中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2009年
9期
765-768
,共4页
普伐他汀%动脉硬化%细胞凋亡
普伐他汀%動脈硬化%細胞凋亡
보벌타정%동맥경화%세포조망
Pravastatin%Atherosclerosis%Apoptosis
目的 研究普伐他汀对载脂蛋白(apo)E-/-小鼠血脂、肿瘤坏死因子(TNF)a及动脉粥样硬化血管B细胞淋巴瘤(Bcl-2)及相关X蛋白(Bax)表达的影响.方法 应用高胆固醇饲料建立apoE-/-小鼠动脉粥样硬化模型,采用普伐他汀混悬液灌胃,实验8周后,酶联免疫吸附法及反转录聚合酶链式扩增法测定血清及主动脉TNFa水平,并应用Westernblot法检测主动脉Bax及Bcl-2蛋白的表达,苏木素伊红(HE)染色观察主动脉组织形态学变化.结果 普伐他汀可降低动脉粥样硬化apoE-/-小鼠血清及动脉TNFa水平(34.8±22.7)μg/L与(180.1±59.1)μg/L,改善主动脉组织病理损伤,调控动脉粥样硬化血管Bax及Bcl-2蛋白表达.结论 普伐他汀可降低血脂,干预动脉粥样硬化的始动环节,并从蛋白水平调控动脉粥样硬化内皮细胞凋亡.
目的 研究普伐他汀對載脂蛋白(apo)E-/-小鼠血脂、腫瘤壞死因子(TNF)a及動脈粥樣硬化血管B細胞淋巴瘤(Bcl-2)及相關X蛋白(Bax)錶達的影響.方法 應用高膽固醇飼料建立apoE-/-小鼠動脈粥樣硬化模型,採用普伐他汀混懸液灌胃,實驗8週後,酶聯免疫吸附法及反轉錄聚閤酶鏈式擴增法測定血清及主動脈TNFa水平,併應用Westernblot法檢測主動脈Bax及Bcl-2蛋白的錶達,囌木素伊紅(HE)染色觀察主動脈組織形態學變化.結果 普伐他汀可降低動脈粥樣硬化apoE-/-小鼠血清及動脈TNFa水平(34.8±22.7)μg/L與(180.1±59.1)μg/L,改善主動脈組織病理損傷,調控動脈粥樣硬化血管Bax及Bcl-2蛋白錶達.結論 普伐他汀可降低血脂,榦預動脈粥樣硬化的始動環節,併從蛋白水平調控動脈粥樣硬化內皮細胞凋亡.
목적 연구보벌타정대재지단백(apo)E-/-소서혈지、종류배사인자(TNF)a급동맥죽양경화혈관B세포림파류(Bcl-2)급상관X단백(Bax)표체적영향.방법 응용고담고순사료건립apoE-/-소서동맥죽양경화모형,채용보벌타정혼현액관위,실험8주후,매련면역흡부법급반전록취합매련식확증법측정혈청급주동맥TNFa수평,병응용Westernblot법검측주동맥Bax급Bcl-2단백적표체,소목소이홍(HE)염색관찰주동맥조직형태학변화.결과 보벌타정가강저동맥죽양경화apoE-/-소서혈청급동맥TNFa수평(34.8±22.7)μg/L여(180.1±59.1)μg/L,개선주동맥조직병리손상,조공동맥죽양경화혈관Bax급Bcl-2단백표체.결론 보벌타정가강저혈지,간예동맥죽양경화적시동배절,병종단백수평조공동맥죽양경화내피세포조망.
Objective To investigate the effects of pravastatin on the serum lipids, the tumor necrosis factor (TNF)α and the expressions of Bax and Bcl-2 in apoE-/- mouse. Methods The atherosclerosis model of apoE-/- mouse was induced by high cholesterol diet;and the suspension of pravastatin was administered intragastrieally. After 8 weeks, the levels of serum TNFα and mRNA of aortic TNFα were detected by enzyme linked immunosorbent assay (ELISA) and reverse transcription polymerase chain reaction (RT-PCR), respectively. The expressions of Bax and Bcl-2 were tested by Western blot analysis and aortic histomorphology changes was observed by Hematoxylin-Eosin (HE) stainning. Results In atherosclerosis model of apoE-/- mouse, the serum lipids, the levels of serum and aortic TNFα[(34.8±22.7) μg/L and (180.1±59.1 )μg/L], the expressions of Bax and Bcl-2 and aortic histomorphology were obviously improved by pravastatin. Conclusions It is suggested that the pravastatin can reduce serum lipid, intervene the initiation step of atherosclerosis and regulate endothelial cells' apoptosis.
