Objective: To explore the mechanism of electroacupuncture(EA) at "Fenglong" (ST 40) in hyperlipidemia (HLP) rats.
Methods: Forty health SD rats were randomly divided into a normal control group (group A), a high fat forage feed group (group B) and a high fat forage feed treatment group (group C), a high fat forage + normal forage feed group (group D) and a high fat forage + normal forage feed treatment group (group E), eight rats in each group. EA was applied at "Fenglong" (ST 40) for the rats in group C and group E, once daily. After treatment of 30 days, blood lipid levels of rats, including total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) in plasma were tested. Real time polymerase chain reaction (RT-PCR) and Western Blotting were applied to detect the gene expression changes of the contents of ATP-binding cassette transporter A1 (ABCA1), peroxisome proliferator-activated receptor alpha (PPARalpha), liver X receptor alpha (LXR-alpha) and retinoid X receptor alpha (RXR-alpha) in liver tissue of rats.
Results: Compared with group A, the contents of TC, LDL-C were significantly elevated in group B and group D (all P < 0.01); compared with group B, above indices were significantly decreased in group D (all P < 0.01). After the treatment of EA at "Fenglong"(ST 40), the contents of TC, LDL-C were significantly decreased (all P < 0.01), and the contents of TG, HDL-C did not change obviously (all P > 0.05). Compared with group A, the mRNA and protein contents of ABCA1, PPARalpha, LXR-alpha and RXR-alpha were decreased obviously in group B and group D (all P < 0.01). But compared with group B, the above indices were decreased in the group D. There were signficantly increasing in the protein content of ABCA1, PPARalpha, RXR-alpha and LXR-alpha mRNA after the treatment of EA (all P < 0.05).
Conclusion: EA at "Fenglong" (ST 40) has some therapeutic effect on decrease the content of TC, LDL-C in rats of hyperlipemia and improve the gene expression of ABCA1, PPARalpha, LXR-alpha and RXR-alpha mRNA so as to promote reverse cholesterol transport.