36</sub> 和過氧化物酶增殖活化受體 γ(PPARγ) 的蛋白和mRNA表達(dá)水平；流式細(xì)胞術(shù)檢測小鼠脾臟組織調(diào)節(jié)性T細(xì)胞（Treg）、抑制輔助性T細(xì)胞(Th17）、濾泡輔助性T細(xì)胞（Tfh)比例。結(jié)果：與正常對照組相比，HFD組小鼠體質(zhì)量升高（ P<0.01 ； CD<sub>36</sub> 、PPARγmRNA及蛋白表達(dá)水平升高（ P<0.01. )；脾臟Th17細(xì)胞比例升高，Treg、Tfh細(xì)胞比例降低（ P<0.01 。與HFD組小鼠相比，經(jīng)山楂提取物與阿托伐他汀干預(yù)的模型小鼠 CD<sub>36</sub> 、PPAR γ mRNA及蛋白表達(dá)水平降低（ ?P<0.01 ,Treg、Tfh細(xì)胞比例升高 (P<0.01 ),Th17細(xì)胞比例降低 P<0.01 ),HFD十高劑量山楂提取物組與HFD十阿托伐他汀組作用效果顯著（ P<0.05 或P<0.01) 。結(jié)論：山楂提取物能夠改善高脂模型小鼠Treg、Th17、Tfh細(xì)胞失衡及 CD<sub>36</sub> 與PPARγ受體表達(dá)，山楂提取物調(diào)脂可能與T細(xì)胞免疫及脂代謝分化相關(guān)。-龍源期刊網(wǎng)" />

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山楂提取物調(diào)控高脂小鼠T細(xì)胞免疫及脂代謝的作用機(jī)制研究

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AbstractObjective：ToxplorethemechanismofhawthoextractregulatingTcelimmunityandiidmetabolisminhyperideic mice.Methods：Sixty healthymale6-weekoldspecicpathogenic（SPF）gradeC57BL/6Jmicewereadaptivelyraisedforoneweekand thenrandomly divided into the normal control group，high-fat diet（HFD） group，HFD + high-dose hawthorn extract group，HFD+mediumdosehawthomextractgroup，HFDlow-dosehawthomextractgroupandHFDatorvastatingroup.Thenormalcontrolgroupwasgiven ordinary feed andraised normaly for8weeks，while the mice in the HFDgroup were fed with high-fatfeed powered by 60% fat for 8 weks.MiceintheHFDhigh-dosehawthomextractgroup，HDmedium-dosehawthomextractgroup，ndHFDlow-dosehawthom extract group were gavaged with 5.2，2.6，and 1.3g/kg hawthorn extract，respectively after 4weeks of high-fat rearing，once a day.Mice in theatorvastatin groupwere given oraladministration of atorvastatinat a dose of 10mg/kg bygavageafter4weeksof high-fat feeding， onceaday.Thecontrolgroupandthe HFDgroupweregavagedwiththesamevolumeof normalsalineatthesamevolume.The intervention period was 4weeks.The mRNA and protein expression levels of CD36 and peroxidase proliferation-activated receptor γ （PPARγ） weredetected by WestemBlotand reverse transcription polymerasechain reaction（qRT-PCR）.Flowcytometry was used to detecthepropiosa）el）neli mice.Results：Compared with the normal group，the body weight of mice in the HFD group increased P<0.01 ）;theexpression levels of CD36 ， PPARγ mRNA，proteinincreased P<0.01 ）;the proportionof Th17 cels in the spleen increased，and the percentages of Treg and Tfhcells increased（ P<0.01 ）.Compared with the mice in the HFD group，the expression levelsof CD36 PPARγ mRNA，and protein inthe model groupmice intervenedwith hawthornextractand atorvastatindecreased P<0.01 ），thepercentagesofTregandTfhcellsincreased （P<0.01） ，andthepercentageofTh17celsdecreased P<0.01 ）.Theeffect of the HFD+high-dose hawthorn extract group and the atorvastatin group were significant（ P<0.05 or P<0.01 ）.Conclusion：Hawthorn extract can improve the imbalance of Treg，Th17 and Tfh cellsand the expression of CD36 PPARγ receptors in mice with dyslipidemiamodels.Lipid regulation by hawthorn extract may be related to T-cell immunity and lipid metabolism differentiation.

Keywordsdyslipidemia;Tcellimmunity; hawthorn extract; peroxisome proliferator-activated receptor γ; experimental study

心血管疾病（cardiovasculardisease，CVD）仍是全球首位死亡原因，據(jù)世界衛(wèi)生組織統(tǒng)計，約13的病人死于CVD，是當(dāng)今嚴(yán)重危害人類健康的疾病之-[1]。（剩余13942字）

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