(t=0.45,P＞0.05)；在骨髓、外週血、甲狀腺未檢齣天然型TSHβ;垂體中TSHβ-Ⅴ mRNA和天然型TSHβ錶達水平(1.99±0.61、- 7.17±1.78)均高于對照組(5.75±0.98、-1.43±0.51,t=-8.02、- 7.60,P均＜0.01].結論 低碘飲食引髮小鼠甲狀腺功能低下,抑製骨髓和外週血TSHβ-Ⅴ mRNA的錶達,提示免疫繫統來源的TSHβ-Ⅴ可能具有比天然型TSHβ更重要的免疫-甲狀腺調節作用.
목적 제비전결핍소서모형,검측촉갑상선격소(TSH)β전접변체(TSHβ-Ⅴ)시부수순배중갑상선격소적조절,탐토면역계통래원적TSHβ-Ⅴ재유지갑상선자은태중적작용.방법 선용리유BALB/c소서20지,자웅각반.소서안체질량화성별수궤분위2조,매조10지.대조조:음거리자수,보통사료위양；저전조:음거리자수,저전사료(함전량20 - 40μg /kg)위양,매일전섭입량약위0.25μg/d.3개월후처사소서,화학발광면역분석법(CIA)검측소서혈청중갑상선격소화TSH수평,실시정량(RT)-PCR법측정소서골수、외주혈、갑상선、수체TSHβ-Ⅴ적표체.결과 저전조소서혈청총갑상선소(TT4)、유리갑상선소(FT4)、총삼전갑선원안산(TT3)、유리삼전갑선원안산(FT3)[ (0.47±0.70)nmol/L、(2.41±0.28)pmol/L、(0.76±0.08 )nmol/L、(4.01±0.40) pmol/L]현저저우대조조[(55.2±3.68)nmol/L、(32.72±1.02) pmol/L、(1.10±0.06)nmol/L、(5.40±0.38 )pmol/L,t=43.81、86.04、9.81、7.51,P균＜0.01]；저전조소서TSH[(35.67±17.39)mU/L]명현고우대조조[(0.24±0.10)mU/L,t =-6.11、,P＜0.001]；저전조소서골수、외주혈TSHβ-Ⅴ mRNA표체수평[(9.62±0.60)、(9.25±0.83)]균저우정상대조조(7.69±0.36、7.11±0.41,t=6.77、5.64,P균＜0.001)；저전조소서갑상선TSHβ-Ⅴ mRNA표체(9.32±0.91)여대조조(9.12±0.62)상비교,차이무통계학의의(t=0.45,P＞0.05)；재골수、외주혈、갑상선미검출천연형TSHβ;수체중TSHβ-Ⅴ mRNA화천연형TSHβ표체수평(1.99±0.61、- 7.17±1.78)균고우대조조(5.75±0.98、-1.43±0.51,t=-8.02、- 7.60,P균＜0.01].결론 저전음식인발소서갑상선공능저하,억제골수화외주혈TSHβ-Ⅴ mRNA적표체,제시면역계통래원적TSHβ-Ⅴ가능구유비천연형TSHβ경중요적면역-갑상선조절작용.
Objective To find out if the immune system derived thyroid stimulating hormone(TSH) β splice variant(TSHβ-Ⅴ) would be regulated by circulating thyroid hormone levels to get a further understanding of the function and mechanism of this TSHβ-Ⅴ in thyroid homeostasis.Methods A total of 20 weaning Balb/c mice (half male and half female) were selected and randomly divided into two groups according to their body mass and gender(n =10).Mice of control group were fed with common diet and deionized water.Mice of the low-iodine(LI) group were fed with low-iodine diet(containing iodine 20 - 40 μg/kg,iodine-intake about 0.25 μg/d) and deionized water.The experimental period was 3 months.At the end of the experiment,mice were executed and the blood was collected to observe the levels of TSH and thyroid hormone by chemiluminescence immunoassay (CIA) ; bone marrow (BM),peripheral blood(PBL),thyroid gland and pituitary were collected to assay the TSHβ-Ⅴ mRNA expression by real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR).Results The serum free thyroxine(FT4) and total thyroxine(TT4) levels in LI group of mice[(0.47 ± 0.70)nmol/L,(2.41 ± 0.28)pmol/L] were significantly lower than that of the control group of mice [(55.2 ± 3.68) nmol/L, (32.72 ± 1.02) pmol/L,t =43.81,86.04 、all P ＜ 0.01 ] and the serum total triiodothyronine(TT3) and free triiodothyronine(FT3) reduction in LI group of mice[ (0.76 ± 0.08)nmol/L,(4.01 ± 0.40)pmol/L] were significantly lower than that of the control group of mice [ (1.10 ± 0.06)nmol/L,(5.40 ± 0.38)pmol/L,t =9.81,7.5 1,P ＜ 0.01 ].Iodine insufficiency strongly elevated the serum TSH in LI group of mice[ (35.67 ± 17.39)mU/L] than that in control group of mice[ (0.24 ± 0.10)mU/L,t =- 6.11,P ＜ 0.01 ].The mRNA levels of TSH β-Ⅴ in BM (9.62 ± 0.60) and in PBL( 9.25 ± 0.83 ) of LI group of mice were lower than those in control group of mice (7.69 ± 0.36,7.11 ± 0.41,t =6.77,5.64,P ＜ 0.01),while the mRNA level of TSH β-Ⅴ in pituitary of LI group of mice (1.99 ± 0.61) was increased compared with that in control group of mice (5.75 ± 0.98,t =- 8.02,P＜ 0.01).Compared with control group of mice(9.12 ± 0.62),the level of thyroid TSH β-Ⅴ mRNA in LI group of mice (9.32 ± 0.91 ) was not significantly changed (t =0.45,P ＞ 0.05).There was no detectable native TSHβ in BM,PBL and thyroid.The mRNA level of native TSHβ in pituitary in LI group of mice( - 7.17 ± 1.78) was dramatically elevated compared to that in control group of mice( - 1.43 ± 0.51,t =- 7.60,P ＜ 0.01 ).Conclusions The mRNA levels of TSHβ-Ⅴ are suppressed in BM and PBL in low iodinediet induced hypothyroidism mice,which suggest that immune system derived TSHβ-Ⅴ may be more important thannative TSHβ in immune-thyroid regulation.
