Objective:To observe effects of Huanglian Jiedu Decoction on expression of insulin receptor substrate 1(IRS-1)and the level of tyrosine phosphorylation in skeletal muscles to explore the molecular mechanism in improving insulin resistance.Methods:Wistar system insulin resistance model rats were developed with injection of small dose of streptozotocin into the caudal vein plus feeding by forage with high sugar and high lipids,and they were treated with Huanglian Jiedu Decoction for 10 weeks.Then blood sugar and serum insulin level were determined,and the changes of IRS-1 protein expression and tyrosine phosphorylation level in the skeletal muscles of the rat with insulin resistence after treatment of Huanglian Jiedu Decoction were detected with immuno- precipitation and Western Blot methods.Results:After treatment with Huanlian Jiedu Decoction,IRS-1 expression and IRS-1 tyrosine phosphorylation level in the muscular tissue increased as compared with those of the model group.Conclusion Huanglian Jiedu Decoction improves IRS-1 protein expression and tyrosine phosphorylation level in the skeletal muscle tissue of the rats with insulin resistance,which is possibly one of the mechanisms of decreasing blood sugar and improving sensitivity of insulin in tissues.

This study investigated the effects and molecular mechanisms of genistein in improving insulin resistance induced by free fatty acids (FFAs) in HepG2 hepatocytes. A model of insulin resistance in HepG2 cells was established by adding palmitic acid (0.5 mmol/L) to the culture medium and the cells were treated by genistein. Glucose consumption of HepG2 cells was determined by glucose oxidase method. The levels of c-jun N-terminal kinase (JNK) phosphorylation, insulin receptor substrate-1 (IRS-1) Ser307 phosphorylation, JNK, IRS-1, phosphatidylinositol-3-kinase p85 (PI-3K p85) and glucose transporter 1 (GLUT1) proteins were detected by Western blotting. The results showed that after the treatment with palmitic acid for 24 h, the insulin-stimulated glucose transport in HepG2 cells was inhibited, and the glucose consumption was substantially reduced. Meanwhile, the expressions of IRS-1, PI-3K p85 protein and GLUT1 were obviously reduced, while the levels of JNK phosphorylation and IRS-1 Ser307 phosphorylation and the expression of JNK protein were significantly increased, as compared with cells of normal control. However, the aforementioned indices, which indicated the existence of insulin resistance, were reversed by genistein at 1-4 μmol/L in a dose-dependent manner. It was concluded that insulin resistance induced by FFAs in HepG2 hepatocytes could be improved by genistein. Genistein might reverse FFAs-induced insulin resistance in HepG2 cells by targeting JNK.

The effects of Cinnamon granules on pharmacokinetics of berberine in Rhizoma Coptidis granules in healthy male volunteers, and the compatibility mechanism of Jiao-Tai-Wan (JTW) composed of Rhizoma Coptidis granules and Cinnamon granules were investigated. The concentration of berberine in plasma of healthy male volunteers was determined directly by high performance liquid chromatography (HPLC) after an oral administration of Rhizoma Coptidis granules alone or combined with Cinnamon granules (JTW). The plasma concentration-time curves of berberine were plotted. The data were analyzed with Drug and Statistics (DAS) 2.0 pharmacokinetic program (Chinese Pharmacology Society) to obtain the main pharmacokinetic parameters. The results showed that the plasma concentration-time curve of berberine was described by a two-compartment model. The C(max), T(max), t(1/2) and CLz/F of berberine in Rhizoma Coptidis granules were 360.883 μg/L, 2.0 h, 3.882 h, 119.320 L·h(-1)·kg(-1) respectively, and those of berberine in JTW were 396.124 μg/L, 1.5 h, 4.727 h, 57.709 L·h(-1)·kg(-1) respectively. It was suggested that Rhizoma Coptidis granules combined with Cinnamon granules could increase the plasma concentration of berberine, promote berberine absorption and lengthen the detention time of berberine in healthy male volunteers.

