Effect of Radix Ilicis Pubescentis on the Rats with Hyperlipidemia

[Objectives]To study the hypolipidemic effect of Radix Ilicis Pubescentis and to provide experimental scientific basis for the study of hypolipidemic mechanism of Radix Ilicis Pubescentis.[Methods]60 healthy(SD)male rats were selected,10 rats were given basic feed and pure water as blank control group,and the other 50 rats were fed with high-fat diet for 4 weeks.After establishing the hyperlipidemic rat model,the rats were randomly divided into model group,high,middle and low dose groups(1000,800,500 mg/kg),and positive control group(simvastatin 0.4 mg/mL).The corresponding drugs were intragastrically administered to the rats in each group(blank control group and model group intragastrically administered with normal saline).Four weeks later,blood samples from abdominal aorta were taken to detect serum total cholesterol(TC),serum triglyceride(TG),low density lipoprotein cholesterol(LDL-C),and high density lipoprotein cholesterol(HDL-C).[Results]Compared with the blank control group,TC,TG and LDL-C increased while HDL-C decreased in the model group(P<0.05);compared with the model group,TC,TG and LDL-C in Radix Ilicis Pubescentis group decreased to varying degrees,and the content of HDL-C in serum of rats had no statistical significance.Compared with the blank control group,the serum TC and TG contents of the model group,positive control group,high,middle and low dose groups of Radix Ilicis Pubescentis extract significantly increased(P<0.01 or 0.05),and the serum LDL-C content of rats decreased(P<0.05).[Conclusions]The extract of Radix Ilicis Pubescentis had a certain lipid-lowering effect on hyperlipidemia in rats,and had obvious preventive and therapeutic effect on hyperlipidemia.

Deficiency of the G protein Gαq ameliorates experimental autoimmune encephalomyelitis with impaired DC-derived IL-6 production and Th17 differentiation

Many G protein-coupled receptors （GPCRs） are reported to be involved in the pathogenesis of multiple sclerosis （MS）, and -40% of all identified GPCRs rely on the Gaq/11 G protein family to stimulate inositol lipid signaling. However, the function of Ga subunits in MS pathogenesis is still unknown. In this study, we attempted to determine the role of Gaq in the pathogenesis of experimental autoimmune encephalomyelitis （EAE）, a well-known mouse model of MS. We discovered that compared with wild-type mice, Gaq-knockout mice exhibited less severe EAE symptoms, with lower clinical scores, reduced leukocyte infiltration and less extensive demyelination. Moreover, a significantly lower percentage of Th17 cells, one of the key players in MS pathogenesis, was observed in Gaq-knockout EAE mice. Studies in vitro demonstrated that deficiency of Gaq in CD4＋ T cells directly impaired Th17 differentiation. In addition, deficiency of Gaq significantly impaired DC-derived IL-6 production, thus inhibiting Th17 differentiation and the Gaq-PLCβ-PKC and Gaq-MAPKs signaling pathways involved in the reduced IL-6 production by DCs. In summary, our data highlighted the critical role of Gaq in regulating Th17 differentiation and MS oathogenesis.