医药导报
醫藥導報
의약도보
HERALD OF MEDICINE
2014年
10期
1310-1313
,共4页
杨波%周承志%张道亮%胡有志%肖金凤
楊波%週承誌%張道亮%鬍有誌%肖金鳳
양파%주승지%장도량%호유지%초금봉
汉黄芩素%高脂血症%氧化代谢%酶活性
漢黃芩素%高脂血癥%氧化代謝%酶活性
한황금소%고지혈증%양화대사%매활성
Wogonin%Dyslipidemia%Oxidative metabolism%Enzyme activity
目的:研究汉黄芩素对饮食诱导下高脂血症小鼠模型的防治作用。方法将30只 C57小鼠随机分为正常对照组、模型对照组和药物干预组,每组10只。正常对照组给予普通饮食,模型对照组给予高脂饲料,药物干预组在高脂饲料基础上添加汉黄芩素500 mg·kg-1。观察汉黄芩素对模型小鼠血脂、脂代谢关键酶的影响,探讨其降脂机制。结果经过12周的高脂饮食,模型小鼠形成了明显的高脂血症,体质量增加,内脏脂肪增多,脂肪指数增加(P<0.05)。药物干预组较模型对照组体质量减轻(P>0.05),内脏脂肪明显减少(P<0.01),脂肪指数显著下降(P<0.05)。汉黄芩素明显降低总胆固醇(TC)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL),但对三酰甘油(TG)影响不大。药物干预组较模型对照组肝脂酶(HL)与脂蛋白脂酶(LPL)活性恢复(P<0.05),羟甲基戊二酸单酰辅酶 A 还原酶活性被抑制(P<0.01);分子生物学研究显示其降脂效果可能与脂合成基因(SREBP-1c,FAS,PPARγ)与脂质代谢基因(PPARα,CPT-1)的转录调控相关。结论汉黄芩素能够很好地治疗高脂血症,这一作用可能与调节脂酶活性和影响脂质合成与氧化基因相关。
目的:研究漢黃芩素對飲食誘導下高脂血癥小鼠模型的防治作用。方法將30隻 C57小鼠隨機分為正常對照組、模型對照組和藥物榦預組,每組10隻。正常對照組給予普通飲食,模型對照組給予高脂飼料,藥物榦預組在高脂飼料基礎上添加漢黃芩素500 mg·kg-1。觀察漢黃芩素對模型小鼠血脂、脂代謝關鍵酶的影響,探討其降脂機製。結果經過12週的高脂飲食,模型小鼠形成瞭明顯的高脂血癥,體質量增加,內髒脂肪增多,脂肪指數增加(P<0.05)。藥物榦預組較模型對照組體質量減輕(P>0.05),內髒脂肪明顯減少(P<0.01),脂肪指數顯著下降(P<0.05)。漢黃芩素明顯降低總膽固醇(TC)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL),但對三酰甘油(TG)影響不大。藥物榦預組較模型對照組肝脂酶(HL)與脂蛋白脂酶(LPL)活性恢複(P<0.05),羥甲基戊二痠單酰輔酶 A 還原酶活性被抑製(P<0.01);分子生物學研究顯示其降脂效果可能與脂閤成基因(SREBP-1c,FAS,PPARγ)與脂質代謝基因(PPARα,CPT-1)的轉錄調控相關。結論漢黃芩素能夠很好地治療高脂血癥,這一作用可能與調節脂酶活性和影響脂質閤成與氧化基因相關。
목적:연구한황금소대음식유도하고지혈증소서모형적방치작용。방법장30지 C57소서수궤분위정상대조조、모형대조조화약물간예조,매조10지。정상대조조급여보통음식,모형대조조급여고지사료,약물간예조재고지사료기출상첨가한황금소500 mg·kg-1。관찰한황금소대모형소서혈지、지대사관건매적영향,탐토기강지궤제。결과경과12주적고지음식,모형소서형성료명현적고지혈증,체질량증가,내장지방증다,지방지수증가(P<0.05)。약물간예조교모형대조조체질량감경(P>0.05),내장지방명현감소(P<0.01),지방지수현저하강(P<0.05)。한황금소명현강저총담고순(TC)、저밀도지단백(LDL)、고밀도지단백(HDL),단대삼선감유(TG)영향불대。약물간예조교모형대조조간지매(HL)여지단백지매(LPL)활성회복(P<0.05),간갑기무이산단선보매 A 환원매활성피억제(P<0.01);분자생물학연구현시기강지효과가능여지합성기인(SREBP-1c,FAS,PPARγ)여지질대사기인(PPARα,CPT-1)적전록조공상관。결론한황금소능구흔호지치료고지혈증,저일작용가능여조절지매활성화영향지질합성여양화기인상관。
Objective To explore the effects of wogonin on hyperlipidemia in mice and clarify the molecule mechanism. Methods Thirty mice were evenly divided into three group normal control group,model control group and treatment group. The normal control group was given normal diet,the model control group received high-fat diet,the treatment group received high-fat diet with wogonin (500 mg·kg-1 ). Results The mice developed hyperlipidemia 12 weeks after starting the high-fat diet. The body weight,visceral fat and fat index were increased (P<0. 05). After treatment,these indices were reduced ( P < 0. 01). Wogonin significantly reduced the total cholesterol ( TC),low density lipoprotein ( LDL),high density lipoprotein (HDL),except the triglyceride (TG). Compared to the model control group,the hepatic lipase(HL) and lipoprotein lipase(LPL) activity in the treatment group were recovered (P<0. 05),but HMG-CoA reductase activity was inhibited ( P<0. 01). Mechanistic study suggested that the lipid-lowering effect might be related to the lipid synthesis genes (SREBP-1c,FAS, PPARγ) and the lipid metabolism genes (PPARα,CPT-1). Conclusion Wogonin can prevent hyperlipidemia,which might be related to the regulation of enzyme activity and the changes of lipid synthesis and oxidative metabolism.