中华内分泌代谢杂志
中華內分泌代謝雜誌
중화내분비대사잡지
CHINESE JOURNAL OF ENDOCRINOLOGY AND METABOLISM
2008年
6期
649-653
,共5页
陈威%滕晓春%单忠艳%范晨玲%关海霞%满娜%李玉姝%佟雅洁%崇巍%滕卫平
陳威%滕曉春%單忠豔%範晨玲%關海霞%滿娜%李玉姝%佟雅潔%崇巍%滕衛平
진위%등효춘%단충염%범신령%관해하%만나%리옥주%동아길%숭외%등위평
碘%甲状腺%细胞凋亡%自由基
碘%甲狀腺%細胞凋亡%自由基
전%갑상선%세포조망%자유기
Iodine%Thyroid gland%Apoptosis%Free radicals
目的 探讨慢性轻中度碘过量对甲状腺细胞凋亡的影响,观察限碘后的恢复情况.方法 将Wistar大鼠分入4组:对照组、1.5倍、3倍和6倍高碘组,每日给碘量分别为4、6、12和24 μg,于实验1至8个月分批处死动物.部分高碘8个月大鼠限碘3个月(4μg/d).采用砷铈催化分光光度法测定尿碘浓度,应用Annexin V染色流式细胞术和电镜对甲状腺细胞凋亡定量定性,碘化丙碇染色流式细胞术测定细胞周期,分子探针(DCFH-DA)荧光定量细胞内活性氧簇(ROS)水平.应用流式细胞术和免疫组织化学方法检测凋亡相关蛋白的表达.结果 3倍和6倍高碘组4个月和8个月时,甲状腺细胞凋亡率和ROS水平显著高于对照(均P<0.05),限碘后恢复正常.6倍碘组4个月和8个月时,甲状腺增殖期细胞比例著升高(5%和6% vs 3%,均P<0.05),静止期细胞比例显著下降(64%和67% vs 80%,均P<0.05).3倍和6倍碘组8个月时,Fas、FasL、TRAIL蛋白表达水平比对照组高2-4倍,限碘后未恢复.Bcl-2和Bax蛋白的表达不变.6倍碘组8个月时,细胞凋亡率、ROS水平及给碘量三者之间显著正相关(r=0.637～0.790,P<0.01).结论 慢性碘过最能增加甲状腺细胞凋亡,ROS过多产生可能涉及其机制.
目的 探討慢性輕中度碘過量對甲狀腺細胞凋亡的影響,觀察限碘後的恢複情況.方法 將Wistar大鼠分入4組:對照組、1.5倍、3倍和6倍高碘組,每日給碘量分彆為4、6、12和24 μg,于實驗1至8箇月分批處死動物.部分高碘8箇月大鼠限碘3箇月(4μg/d).採用砷鈰催化分光光度法測定尿碘濃度,應用Annexin V染色流式細胞術和電鏡對甲狀腺細胞凋亡定量定性,碘化丙碇染色流式細胞術測定細胞週期,分子探針(DCFH-DA)熒光定量細胞內活性氧簇(ROS)水平.應用流式細胞術和免疫組織化學方法檢測凋亡相關蛋白的錶達.結果 3倍和6倍高碘組4箇月和8箇月時,甲狀腺細胞凋亡率和ROS水平顯著高于對照(均P<0.05),限碘後恢複正常.6倍碘組4箇月和8箇月時,甲狀腺增殖期細胞比例著升高(5%和6% vs 3%,均P<0.05),靜止期細胞比例顯著下降(64%和67% vs 80%,均P<0.05).3倍和6倍碘組8箇月時,Fas、FasL、TRAIL蛋白錶達水平比對照組高2-4倍,限碘後未恢複.Bcl-2和Bax蛋白的錶達不變.6倍碘組8箇月時,細胞凋亡率、ROS水平及給碘量三者之間顯著正相關(r=0.637～0.790,P<0.01).結論 慢性碘過最能增加甲狀腺細胞凋亡,ROS過多產生可能涉及其機製.
목적 탐토만성경중도전과량대갑상선세포조망적영향,관찰한전후적회복정황.방법 장Wistar대서분입4조:대조조、1.5배、3배화6배고전조,매일급전량분별위4、6、12화24 μg,우실험1지8개월분비처사동물.부분고전8개월대서한전3개월(4μg/d).채용신시최화분광광도법측정뇨전농도,응용Annexin V염색류식세포술화전경대갑상선세포조망정량정성,전화병정염색류식세포술측정세포주기,분자탐침(DCFH-DA)형광정량세포내활성양족(ROS)수평.응용류식세포술화면역조직화학방법검측조망상관단백적표체.결과 3배화6배고전조4개월화8개월시,갑상선세포조망솔화ROS수평현저고우대조(균P<0.05),한전후회복정상.6배전조4개월화8개월시,갑상선증식기세포비례저승고(5%화6% vs 3%,균P<0.05),정지기세포비례현저하강(64%화67% vs 80%,균P<0.05).3배화6배전조8개월시,Fas、FasL、TRAIL단백표체수평비대조조고2-4배,한전후미회복.Bcl-2화Bax단백적표체불변.6배전조8개월시,세포조망솔、ROS수평급급전량삼자지간현저정상관(r=0.637～0.790,P<0.01).결론 만성전과최능증가갑상선세포조망,ROS과다산생가능섭급기궤제.
Objective To explore the chronic effects of mild and moderate iodine excess and iodine restriction on apoptosis of thyrocytes. Methods Wistar rats were exposed to 4 different doses of iodine: 4 μg/d (control), 6 μg/d (1.5 fold iodine excess), 12 μg/d (3 fold iodine excess), and 24 μg/d (6 fold iodine excess) for 1, 2, 4 and 8 months. Some rats treated for 8 months were fed with 4 μg/d iodine for another 3 months. Urinary iodine concentration was monitored by arscnic/cerium catalyzing spectrophotography. Apoptosis was determined by flow cytometry after Annexin V-FTTC staining and uhrastructure assessment under electronic microscope. Cell cycle kinetics was analyzed by flow eytometry after propidium iodine staining. Fluorescent measurement by DCFH-DA probe was used to determine the intracellular reactive oxygen species (ROS) level. Expressions of apoptic proteins were analyzed by flow cytometry and immunohistochemistry. Results Apoptotosis rate and ROS production in thyrocytes were significantly increased in 3 and 6 fold iodine excess groups after 4 months and 8 months (all P < 0.05), which was reversed with iodine restriction. 6 fold iodine exposure was proved to cause a reduction of cells in GOG1-phase (64% and 67% vs 80%, both P < 0. 05) and a concomitant accumulation in S-phase (5% and 6% vs 3%, both P <0.05) after 4 months and 8 months. Expressions of Fas, FasL and TRAIL proteins in 3 and 6 fold iodine excess groups after 8 months were increased by 2 to 4 times compared with control group and did not return to normal after iodine restriction. Bcl-2 and Bax remained constant. Positive correlations were observed among iodine amount, apoptosis rate and ROS level in 6 fold iodine excess group after 8 months (r = 0. 637-0.790, P < 0.01). Conclusion Chronic iodine excess results in thyrocyte apoptosis due probably to generation of ROS.
