Effects Of LPS On Lipid Metabolism Genes Transcription Level In Mice Liver Injury

In order to research the effefts of lipopolysaccharide (LPS) to the liver injury onlipid metabolism gene transcription level, the test use kunming mice as the researchobject, the LPS was injected to the abdominal cavity of the mice,from themorphology, liver function index and inflammatory signal molecule transcription,judged liver injury model, using fluorescence quantitative polymerase chain reaction(PCR) detection mice lipid metabolism genes of liver, fat and muscle tissuetranscription, explained the effects of LPS on lipid metabolism genes transcriptionlevel in mice liver injury. The results are as follows:Mice liver injury model: With the increase of LPS dose effect and the extensionof time, the liver tissue pathology significantly different, the only parts of the cellnuclei dissolve, liver sinus congestion, a few mild liver cells turbidity is swollen, afew inflammatory cells infiltrating until the liver sinus expansion, marked hyperemia,passive congestion, a large number of inflammatory cells infiltration, liver cellspunctiformp, small patch of necrosis; LPS can make blood and liver liver functionindex (GOP and GOT) activity increased, increased inflammatory signals moleculestranscription level. The results indicated that LPS induced liver damage model wassuccessfully established. LPS dosage was3mg/kg, reaction time was6-9h.The liver of Fat synthesis and transport key gene transcription results: time effectexperiment,LPS can significantly cut SREBP, ACC mRNA transcription level, withextension of time significantly cut;12-24h can significantly cut CD36, SCD mRNAtranscription level,3-6h cut significantly PPAR α mRNA transcription,6-9hsignificantly raised LXR β mRNA transcription level, LXR α and FAS mRNAtranscription is not significantly; Dose effect experiment, LPS can significantly cutPPAR α, LXR α, SREBP, ACC mRNA transcription level, LXR β, CD36, FAS, SCDmRNA transcription level is not significantly. It showed that LPS can reducedhepatic synthetic fatty acids ability by cut nuclear transcription factors PPAR α, LXRα, SREBP mRNAtranscription, and theACC mRNAtranscription level. Fat tissue lipid metabolism key gene transcription: time effect experiment, LPScan cut fat tissue PPAR α, SREBP, FAS, ACC mRNA transcription level, the effect onLXR α, CD36mRNA transcription levelt is not significantly, but can increase whitefat LXR β mRNA transcription, reduce fat brown SCD mRNA transcription, the effecton white and brown fat SCD mRNA,fat LXR β mRNA transcription level is notsignificantly; Dose effect experiment, LPS can cut fat tissue LXR α, SREBP mRNAtranscription level, the effect on LXR β, FAS, ACC mRNA transcription is notsignificantly, can cut white fat CD36, SCD, ACC mRNA transcription level, cut fatbrown PPAR α mRNA transcription, ACC, SCD, CD36mRNA of brown fat andPPAR α mRNA of white fat transcription is not significantly,the regulation rangedoes not rely on LPS effect time and dose.Muscles and transshipment fat synthesis key genetic transcription results showthat: time effect trial, LPS can raise SCD (P<0.05) and PPARα, LXR α, LXR β, FAS,ACC, CD36mRNA transcription level (P>0.05), the transcription of the impact is notbig to SREBP; Dose effect in the test, LPS raised PPAR α (P<0.05) and SCD, FAS,ACC mRNA transcription level (P>0.05), cut LXRα, LXRβ, CD36transcription(P>0.05), the impact is not significantly, the transcription regulation range does notrely on LPS effect time and dose.Comprehensive above results, LPS induced liver injury by increasinginflammatory signal molecules in mice,liver injury degree depends on the dose ofLPS and effect time; LPS can cut PPAR α, LXR α, SREBP mRNA transcription, thencut its target gene transcription level, reduce the body’s synthesis and transport fattyacids ability finally,The magnitude of reduction with tissue specific.