医药导报
醫藥導報
의약도보
HERALD OF MEDICINE
2015年
4期
440-444
,共5页
荷叶碱%高脂血症%脂酶%氧化应激%合成代谢
荷葉堿%高脂血癥%脂酶%氧化應激%閤成代謝
하협감%고지혈증%지매%양화응격%합성대사
Nuciferine%Hyperlipidemia%Lipase%Oxidative stress%Constructive metabolism
目的：研究荷叶碱对饮食诱导的高脂血症小鼠的影响并了解其降脂机制。方法将小鼠根据饲料分为3组：正常对照组(n=10)、模型对照组(n=10)、干预组(n=10)。正常对照组采取普通饮食(ANI-76A饲料：12.4%脂肪,68.8%碳水化合物,18.8%蛋白质)；模型对照组采用高脂饮食诱导(高脂饲料：37.1%脂肪,42.4%碳水化合物,20.5%蛋白质)；干预组在高脂饲料基础上添加了0.5%荷叶碱。小鼠自由食用,共10周。比较3组小鼠体质量、血脂、脂代谢关键酶、肝脏氧化应激的变化并研究脂质代谢通路。结果高脂饮食成功诱导出高脂血症模型小鼠：肥胖、血脂增高(P<0.05)。干预组与模型对照组比较：小鼠体质量降低[(33.97±3.46) g比(27.62±2.87) g],血脂降低[(2.73±0.26) g比(1.91±0.21)g],均P<0.05,但不能改善其高甘油三酯血症(P>0.05)；肝脂酶活性[(4.15±1.26) U·mL-1比(9.01±1.34) U·mL-1]及脂蛋白脂酶活性提高[(8.12±3.07) U·mL-1比(13.48±3.75) U·mL-1],且降低了肝脏氧化应激(P<0.05)。高脂饮食诱导脂质合成基因SREBP-1c、FAS、SCD-1及PPARγ mRNA显著上调(P<0.05),而使脂质氧化代谢基因PPARα、CPT-1a mRNA下调(P<0.05),干预组则逆转了这些变化(P<0.05)。结论荷叶碱能改善小鼠高脂血症,且可能与增加脂酶活性、减少氧化应激及调控脂质合成与氧化代谢相关。
目的：研究荷葉堿對飲食誘導的高脂血癥小鼠的影響併瞭解其降脂機製。方法將小鼠根據飼料分為3組：正常對照組(n=10)、模型對照組(n=10)、榦預組(n=10)。正常對照組採取普通飲食(ANI-76A飼料：12.4%脂肪,68.8%碳水化閤物,18.8%蛋白質)；模型對照組採用高脂飲食誘導(高脂飼料：37.1%脂肪,42.4%碳水化閤物,20.5%蛋白質)；榦預組在高脂飼料基礎上添加瞭0.5%荷葉堿。小鼠自由食用,共10週。比較3組小鼠體質量、血脂、脂代謝關鍵酶、肝髒氧化應激的變化併研究脂質代謝通路。結果高脂飲食成功誘導齣高脂血癥模型小鼠：肥胖、血脂增高(P<0.05)。榦預組與模型對照組比較：小鼠體質量降低[(33.97±3.46) g比(27.62±2.87) g],血脂降低[(2.73±0.26) g比(1.91±0.21)g],均P<0.05,但不能改善其高甘油三酯血癥(P>0.05)；肝脂酶活性[(4.15±1.26) U·mL-1比(9.01±1.34) U·mL-1]及脂蛋白脂酶活性提高[(8.12±3.07) U·mL-1比(13.48±3.75) U·mL-1],且降低瞭肝髒氧化應激(P<0.05)。高脂飲食誘導脂質閤成基因SREBP-1c、FAS、SCD-1及PPARγ mRNA顯著上調(P<0.05),而使脂質氧化代謝基因PPARα、CPT-1a mRNA下調(P<0.05),榦預組則逆轉瞭這些變化(P<0.05)。結論荷葉堿能改善小鼠高脂血癥,且可能與增加脂酶活性、減少氧化應激及調控脂質閤成與氧化代謝相關。
목적：연구하협감대음식유도적고지혈증소서적영향병료해기강지궤제。방법장소서근거사료분위3조：정상대조조(n=10)、모형대조조(n=10)、간예조(n=10)。정상대조조채취보통음식(ANI-76A사료：12.4%지방,68.8%탄수화합물,18.8%단백질)；모형대조조채용고지음식유도(고지사료：37.1%지방,42.4%탄수화합물,20.5%단백질)；간예조재고지사료기출상첨가료0.5%하협감。소서자유식용,공10주。비교3조소서체질량、혈지、지대사관건매、간장양화응격적변화병연구지질대사통로。결과고지음식성공유도출고지혈증모형소서：비반、혈지증고(P<0.05)。간예조여모형대조조비교：소서체질량강저[(33.97±3.46) g비(27.62±2.87) g],혈지강저[(2.73±0.26) g비(1.91±0.21)g],균P<0.05,단불능개선기고감유삼지혈증(P>0.05)；간지매활성[(4.15±1.26) U·mL-1비(9.01±1.34) U·mL-1]급지단백지매활성제고[(8.12±3.07) U·mL-1비(13.48±3.75) U·mL-1],차강저료간장양화응격(P<0.05)。고지음식유도지질합성기인SREBP-1c、FAS、SCD-1급PPARγ mRNA현저상조(P<0.05),이사지질양화대사기인PPARα、CPT-1a mRNA하조(P<0.05),간예조칙역전료저사변화(P<0.05)。결론하협감능개선소서고지혈증,차가능여증가지매활성、감소양화응격급조공지질합성여양화대사상관。
