中国现代药物应用
中國現代藥物應用
중국현대약물응용
CHINESE JOURNAL OF MODERN DRUG APPLICATION
2015年
1期
12-13
,共2页
信号转导及转录激活因子3%动脉粥样硬化%炎症%瑞舒伐他汀
信號轉導及轉錄激活因子3%動脈粥樣硬化%炎癥%瑞舒伐他汀
신호전도급전록격활인자3%동맥죽양경화%염증%서서벌타정
Signal transducers and activators of transcription 3%Atherosclerosis%Inflammation%Rosuvastatin
目的:研究瑞舒伐他汀对家兔动脉粥样硬化的影响及其机制。方法随机将30只纯种雄性大白兔分成三组,正常饮食组(对照组),高脂饮食组(高脂组),高脂饮食加瑞舒伐他汀组(瑞舒伐他汀组)。实验动物喂养8周后检测各实验组血清低密度脂蛋白胆固醇(LDL-C)、甘油三酯(TG)、总胆固醇(TC),用免疫组化的方法检测信号转导及转录激活因子3(STAT3)、白细胞介素-6(IL-6)在组织中的表达。结果实验显示高脂组、瑞舒伐他汀组中LDL-C、TG、TC水平较对照组明显增高(P<0.05);瑞舒伐他汀组LDL-C、TG、TC水平较高脂组降低(P<0.05)。IL-6、STAT3在瑞舒伐他汀组中表达较高脂组明显减少,两者的表达为正相关。结论瑞舒伐他汀可通过抑制炎症反应抑制动脉粥样硬化的发生,其机制与阻断JAK-STAT3信号转导通路有关。
目的:研究瑞舒伐他汀對傢兔動脈粥樣硬化的影響及其機製。方法隨機將30隻純種雄性大白兔分成三組,正常飲食組(對照組),高脂飲食組(高脂組),高脂飲食加瑞舒伐他汀組(瑞舒伐他汀組)。實驗動物餵養8週後檢測各實驗組血清低密度脂蛋白膽固醇(LDL-C)、甘油三酯(TG)、總膽固醇(TC),用免疫組化的方法檢測信號轉導及轉錄激活因子3(STAT3)、白細胞介素-6(IL-6)在組織中的錶達。結果實驗顯示高脂組、瑞舒伐他汀組中LDL-C、TG、TC水平較對照組明顯增高(P<0.05);瑞舒伐他汀組LDL-C、TG、TC水平較高脂組降低(P<0.05)。IL-6、STAT3在瑞舒伐他汀組中錶達較高脂組明顯減少,兩者的錶達為正相關。結論瑞舒伐他汀可通過抑製炎癥反應抑製動脈粥樣硬化的髮生,其機製與阻斷JAK-STAT3信號轉導通路有關。
목적:연구서서벌타정대가토동맥죽양경화적영향급기궤제。방법수궤장30지순충웅성대백토분성삼조,정상음식조(대조조),고지음식조(고지조),고지음식가서서벌타정조(서서벌타정조)。실험동물위양8주후검측각실험조혈청저밀도지단백담고순(LDL-C)、감유삼지(TG)、총담고순(TC),용면역조화적방법검측신호전도급전록격활인자3(STAT3)、백세포개소-6(IL-6)재조직중적표체。결과실험현시고지조、서서벌타정조중LDL-C、TG、TC수평교대조조명현증고(P<0.05);서서벌타정조LDL-C、TG、TC수평교고지조강저(P<0.05)。IL-6、STAT3재서서벌타정조중표체교고지조명현감소,량자적표체위정상관。결론서서벌타정가통과억제염증반응억제동맥죽양경화적발생,기궤제여조단JAK-STAT3신호전도통로유관。
Objective To study the influence and mechanism of rosuvastatin on atherosclerosis in rabbits. Methods A total of 30 male purebred rabbits were randomly divided into 3 groups, as normal diet group (control group), high fat diet group (high fat group), and high fat diet plus rosuvastatin group (rosuvastatin group). After feeding for 8 weeks, the levels of low density lipoprotein cholesterol (LDL-C), triglyceride (TG), and total cholesterol (TC) were detected in each group. The expressions of signal transducer and activator of transcription 3 (STAT3) and interleukin-6 (IL-6) were detected by immunohistochemical method. Results The levels of LDL-C, TG, and TC in high fat group and rosuvastatin group were all obviously increased than those in the control group (P<0.05). The levels of LDL-C, TG, and TC were decreased in the rosuvastatin group, compared with that in the high fat group (P<0.05). The expressions of IL-6 and STAT3 in the rosuvastatin group were obviously decreased, compared with those in the high fat group, and their expressions were positively correlated. Conclusion Rosuvastatin can suppress atherosclerosis by inhibiting inflammatory reaction, and its mechanism is related with JAK-STAT3 signal transduction pathway.