中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2013年
7期
782-785
,共4页
刘相菊%邱洁%由倍安%高海青
劉相菊%邱潔%由倍安%高海青
류상국%구길%유배안%고해청
原花青素%哇巴因%高血压
原花青素%哇巴因%高血壓
원화청소%왜파인%고혈압
Proanthocyanidins%Ouabain%Hypertension
目的 观察葡萄籽原花青素(GSPE)对哇巴因高血压大鼠血管重构的作用. 方法 30只雄性SD大鼠,随机分为3组(每组10只):(1)对照组:每日清晨给予0.9％生理盐水1 ml腹腔注射,同时0.9％生理盐水1 ml灌胃；(2)哇巴因组:每日清晨给予腹腔注射畦巴因2mg/kg,并给予1ml 0.9％生理盐水灌胃；(3)GSPE组:每日清晨给予腹腔注射哇巴因2mg/kg,并给予250 mg· kg-1·d-1 GSPE灌胃.实验前、实验5周后测定大鼠血压,5周后处死大鼠,留取主动脉,通过反转录聚合酶链反应(RT-PCR)、免疫印迹分析(Westen blot)进行形态学观察和分子生物学检查. 结果 5周末,GSPE治疗组大鼠血压较哇巴因组下降,分别为(133.6±6.0)mm Hg(1 mm Hg=0.133 kPa)与(146.5±7.9)mm Hg(P＜0.01).形态学观察结果显示,哇巴因组大鼠主动脉内膜增厚,结构紊乱,而GSPE组与对照组血管内膜结构完整.核因子κB p65 (NF-κB p65)和转化生长因子(TGF)-β1的mRNA表达及其与内参蛋白的对比中,GSPE可降低哇巴因组大鼠主动脉核因子κB(NF-κB) p65和TGF-β1的表达3.14±0.64与2.77±0.58、6.09±0.95与5.80±0.67、0.93±0.21与0.73±0.20)、0.69±0.16与0.42±0.14,均P＜0.05. 结论 GSPE具有拮抗内源性哇巴因的作用,可以通过抑制NF-κB和(或)TGF-β1途径,延缓了血压的升高和血管重构的过程.
目的 觀察葡萄籽原花青素(GSPE)對哇巴因高血壓大鼠血管重構的作用. 方法 30隻雄性SD大鼠,隨機分為3組(每組10隻):(1)對照組:每日清晨給予0.9％生理鹽水1 ml腹腔註射,同時0.9％生理鹽水1 ml灌胃；(2)哇巴因組:每日清晨給予腹腔註射畦巴因2mg/kg,併給予1ml 0.9％生理鹽水灌胃；(3)GSPE組:每日清晨給予腹腔註射哇巴因2mg/kg,併給予250 mg· kg-1·d-1 GSPE灌胃.實驗前、實驗5週後測定大鼠血壓,5週後處死大鼠,留取主動脈,通過反轉錄聚閤酶鏈反應(RT-PCR)、免疫印跡分析(Westen blot)進行形態學觀察和分子生物學檢查. 結果 5週末,GSPE治療組大鼠血壓較哇巴因組下降,分彆為(133.6±6.0)mm Hg(1 mm Hg=0.133 kPa)與(146.5±7.9)mm Hg(P＜0.01).形態學觀察結果顯示,哇巴因組大鼠主動脈內膜增厚,結構紊亂,而GSPE組與對照組血管內膜結構完整.覈因子κB p65 (NF-κB p65)和轉化生長因子(TGF)-β1的mRNA錶達及其與內參蛋白的對比中,GSPE可降低哇巴因組大鼠主動脈覈因子κB(NF-κB) p65和TGF-β1的錶達3.14±0.64與2.77±0.58、6.09±0.95與5.80±0.67、0.93±0.21與0.73±0.20)、0.69±0.16與0.42±0.14,均P＜0.05. 結論 GSPE具有拮抗內源性哇巴因的作用,可以通過抑製NF-κB和(或)TGF-β1途徑,延緩瞭血壓的升高和血管重構的過程.
목적 관찰포도자원화청소(GSPE)대왜파인고혈압대서혈관중구적작용. 방법 30지웅성SD대서,수궤분위3조(매조10지):(1)대조조:매일청신급여0.9％생리염수1 ml복강주사,동시0.9％생리염수1 ml관위；(2)왜파인조:매일청신급여복강주사휴파인2mg/kg,병급여1ml 0.9％생리염수관위；(3)GSPE조:매일청신급여복강주사왜파인2mg/kg,병급여250 mg· kg-1·d-1 GSPE관위.실험전、실험5주후측정대서혈압,5주후처사대서,류취주동맥,통과반전록취합매련반응(RT-PCR)、면역인적분석(Westen blot)진행형태학관찰화분자생물학검사. 결과 5주말,GSPE치료조대서혈압교왜파인조하강,분별위(133.6±6.0)mm Hg(1 mm Hg=0.133 kPa)여(146.5±7.9)mm Hg(P＜0.01).형태학관찰결과현시,왜파인조대서주동맥내막증후,결구문란,이GSPE조여대조조혈관내막결구완정.핵인자κB p65 (NF-κB p65)화전화생장인자(TGF)-β1적mRNA표체급기여내삼단백적대비중,GSPE가강저왜파인조대서주동맥핵인자κB(NF-κB) p65화TGF-β1적표체3.14±0.64여2.77±0.58、6.09±0.95여5.80±0.67、0.93±0.21여0.73±0.20)、0.69±0.16여0.42±0.14,균P＜0.05. 결론 GSPE구유길항내원성왜파인적작용,가이통과억제NF-κB화(혹)TGF-β1도경,연완료혈압적승고화혈관중구적과정.
Objective To observe the effect of grape seed proanthocyanidin extract (GSPE) on vascular remodeling in ouabain-induced hypertensive rats.Methods A total of 30 male SpragueDawley rats were randomized into 3 groups:control group (received 0.9％ 1 ml normal saline by intraperitoneal injection and oral gavage in the morning),ouabain treatment group (received 2 mg/kg ouabain by intraperitoneal injection and 0.9 ％ 1 ml normal saline by oral gavage in the morning),and GSPE treatment group (received 2 mg/kg ouabain by intraperitoneal injection and 250 mg Kg 1 d-1 GSPE by oral gavage in the morning).Blood pressure was determined before and 5 weeks after the treatment.The aortas were observed 5 weeks after the treatment.The mRNA and protein levels of nuclear factor-κB (NF-κB p65) and transforming growth factor-β1 (TGF-β1) in rat aorta were detected using real-time PCR and Western blot,respectively.Morphological observations were obtained by Hemotoxylin and Eosin staining and Electron microscope.Results The systolic blood pressure was significantly lower in GSPE treatment group than in ouabain treatment group [(133.6±6.0) mm Hg vs.(146.5±7.9) mm Hg,1 mm Hg=0.133 kPa,P＜0.01].Morphological observation showed that the thickening aortic intimal and structural disorder were found in the ouabain treatment group,and aortic intimal structural integrity were normal in the other two groups.The mRNA and protein levels of NF-κB p65 and TGF-β1 were significantly lower in GSPE treatment group than in the ouabain treatment group (NF-κBp65:2.77±0.58 vs.3.14±0.64,0.73±0.20 vs.0.93±0.21,both P＜0.05; TGF-β1:5.80±0.67 vs.6.09±0.95,0.42±0.14 vs.0.69±0.16,both P＜0.05).Conclusions GSPE may inhibit endogenous ouabain,and delay the process of elevated blood pressure and vascular remodeling by inhibiting NF-κ B p65 and (or) TGF-β3 1 pathways.
