CAJ | 학술논문

目的研究甲减大鼠肾脏抗氧化能力的变化,探讨甲状腺激素水平对肾脏的影响.方法 Wistar大鼠随机分2组:甲减组(HT)和对照组(Control).2组大鼠通过不同碘含量饮食复制甲减动物模型;肾脏形态定量学观察;比色法测定肾脏组织丙二醛(MDA)含量、谷胱甘肽过氧化物酶(GPx)、超氧化物歧化酶(SOD)及生物膜Na~+,K~+-ATPase活性;RT-PCR方法测定肾脏Na~+,K~+-ATPase αl亚基的基因表达.结果与对照组比较,HT组FT3、FT4、TT3、TT4显著降低(P<0.01);肾小球萎缩;MDA含最和GPx活性显著升高(P<0.05),而 SOD和Na~+,K~+-ATPase活性显著降低(P<0.05);Na~+,K~+-ATPase αl亚基的基因表达下降(P<0.05).结论甲状腺激素不足可导致肾脏抗氧化能力下降,肾小球萎缩.
목적 연구갑감대서신장항양화능력적변화,탐토갑상선격소수평대신장적영향.방법 Wistar대서수궤분2조:갑감조(HT)화대조조(Control).2조대서통과불동전함량음식복제갑감동물모형;신장형태정량학관찰;비색법측정신장조직병이철(MDA)함량、곡광감태과양화물매(GPx)、초양화물기화매(SOD)급생물막Na~+,K~+-ATPase활성;RT-PCR방법측정신장Na~+,K~+-ATPase αl아기적기인표체.결과 여대조조비교,HT조FT3、FT4、TT3、TT4현저강저(P<0.01);신소구위축;MDA함최화GPx활성현저승고(P<0.05),이 SOD화Na~+,K~+-ATPase활성현저강저(P<0.05);Na~+,K~+-ATPase αl아기적기인표체하강(P<0.05).결론 갑상선격소불족가도치신장항양화능력하강,신소구위축.
Objective To observe the antioxidative capability and the mRNA expression of sodium pump αl-subunit in kidney of hypothyroid rats by iodine deficiency and illuminate the pathogenesis of kidney damage.Methods Wistar rats were randomly divided into two groups as control group (NT) and hypothyroid group (HT).The rats were all fed with low-iodine diet derived from an endemic goiter area and drank deionized water containing different potassium iodide to duplicate hypothyriod animal models.We determined the morphometric parameters of kidney by routine histology method.The contents of malondialdehyde and free radical scavengers (GSH-PX and SOD) in kid-ney,as well as the activity of Na~+-K~+ ATPase were measured in two groups.The mRNA expression of sodium pump α1 subunit was determined by reverse transcription-polymerase chain reaction.Results Compared with that in the control group,in hypothyroid group (1) serum free T3,free T4,total T3 and total T4 were markedly lower.(2) mean glomerular area and volum diminished markedly.(3)the content of MDA and activity of PGx increased markedly,but the activity of SOD decreased significantly,as well as the one of Na~+-K~+-ATPase.(4)the mRNA expression level of sodium pump α1 subunit was lower.Conclusion In a hypothyroid state,the decrease of antiox-idative capability of kidney resulted in lipid peroxidative damage,atrophy of kidney,decreased activity of Na~+-K~+ -ATPase and degression of sodium pump α1 subunit mRNA expression.