[Effects of pure total flavonoids from Citrus changshan-huyou on blood lipid metabolism in hyperlipidemic rats].
To observe and investigate the effects and mechanisms of the pure total flavonoids from Citrus changshan-huyou(PTFC) on blood lipid metabolism in hyperlipidemic rats. SD rats were fed with high fat diet for 4 weeks to induce hyperlipidemic rats model, meanwhile three dosages (50, 100, 200 mg•kg ⁻¹•d ⁻¹) of PTFC were administrated intragastrically for 4 weeks respectively.After 2 weeks of modeling, their tail blood was taken and serum TC, TG, and HDL-C levels were detected by biochemical method and their body weight was measured. After 4 weeks of modeling, their body weight was measured and liver weight was measured, then the levels of TC, TG, HDL-C, LDL-C, ALT, AST, MDA and SOD in serum were detected to calculate lipid comprehensive index(LDL-C/HDL-C and LDL-C/TC ratios) and atherogenic index(AI); in addition, MDA and SOD levels were detected by biochemical method. The hitopathological changes of the liver tissues were observed by HE staining; the protein expression levels of PPAR-α, Lpl, and Lipc were detected by ELISA; and the mRNA expression levels of PPAR-α in the liver tissue were detected by Real-time PCR. The results showed that gavage administration of the PTFC significantly decreased the body weight, liver weight, liver index, serum ALT and AST activities, the levels of serum TC, TG, LDL-C, LDL-C/HDL-C, AI and increased serum HDL and LDL/TC level. Moreover, the PTFC significantly enhanced SOD activity and decreased the concentration of MDA in serum and liver tissue. Further mechanism investigation indicated that PTFC inhibited serum lipid accumulation by increasing the expressions PPAR-α, Lpl, Lipc protein and PPAR-α mRNA of the liver tissues. PTFC could actively regulate blood lipid metabolism by ameliorating hepatic function, improving the body's antioxidant capacity, lowering levels of oxidative stress, as well as positively regulating the expression levels of PPAR-α, Lpl, Lipc protein and PPAR-α mRNA of the liver tissues in rats.
Yang PL
，Jiang JP
，Li QQ
，Wu XM
，Chen ZY
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Pure total flavonoids from citrus improve non-alcoholic fatty liver disease by regulating TLR/CCL signaling pathway: A preliminary high-throughput 'omics' study.
This study investigated the possible molecular mechanisms of pure total flavonoids from citrus (PTFC) for the treatment of non-alcoholic fatty liver disease (NAFLD) via toll-like receptor/C-C chemokine ligand (TLR/CCL) signaling pathways by monitoring the changes in gene expression profile in liver tissues induced by high-fat diet.
We performed systematical analyses on hepatic expression profiles of mRNAs in a high-fat diet (HFD)-induced steatotic animal model with or without PTFC treatment. The study was conducted by using MouseOneArray® v2 gene chip, and analyzed by bioinformatics tools for differential gene expression. Real time-PCR, Western blot and liquid suspension array analysis were used to validate specific genes in the NAFLD liver expression profile in which PTFC plays a role in the TLR/CCR pathway.
We found that a total of 562 genes showed varying degrees of reversal after PTFC intervention. Pathway analysis of the differential gene expression in the HFD group and the normal diet group (ND group) revealed six signaling pathways related to inflammatory responses in the top ten results. Comparison of genes between the HFD+PTFC and the HFD groups indicated seven signaling pathways correlated with inflammatory response in the top ten results of the pathway analysis. The TLR/CCL inflammatory signaling pathways played an essential role during liver inflammation in NAFLD mice induced by high-fat diet. Real-time PCR, Western blot and liquid suspension array analysis of the differential gene expression involving the TLR/CCL signaling pathways validated the results of microarray detection.
PTFC may improve NAFLD by regulating TLR/CCL signaling pathways. Genomic studies provide additional evidence supporting the role of PTFC in the treatment of NAFLD.
Wu L
，Yan M
，Jiang J
，He B
，Hong W
，Chen Z
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