摘要
目的探讨脂肪细胞对HepG2细胞载脂蛋白A5(apoA5)表达的影响及其调节机制。方法取人的皮下脂肪组织,经培养、促分化后获得成熟脂肪细胞,用脂多糖(LPS)刺激使其成为炎症状态下脂肪细胞。通过Transwell系统,脂肪细胞与HepG2细胞共培养,R T-PCR测定HepG2细胞的apoA5、血清淀粉样蛋白A(SAA)、过氧化物酶增殖物激活受体-α(PPAR-α)、肝X受体-α(LXR-α)mRNA的表达,并观察MK886对HepG2细胞的apoA5、PPAR-αmRNA表达的影响。结果①成熟脂肪细胞可使HepG2细胞的apoA5、PPAR-α、SAA mR NA的表达升高,且共培养48 h后表达水平高于24 h(P<0.05),但LXR-α的表达无明显改变(P>0.05)。②炎症状态下脂肪细胞对HepG2细胞的apoA5、PPAR-α、SAA mRNA表达的上调作用比成熟脂肪细胞更强(P<0.05),但LXR-αmRNA的表达无明显变化(P>0.05)。③MK886可抑制脂肪细胞对HepG2细胞apoA5 mR NA表达的上调作用(P<0.05)。结论脂肪细胞可通过PPAR-α而不是通过LXR-α途径上调HepG2细胞apoA5 mR NA的表达,此作用可能与其分泌的炎症因子刺激有关。
[Objectives] To investigate the effects and potential mechanisms of human adipocytes on the expression of apolipoprotein A5 （apoA5） in HepG2 cells. [Methods] Subcutaneous adipose tissue from human differentiated into mature adipocytes after culture and stimulation, then mature adipocytes were stimulated by lipopolysaccharide （LPS） into inflammatory adipocytes. Both of them cocaltured with HepG2 cells by transwell system respectively. Reverse transcription polymerase chain reaction （RT-PCR） was used to evaluate mRNA expression of apoA5, serum amyloid A （SAA）, peroxisome proliferator-activated receptor-alpha （PPAR-a） and liver X receptor-alpha （LXR-α. MK886 was used to evaluate its influence on the expressions of apoA5 and PPAR-α in HepG2 cells. [ Results ] （1）Mature adipocytes could upregulate the expression of apoA5, PPAR-α and SAA mRNA in HepG2 cells, and the HepG2 ceils had higher expression of them in cocultured for 48h （all P 〈0.05） compared with cocultured for 24 h. But there were no changes in the expression of LXR-α in both group compared with control group （uncocultured group） （all P 〉0.05）. （2）Inflammatory adipocytes upregulate the expression of apoA5, PPAR-αand SAA mRNA in HepG2 ceils stronger than mature adipocytes （P 〈0.05）, but there were no differences in LXR-α mRNA between them （P 〉0.05）. （3）Upregulation of apoA5 mRNA in HepG2 cells by adipocytes can be inhibited by MK886 （P 〈0.05）. [ Conclusions ] Adipocytes may upregulate the expression of apoA5 in HepG2 cells by PPAR-α but not LXR-α pathyway, and this may associate with the inflammation.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2011年第27期3349-3355,共7页
China Journal of Modern Medicine
