Electrophysiologic effects of 17β-estradiol on pacemaker cells in sinoatrial nodes of rabbits / 生理学报

To investigate the electrophysiological effects of 17β-estradiol on pacemaker cells in sinoatrial (SA) nodes of rabbits and the underlying mechanism, intracellular microelectrode technique was used to record action potential (AP) in SA node cells of rabbits. The results showed that: (1) 17β-estradiol (1, 10, 100 μmol/L) not only significantly decreased the amplitude of action potential (APA) and the maximal rate of depolarization (V(max)), but also decreased the velocity of diastolic (phase 4) depolarization (VDD) and rate of pacemaker firing (RPF) in a concentration-dependent manner. The AP duration at 50% repolarization (APD(50)) and at 90% repolarization (APD(90)) were prolonged. But the maximal diastolic potential (MDP) was not affected. (2) Pretreatment with tamoxifen (10 μmol/L), an inhibitor of estrogen receptor, did not block the electrophysiological effects of 17β-estradiol (10 μmol/L) on SA node cells. (3) Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 100 μmol/L), a nitric oxide (NO) synthase inhibitor, completely abolished the electrophysiological effects of 17β-estradiol (10 μmol/L) on SA node cells. The results suggest that 17β-estradiol inhibits the electrophysiological activity of pacemaker cells in SA nodes of rabbits in a concentration-dependent manner possibly through a non-genomic mechanism related with NO.

Adipokine and metabolic syndrome / 中国医学科学院学报

Adipose tissue is not simply a depot of energy, but is an active endocrine organ. The adipokines play an important role in the pathogenesis of metabolic syndrome. The proinflammatory adipokines secreted from expanded visceral adipose tissue directly induce insulin resistance and vascular injuries. A better understanding of the endocrine function of adipose tissue may lead to more rational therapy for metabolic syndrome.

Ginsenoside Rb_1 facilitates adipocyte differentiation and inhibits lipolysis in 3T3-L1 adipocytes / 中华内分泌代谢杂志

Objective To observe the effect of ginsenoside Rb1,the most abundant ginsenoside in ginseng root,on differentiation and lipolysis of 3T3-L1 cells and to explore its anti-diabetic mechanism.Methods 3T3-L1 preadipoeytes were induced under standard differentiation process in the presence of 0.1,1,10,100?mol/L ginsenoside Rb_1 for 6 days.Oil red O staining,measurement of triglyceride contents and glucose uptake assay were performed.The expressions of mRNA and protein of PPAR?2,C/EBP?,ap2,glucose transporter (Glut) 1,and Glut4 were analysed with quantitative real time-PCR and Western blot.The binding affinity of Rb_1 to PPAR?-LBD was evaluated by Surface Plasmon Resonance (SPR).Lipolysis of adipocytes was examined by the measurement of glycerol released from adipoeytes treated with Rb_1 for 1 h.Results Ginsenoside Rb_1 facilitated differentiation of 3T3-L1 preadipoeytes in a dose-depondent manner.10?mol/L ginsenoside Rb_1 increased lipid accumulation by about 56%.Treatment of differentiating adipocytes with 10?mol/L ginsenoside Rb_1 increased the expressions of PPAR?2 and C/EBP?mRNA and protein,as well as mRNA expression of ap2,one of their target genes.After treatment of differentiating adipoeytes with Rb_1,basal and insulin-mediated glucose transport augmented significantly accompanied by up-regulations of mRNA and protein level of Glut4,but not of Glutl.SPR showed Rb_1 could bind to PPAR?which suggested Rb_1 was a ligand of PPAR?.Ginsenoside Rb_1 inhibited basal lipolysis in adipoeytos in a dose-dependent manner.However,it did not affect isoproterenol-stimulated lipolysis.Conclusion As a PPAR?ligand,ginsenoside Rb_1 promotes adipogenesis,inhibitas basal lipolysis and inereasos basal and insulin-mediated glucose transport in cultured adipoeytes.Therefore,anti-diabetic and insulin-sensitizing activity of ginsenosides is,at least in part,involved in the enhancing effect on PPAR?2 and C/EBP?expressions,hence promoting adipogenesis and glucose uptake,and inhibiting lipolysis in adipocytes.