中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2010年
4期
305-309
,共5页
王慧智%代莉%张宇%韦灵%王洪浩%张婉斌%谭松
王慧智%代莉%張宇%韋靈%王洪浩%張婉斌%譚鬆
왕혜지%대리%장우%위령%왕홍호%장완빈%담송
血管紧张素Ⅱ1型受体拮抗剂%Janus激酶类%衔接蛋白质类,信号转导%转录激活因子类%细胞凋亡
血管緊張素Ⅱ1型受體拮抗劑%Janus激酶類%銜接蛋白質類,信號轉導%轉錄激活因子類%細胞凋亡
혈관긴장소Ⅱ1형수체길항제%Janus격매류%함접단백질류,신호전도%전록격활인자류%세포조망
Angiotensin Ⅱ type 1 receptor blockers%Janus kinases%Adaptor proteins,signal transducing%Activating transcription factors%Apoptosis
目的 探讨厄贝沙坦对自发性高血压大鼠(SHR)心肌组织Janus激酶-信号转导蛋白和转录激活蛋白(JAK-STAT)信号转导通路及细胞凋亡的影响. 方法 30周龄WKY大鼠13只,设为WKY对照组;30周龄SHR 26只,随机分为SHR对照组和厄贝沙坦组.反转录-聚合酶链反应(RT-PCR)法检测血管紧张素Ⅱ1型(AT1)与2型(AT2)受体mRNA在心肌中的表达,免疫组化法检测心肌组织STAT1、STAT3表达,TUNEL细胞凋亡显色法进行细胞凋亡检测. 结果 (1)厄贝沙坦组与SHR对照组比较,AT1 mRNA表达水平显著降低(0.72±0.55对1.08±0.13,P<0.01),AT2 mRNA表达水平显著增高(0.30±0.32对0.25±0.35,P<0.01);(2)与SHR对照组比较,厄贝沙坦能降低STAT1表达(7.27±0.53对13.16±0.35,P<0.01),升高STAT3表达(5.41±0.37对4.82±0.34,P<0.01);(3)厄贝沙坦组心肌细胞凋亡率显著低于SHR对照组(P<0.01). 结论厄贝沙坦能调节心肌组织JAK-STAT信号转导通路,抑制细胞凋亡,从而发挥其心脏保护作用.
目的 探討阨貝沙坦對自髮性高血壓大鼠(SHR)心肌組織Janus激酶-信號轉導蛋白和轉錄激活蛋白(JAK-STAT)信號轉導通路及細胞凋亡的影響. 方法 30週齡WKY大鼠13隻,設為WKY對照組;30週齡SHR 26隻,隨機分為SHR對照組和阨貝沙坦組.反轉錄-聚閤酶鏈反應(RT-PCR)法檢測血管緊張素Ⅱ1型(AT1)與2型(AT2)受體mRNA在心肌中的錶達,免疫組化法檢測心肌組織STAT1、STAT3錶達,TUNEL細胞凋亡顯色法進行細胞凋亡檢測. 結果 (1)阨貝沙坦組與SHR對照組比較,AT1 mRNA錶達水平顯著降低(0.72±0.55對1.08±0.13,P<0.01),AT2 mRNA錶達水平顯著增高(0.30±0.32對0.25±0.35,P<0.01);(2)與SHR對照組比較,阨貝沙坦能降低STAT1錶達(7.27±0.53對13.16±0.35,P<0.01),升高STAT3錶達(5.41±0.37對4.82±0.34,P<0.01);(3)阨貝沙坦組心肌細胞凋亡率顯著低于SHR對照組(P<0.01). 結論阨貝沙坦能調節心肌組織JAK-STAT信號轉導通路,抑製細胞凋亡,從而髮揮其心髒保護作用.
목적 탐토액패사탄대자발성고혈압대서(SHR)심기조직Janus격매-신호전도단백화전록격활단백(JAK-STAT)신호전도통로급세포조망적영향. 방법 30주령WKY대서13지,설위WKY대조조;30주령SHR 26지,수궤분위SHR대조조화액패사탄조.반전록-취합매련반응(RT-PCR)법검측혈관긴장소Ⅱ1형(AT1)여2형(AT2)수체mRNA재심기중적표체,면역조화법검측심기조직STAT1、STAT3표체,TUNEL세포조망현색법진행세포조망검측. 결과 (1)액패사탄조여SHR대조조비교,AT1 mRNA표체수평현저강저(0.72±0.55대1.08±0.13,P<0.01),AT2 mRNA표체수평현저증고(0.30±0.32대0.25±0.35,P<0.01);(2)여SHR대조조비교,액패사탄능강저STAT1표체(7.27±0.53대13.16±0.35,P<0.01),승고STAT3표체(5.41±0.37대4.82±0.34,P<0.01);(3)액패사탄조심기세포조망솔현저저우SHR대조조(P<0.01). 결론액패사탄능조절심기조직JAK-STAT신호전도통로,억제세포조망,종이발휘기심장보호작용.
Objective To investigate the effects of irbesartan on regulating JAK-STAT signal pathway and apoptosis in myocardium of spontaneous hypertensive rat (SHR). Methods There were 13 Wistar-Kyoto (WKY) rats aged 30 weeks as WKY control group, and 26 SHRs at the same age were randomly divided into SHR control group and irbesartan treatment group (n=13, respectively). The mRNA expression levels of AT1 and AT2 were detected by RT-PCR. The STAT1 and STAT3 expression levels in myocardium were determined by immunohistochemical methods. The apoptosis rate of myocardial cells was measured by Colorimetric TUNEL. Results The mRNA expression level of AT1 was significantly lower in irbesartan group than in SHR control group (0.72±0.55 vs. 1.08±0. 13, P<0.01), while in study of irbesartan versus SHR control group, the mRNA expression level of AT2 was significantly higher (0.30±0.32 vs. 0.25±0.35, P<0.01), the STAT1 expression in protein level was significantly lower (7.27±0.53 vs. 13.16±0.35, P<0.01),and the STAT3 expression in protein level was significantly higher (5.41±0.37 vs. 4.82±0.34, P< 0.01). The apoptosis rate was significantly higher in SHR control group than in irbesartan group (P<0.01). Conclusions Irbesartan can regulate JAK-STAT signal transduction pathway in myocardium of SHR, and inhibit apoptosis of myocardium to produce a protective effect on the heart.