OBJECTIVETo explore the molecular mechanism of jiantai liquid (JTL) in improving endometrial receptivity of mice with embryo implantation dysfunction (EID).

METHODSMice model of EID induced by mifepristone were intervened with JTL (Twig of Chinese Taxillus, Red Sage root, Chinese Angelica, Milkvetch root, Chuanxiong rhizome), and sacrificed on day 8 of pregnancy. The endometrial estrogen receptor (ER) and progesterone receptor (PR) protein and their gene expressions were assessed by Western blot and semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR).

RESULTSLevels of ER and PR protein and their gene expressions in the JTL treated group were significantly higher than those in the model group respectively (all P < 0.05), and showed insignificant difference from those in the normal control group (all P > 0.05).

CONCLUSIONJTL could promote the development of endometrium and improve the embryo implantation by way of regulating the levels of ER and PR protein and gene expression in mice with EID.

Animals ; Drugs, Chinese Herbal ; pharmacology ; Embryo Implantation ; drug effects ; Female ; Luteolytic Agents ; antagonists & inhibitors ; pharmacology ; Male ; Mice ; Mifepristone ; antagonists & inhibitors ; pharmacology ; Receptors, Estrogen ; biosynthesis ; genetics ; Receptors, Progesterone ; biosynthesis ; genetics ; Uterus ; metabolism

The effects of Cinnamon granules on pharmacokinetics of berberine in Rhizoma Coptidis granules in healthy male volunteers,and the compatibility mechanism of Jiao-Tai-Wan (JTW) composed of Rhizoma Coptidis granules and Cinnamon granules were investigated.The concentration of berberine in plasma of healthy male volunteers was determined directly by high performance liquid chromatography (HPLC) after an oral administration of Rhizoma Coptidis granules alone or combined with Cinnamon granules (JTW).The plasma concentration-time curves of berberine were plotted.The data were analyzed with Drug and Statistics (DAS) 2.0 pharmacokinetic program (Chinese Pharmacology Society)to obtain the main pharmacokinetic parameters.The results showed that the plasma concentration-time curve of berberine was described by a two-compartment model.The Cmax,Tmax,t1/2 and CLz/F of berberine in Rhizoma Coptidis granules were 360.883 μg/L,2.0 h,3.882 h,119.320 L·h-1·kg-1 respectively,and those of berberine in JTW were 396.124 μg/L,1.5 h,4.727 h,57.709 L·h-1·kg-1 respectively.It was suggested that Rhizoma Coptidis granules combined with Cinnamon granules could increase the plasma concentration of berberine,promote berberine absorption and lengthen the detention time of berberine in healthy male volunteers.

This study investigated the effects and molecular mechanisms of genistein in improving insulin resistance induced by free fatty acids (FFAs) in HepG2 hepatocytes.A model of insulin resistance in HepG2 cells was established by adding palmitic acid (0.5 mmol/L) to the culture medium and the cells were treated by genistein.Glucose consumption of HepG2 cells was determined by glucose oxidase method.The levels of c-jun N-terminal kinase (JNK) phosphorylation,insulin receptor substrate-1 (IRS-1) Ser307 phosphorylation,JNK,IRS-1,phosphatidylinositol-3-kinase p85 (PI-3K p85) and glucose transporter 1 (GLUT1) proteins were detected by Western blotting.The results showed that after the treatment with palmitic acid for 24 h,the insulin-stimulated glucose transport in HepG2 cells was inhibited,and the glucose consumption was substantially reduced.Meanwhile,the expressions of IRS-1,PI-3K p85 protein and GLUT1 were obviously reduced,while the levels of JNK phosphorylation and IRS-1 Ser307 phosphorylation and the expression of JNK protein were significantly increased,as compared with cells of normal control.However,the aforementioned indices,which indicated the existence of insulin resistance,were reversed by genistein at 1-4 μmol/L in a dose-dependent manner.It was concluded that insulin resistance induced by FFAs in HepG2 hepatocytes could be improved by genistein.Genistein might reverse FFAs-induced insulin resistance in HepG2 cells by targeting JNK.