[Studies on separation and purification of phenylethanoid glycosides from leaves of Forsythia suspensa by macroporous adsorption resin].

OBJECTIVE: To study the technology for separation and purification of phenylethanoid glycosides from leaves of Forsythia suspensa by macroporous adsorption resin. METHODS: The absorption and separation abilities of 10 kinds of adsorption resin were studied and the separation and purification technological process of phenylethanoid glycosides from leaves of Forsythia suspensa was investigated by HPLC with the content of Forsythoside A as an index. RESULTS: The optimal conditions were as follows: taking AB-8 resin column as adsorbent, the resin was washed by 20BV distilled water to remove impurity and 8BV 30% ethanol to elute phenylethanoid glycosides, the eluting velocity was 2BV/h, the content of Forsythoside A in the extract was 34.8%. CONCLUSION: The process with AB-8 resin is an effective method to separate and purify phenylethanoid glycosides.

[Protective effect of Buyanghuanwu Decoction on myocardial ischemia induced by isoproterenol in rats].

OBJECTIVE: To study the protective effect of Buyanghuanwu Decoction on myocardial ischemia induced by isoproterenol in rats. METHODS: Buyanghuanwu Decoction was given in different dose and the rat model of myocardial ischemia was established by peritoneal injection of isoproterenol. The expression of CD40 in whole blood was detected by flow cytometry,and the expression of CD40L in myocardial tissues was detected by immunohistochemistry. The activities of lactate dehydrogenase (LDH), creatine kinase (CK) and aspartate aminotransferase (AST) in blood serum were detected by biochemistry detector. RESULTS: Compared with the model group, Buyanghuanwu Decoction in high and middle dose significantly inhibited the expression of CD40 in blood serum and CD40L in myocardial tissues (P < 0.01), and obviously decreased the activities of LDH, CK and AST in blood serum (P < 0.01). CONCLUSION: Buyanghuanwu Decoction has a protective effect on myocardial ischemia induced by isoproterenol in rats, and it may be relevant to the decrease of the expression of CD40-CD40L and the activities of myocardial enzymes.

[Effects of bazheng mixture on urinary amount and contractile-relaxant function of isolated urethral smooth muscle in rabbits].

OBJECTIVE: To explore the pharmacological mechanism of Bazheng Mixture (BZM) in promoting diuresis and relieving stranguria. METHODS: By means of urine collection through indwelling catheter and urethral ring isolation test to observe the effects of BZM on the urinary amount of conscious rabbits and contractile-relaxant function of urethral smooth muscle isolated from rabbits. RESULTS: BZM, at dosage of 5.0 g/kg or 10.0 g/kg by gastrogavage, could increase the urinary amount in 60 min obviously (P < 0.05). For the isolated urethral rings, the maximal contractile and maximal relaxant forces reduced significantly (P < 0.05 or P < 0.01) when the concentration of BZM applied ranged between 9.9-90.9 g/L; the frequency increased significantly (P < 0.05 or P < 0.01) when the concentration ranged 29.1-90.9 g/L and the amplitude increased significantly when the concentration were 56.6 and 90.0 g/L. Along with the concentration of BZM increased from 9.9 g/L to 90.9 g/L, the changes occurred in the above-mentioned parameters of urethral ring were in order of potency amplitude > frequency > maximal relaxant force > maximal contractile force. CONCLUSION: The effects of BZM in enhancing urethral peristalsis may be stronger than that in dilating the urethral caliber. Its mechanism in promoting diuresis and relieving stranguria may be related with its action of urethral dilatation and potential peristalsis promotion.

Ginsenoside Re reduces insulin resistance through activation of PPAR-γ pathway and inhibition of TNF-α production.

ETHNOPHARMACOLOGICAL RELEVANCE: Panax ginseng is a well-known traditional Chinese medicine and has been used for treatment of various diseases for more than four thousand years in Asia. Ginseng saponins or ginsenosides, the active constituents are reported to possess antidiabetic activity, but their antihyperglycemic mechanisms are not fully elucidated. In the present study, the mechanisms of action of ginsenoside Re were investigated in vitro models. MATERIALS AND METHODS: 3T3-L1 cells were chosen as the model to investigate the molecular mechanisms of action of ginsenoside Re. Influence of ginsenoside Re on the adipogenesis was examined by determining TG levels in 3T3-L1 adipocytes by the method of TG oxidation enzyme. Glucose uptake in 3T3-L1 cells stimulated by insulin in the absence or presence of ginsenoside Re were quantified by measuring (3)H-2-deoxy-d-glucose levels. Cytokine proteins released into the medium including adiponectin and TNF-α were tested using respective ELISA kits. In addition, real time RT-PCR was conducted to investigate the expression changes of PPAR-γ and its responsive genes, ap2, adiponectin, IRS-1, GLUT4 and TNF-α. And western blot analysis was performed to determine the translocation of GLUT4. Finally, effects of ginsenoside Re on NO production in 3T3-L1 adipocytes and in macrophages were investigated through measurement of nitrite concentration by Griess reagent. RESULTS: Ginsenoside Re induced adipogenesis of 3T3-L1 adipocytes by accumulating TG, increased glucose uptake and up-regulated PPAR-γ2, IRS-1, ap2 and adiponectin genes expressions. Meanwhile, Re also increased production and release of adiponectin. Although having no effects on GLUT4 gene expression, Re facilitated GLUT4 protein translocation to the membranes. In addition, Re inhibited the expression and release of TNF-α. Finally, Re did not show inhibitory effects on NO production both in 3T3-L1 cells stimulated by LPS, TNF-α and IFN-γ and in LPS-stimulated mouse peritoneal macrophages. CONCLUSIONS: Ginsenoside Re exhibited the action of reducing insulin resistance through activation of PPAR-γ pathway by directly increasing the expressions of PPAR-γ2 and its responsive genes, adiponectin, IRS-1, ap2, inhibiting TNF-α production and facilitating the translocation of GLUT4 to promote glucose uptake and disposal in 3T3-L1 adipocytes.