中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2001年
1期
46-49
,共4页
原卫清%王颢%吕卓人%张明娟%杨军
原衛清%王顥%呂卓人%張明娟%楊軍
원위청%왕호%려탁인%장명연%양군
高血压%大鼠%肾皮质%钠钾泵%基因表达
高血壓%大鼠%腎皮質%鈉鉀泵%基因錶達
고혈압%대서%신피질%납갑빙%기인표체
目的:探讨“一肾一夹(1k1c)”高血压大鼠肾脏皮质钠泵α亚单位各异构体基因表达的改变,为高血压发病机制的深入研究提供理论及实验依据。方法:分别应用RT-PCR及免疫组化技术,探讨1k1c高血压大鼠肾脏皮质钠泵α1、α2及α3亚单位mRNA及蛋白水平基因表达的改变。结果:正常大鼠肾脏皮质主要表达钠泵α1亚单位,α2与α3亚单位表达较弱;在mRNA水平,1k1c高血压大鼠肾脏皮质钠泵α1亚单位表达明显较强,α2与α3亚单位表达无改变,而在蛋白水平各亚单位基因表达与对照组比较均无明显差异。结论:1k1c高血压大鼠肾皮质钠泵α亚单位基因表达发生改变,这种改变可能参与该模型的血压升高机制。
目的:探討“一腎一夾(1k1c)”高血壓大鼠腎髒皮質鈉泵α亞單位各異構體基因錶達的改變,為高血壓髮病機製的深入研究提供理論及實驗依據。方法:分彆應用RT-PCR及免疫組化技術,探討1k1c高血壓大鼠腎髒皮質鈉泵α1、α2及α3亞單位mRNA及蛋白水平基因錶達的改變。結果:正常大鼠腎髒皮質主要錶達鈉泵α1亞單位,α2與α3亞單位錶達較弱;在mRNA水平,1k1c高血壓大鼠腎髒皮質鈉泵α1亞單位錶達明顯較彊,α2與α3亞單位錶達無改變,而在蛋白水平各亞單位基因錶達與對照組比較均無明顯差異。結論:1k1c高血壓大鼠腎皮質鈉泵α亞單位基因錶達髮生改變,這種改變可能參與該模型的血壓升高機製。
목적:탐토“일신일협(1k1c)”고혈압대서신장피질납빙α아단위각이구체기인표체적개변,위고혈압발병궤제적심입연구제공이론급실험의거。방법:분별응용RT-PCR급면역조화기술,탐토1k1c고혈압대서신장피질납빙α1、α2급α3아단위mRNA급단백수평기인표체적개변。결과:정상대서신장피질주요표체납빙α1아단위,α2여α3아단위표체교약;재mRNA수평,1k1c고혈압대서신장피질납빙α1아단위표체명현교강,α2여α3아단위표체무개변,이재단백수평각아단위기인표체여대조조비교균무명현차이。결론:1k1c고혈압대서신피질납빙α아단위기인표체발생개변,저충개변가능삼여해모형적혈압승고궤제。
AIM: To investigate the regulation of sodium pump α-subunit geneexpression in the cortex of kidneys from one kidney one clip (1k1c) hypertensive rats. METHODS: 1k1c hypertensive rats were prepared by partially ligating the left renal artery and removing the right kidney. 4 weeks later, all the rats were killed, the levels of sodium pump α1-, α2-, and α3-subunit mRNA and protein in the cortex of kidney were detected with reverse transcription polymerase chain reaction (RT-PCR) method and immunohistochemical assay, respectively. RESULTS: The mRNA levels of sodium pump α1-subunit increased and α2- and α3-subunit were unchanged in the cortex of kidneys from 1k1c hypertensive rats compared with control rats, while no change has been found for all the three subunits gene expressions at protein level. CONCLUSION: There were some changes in the expression of sodium pump α-subunit gene in the cortex of kidney of the 1k1c hypertensive rat, which might be related to the development of hypertension in this hypertensive model.