Abstract

To study the effect of polysaccharides from Polygonatum sibiricum on mRNA and protein expressions of blood lipid metabolism in hyperlipidemic mice. The mice were randomly divided into 6 groups, namely the blank control group, the hyperlipidemia model group, the simvastatin group, and low, middle and high-dose PSP groups (200, 400, 800 mg·kg⁻¹·d⁻¹). Each group of the mice was administrated intragastrically for 14 days, respectively. Subsequently, every group of mice, except for the blank control group, was intraperitoneally injected with 75% fresh egg yolk emulsion for establishing the hyperlipidemic mice model. Upon completion of the administration, the contents of TC, TG, LDL-C and HDL-C in serum of each group were investigated in details. In particular, the mRNA expression levels of PPAR-α, PPAR-β, PPAR-γ, SREBP-1c, IL-6 and TNF-α of the liver tissues were detected by Real-time PCR, and the protein expression levels (including PPAR-α, PPAR-β, PPAR-γ, SREBP-1c, IL-6, TNF-α) were examined by Western blot. Consequently, the obtained results showed that the contents of the serum TC, TG, LDL-C of low, middle and high-dose PSP groups significantly decreased compared with those of the hyperlipidemia model group. Simultaneously, there were significant differences between middle-dose and high-dose PSP groups (P<0.01). In striking contrast, the contents of serum HDL-C of low, middle and high-dose PSP groups significantly increased, while obvious differences were also observed between middle-dose and high-dose PSP groups (P<0.01). Moreover, middle-dose and high-dose PSR groups could up-regulate the protein and mRNA expressions of PPAR-α, PPAR-β (P<0.05) compared with those of the hyperlipidemia model group, and down-regulate the expressions of PPAR-γ,SREBP-1c, IL-6 and TNF-α(P<0.05) compared with those of liver tissues of the hyperlipidemia model group. In conclusion, all of the above results suggested that PSP could inhibit the oxidation of the liver lipid, and regulate the expression levels of the corresponding genes and proteins relating to the lipid metabolism, so as to play a critical role for preventing hyperlipidemia.

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