| [Objective]:Observe the Proliferator-Activated Receptorγ(PPARγ) and sterol regulatory element-binding protein-1c (SREBP-lc) in rat nonalcoholic fatty liver disease (NAFLD), in order to investigate the expression changes in both formation of NAFLD interaction and the possible mechanism.[Methods]:40 SD rats were randomly divided into control and experimental groups.Experimental group received 40% CCL4 subcutaneously 2 times a week and were fed high fat diet combined to obtain the rat model of NAFLD, Use enzymatic analysis in 2,4,6,8 weeks of each group in the 4 time points of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG), total cholesterol (TC) levels, use ELISA method to detection of the observation points of tumor necrosis factor (TNF-α) levels, and immunohistochemical methods RT-PCR methods were used to analysis liver tissue PPARy and SREBP-lc expression[Results]:1,With prolonged, experimental group liver fatty change is more and more obvious, serum ALT, AST, TG, TC gradually increased, compared with controls difference was statistically significant (p<0.05).2,Rat liver cells in the experimental group TNF-αin the first 2 weeks from the start since there is weak expression, with the prolonged expression of the modeling gradually increased, compared with the control group significantly (p<0.05).3,Immunohistochemical staining showed that the experimental group, SREBP-lc expression in the cytoplasm early in the second weekend you can see the expression of brown particles such as extended and enhanced modeling and stronger than the control group (p <0.05), to the 8th weekend can be seen a lot of brown cytoplasmic particle deposition, while most of the nuclei also showed positive staining (p<0.05).And in the experimental group PPARγexpress began to strengthen, liver cytoplasm tan particles increase. With the increasing degree of fatty degeneration of liver cells, PPARγexpression increased, 8 the weekend cytoplasm visible large brown particle deposition (p< 0.05).4,RT-PCR detection to 2 weekend rat liver tissue experimental SREBP-1c mRNA transcription started to increase, With the extension of the enhanced modeling time, compared with the control group significantly (P<0.01). The RT-PCR, the expression of PPARγin liver found that:the experimental group in each group PPARγmRNA expression was increased from 4 weeks, then mRNA transcription increased significantly compared with the control group, With the severity of fatty liver gradually increased, compared with the control group was significantly (P<0.05).5,With the extended modeling of fatty liver, inflammation and necrosis becoming significantly more severe liver damage.Experimental group, ALT, AST, TG and TC increased gradually, the serum TNF-αwas also found an upward trend. Statistical correlation analysis showed that serum TNF-αand ALT, AST, TG, TC were positively correlated, Correlation coefficient 0.782,P<0.05; 0.863,P<0.05; 0.356,P<0. 05; 0.786,P<0.05. Correlation Analysis of RT-PCR results showed that SREBP-1c, PPARγpositive correlation between, Correlation coefficient of r= 0.951, P<0.05. Further analysis of SREBP-1c, PPARγthe RT-PCR results and serum TNF-αresults were also positively correlated, TNF-αand SREBP-1c, PPARγcorrelation coefficients were 0.922,0.903 (P<0.05)[Conclusions]:1,PPARγand SREBP-1c, TNF-αcan be used as sensitive indicators of the non-alcoholic fatty liver disease occurrence and development.2,PPARγand SREBP-1c and the severity of liver cells are in good agreement between,Possible synergies between the promotion of participation and non-alcoholic fatty liver disease occurrence and development. Further suggest that PPARγand SREBP-1c intervention the inappropriate expression may be the prevention and treatment of NAFLD an efficient way. Also speculated that SREBP-1c and PPARγis also involved in inflammation, necrosis, and inhibition of its expression may inhibit cell proliferation of a variety of inflammatory stimulation reaction. |
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