ABSTRACT
Objective To explore the effects of wogonin on hyperlipidemia in mice and clarify the molecule mechanism. Methods Thirty mice were evenly divided into three group normal control group,model control group and treatment group. The normal control group was given normal diet,the model control group received high-fat diet,the treatment group received high-fat diet with wogonin (500 mg·kg-1 ). Results The mice developed hyperlipidemia 12 weeks after starting the high-fat diet. The body weight,visceral fat and fat index were increased (P<0. 05). After treatment,these indices were reduced ( P < 0. 01). Wogonin significantly reduced the total cholesterol ( TC),low density lipoprotein ( LDL),high density lipoprotein (HDL),except the triglyceride (TG). Compared to the model control group,the hepatic lipase(HL) and lipoprotein lipase(LPL) activity in the treatment group were recovered (P<0. 05),but HMG-CoA reductase activity was inhibited ( P<0. 01). Mechanistic study suggested that the lipid-lowering effect might be related to the lipid synthesis genes (SREBP-1c,FAS, PPARγ) and the lipid metabolism genes (PPARα,CPT-1). Conclusion Wogonin can prevent hyperlipidemia,which might be related to the regulation of enzyme activity and the changes of lipid synthesis and oxidative metabolism.
ABSTRACT
Objective: To study the effect of ghrelin on L-type calcium channel current (ICa-L) of ventricular myocytes in experimental rats. Methods: The single ventricular myocyte in experimental rats were obtained by enzymolysis method, and the whole-cell patch-clamp technique was used to investigate the effect of ghrelin on ICa-L of ventricular myocytes at different doses of 10 nmol/L, 100 nmol/L and 1μmol/L respectively. Results: Ghrelin at 10 nmol/L, 100 nmol/L and 1μmol/L may inhibit ICa-L at (8.95 ± 2.13) %, (31.18 ± 4.78) % and (64.63 ± 8.57)% respectively,P<0.05, and the current-voltage curve was shifted upwards. The channel half inactivation curve decreased from (-1.34 ± 1.9) mV to (-8.04 ± 1.32 ) mV, (9.76 ± 1.17) mV and (-11.81 ± 0.73) mV respectively,P<0.05, and the recovery time after inactivation was prolonged as τ value from (63.23 ± 9.32) to (98.95 ± 10.74), (109.56 ± 13.42) and (127.39 ± 16.13) respectively,P<0.05. Conclusion: Ghrelin may accelerate ICa-L inactivation and prolong the recovery time after inactivation. Ghrelin inhibits ICa-L in a dose-dependent manner.