Objective To investigate the effects of nuciferine on hyperlipidemia in mice and to clarify the molecular mechanism. Methods Mice were divided into three groups according to the diet: normal control group ( n=10 ) , model control group (n=10), and the intervention group (n=10). The normal control group was treated with common diet (ANI-76A feed:12. 4% fat, 68. 8% carbohydrate, 18. 8% protein). The model control group was induced with high fat diet (37. 1% fat, 42. 4% carbohydrate, 20. 5% protein). The intervention group was supplemented with 0. 5% nuciferine based on high fat diet. The mice were allowed free access to food and water for a total of 10 weeks. Several indices were analyzed in the 3 groups, including the body weight, serum lipid, lipid metabolism key enzyme, oxidative stress and metabolic pathway. Results Our results suggested that the high-fat diet-induced animal models developed obesity and dyslipidemia (P<0. 05). The body weight [(33.97±3.46) g vs. (27. 62±2. 87) g] and the serum lipid[(2. 73±0. 26) g vs. (1. 91±0. 21) g] were significantly decreased in the intervention group compared to the model control group (P<0. 05), except for the hypertriglyceridemia (P>0.05).Theactivityofhepaticlipidmetabolismkeyenzymes[(4.15±1.26) U·mL-1vs.(9.01±1.34) U·mL-1] andthe activity of hepatic lipase and lipoprotein lipase[(8.12±3.07) U·mL-1 vs.(13.48±3.75) U·mL-1] were elevated.Oxidative stress was also affected by nuciferine (P<0. 05). Mechanism study suggested that lipid synthesis genes (like SREBP-1c, FAS, SCD-1 and PPAR gamma mRNA) were up-regulated by high fat diet (P<0. 05), and the lipid oxidation metabolism genes, PPARαand CPT-1a mRNA, were down-regulated (P<0. 05), while the intervention group treatment reversed these changes (P<0. 05). Conclusion Nuciferine can improve hyperlipidemia, which might be related to the regulation of enzyme activity, oxidative stress and the changes of lipid synthesis and oxidative metabolism.
