Effects of total flavones from Dendranthema morifolium on vasocontraction and proliferation of vascular smooth muscle cells.

Pharmacological studies have shown that the active components in Dendranthema morifolium exhibit protective effects against ischemia/reperfusion injury; however, its pharmacological action on blood vessels has not yet been investigated. The purpose of the present study was to assess the effects of the total flavones extracted from D. morifolium (Ramat.) Tzvel. cv. Hangju (FDM) on the vasocontraction and proliferation of vascular smooth muscle cells (VSMCs). The tension of rat thoracic aortic rings was measured using a mechanical force transducer attached to a recording system. FDM induced a dose­dependent relaxation of rings with endothelium pre­contracted by either phenylephrine (PE; 10(­6) mol/l) or a high concentration of potassium chloride (KCl; 60 mmol/l). FDM did not significantly affect the vasorelaxant effects on mechanically removed endothelium. In endothelium­denuded aortic rings depolarized by 60 mmol/l KCl, FDM inhibited the contraction induced by Ca2+. FDM reduced the transient contraction caused by PE in a Ca2+­free solution, but did not affect the contraction induced by phorbol ester. Furthermore, FDM inhibited the proliferation of VSMCs with or without growth stimulation by insulin. In conclusion, that the vasorelaxation induced by FDM in rat aortic rings is not dependent on the endothelium but is mediated via a reduction of the influx of extracellular Ca2+ through the voltage­dependent and receptor­operated channels and via the inhibition of the release of intracellular Ca2+ in VSMCs. The anti­proliferative activity of FDM suggests that it may be beneficial in inhibiting atherosclerosis.

Effects of Radix Ginseng and Radix Ophiopogonis extract (SMF) on protein S-nitrosylation in ischemic myocardial tissue / 中国中药杂志

<p><b>OBJECTIVE</b>To observe the effect of Radix Ginseng and Radix Ophiopogonis extract (SMF) on protein S-nitrosylation in rats myocardial with ischemia/reperfusion injury (MI/RI).</p><p><b>METHOD</b>Myocardial ischemia/reperfusion in rats were produced by occlusion of the left anterior descending coronary artery. To study the cardioprotective effects of SMF on the acute MI/RI rats, the serum levels of creatine kinase (CK), lactate dehydrogenase (LDH), and nitric oxide (NO) were determined. The change of the expression of endothelial nitric oxide synthase (eNOS) was detected by Western blot. The content of related S-nitrosylation proteins in myocardial tissue was measured by Biotin-Switch method.</p><p><b>RESULT</b>SMF significantly decreased the serum levels of CK and LDH as well as increased the serum levels of NO and the expression of eNOS in myocardial tissue. The contents of S-nitrosylation proteins were significantly increased from (4.42 +/- 0.60) micromol x g(-1) to (8.78 +/- 1.37) micromol x g(-1). The molecular weight of the majority S-nitrosylation proteins were in the range of 90 x 10(3)-117 x 10(3).</p><p><b>CONCLUSION</b>Increased expression of eNOS and NO induced by SMF may activate S-nitrosylation of many proteins in rat hearts. The change of the activities or functions of those proteins by S-nitrosylation may be an important mechanism for myocardial protective effects of SMF.</p>

[Treatment of interferon-alpha in reducing the endothelium-dependent relaxation of rat thoracic aorta].

OBJECTIVE: To investigate the vascular effect of acute and chronic treatment of interferon-alpha (IFN-alpha) in rat aortic rings. METHODS: Isolated thoracic aortic rings were mounted on the organ bath and the tension of the vessel was recorded. RESULTS: IFN-alpha(10, 100, 1,000 and 10,000 U/ml) caused concentration -dependent relaxation of endothelium-intact aorta rings preconstricted with phenylephrine (PE,10(-6)mol/L), to(90.1+/-0.91)%, (65.1+/-5.21)%, (39.5+/-8.22)% and (35.3+/-8.27)% of pre-drug control, respectively. Removal of the endothelium inhibited the relaxation by IFN-alpha. The vasorelaxant effect of IFN-alpha (100 U/ml ) was attenuated by pretreatment with L-NAME (10(-4)mol/L), methylene blue (10(-5)mol/L) or AMG (10(-4)mol/L), to (97.2+/-5.34)%, (95.1+/-6.25)% and (93.7+/-8.82)% of the control, respectively. Pretreatment with IFN-alpha (1,000,000 U/d, i.p.) for five days markedly inhibited the endothelium-dependent relaxation of the aortic rings to acetylcholine. But the endothelium-dependent relaxation to acetylcholine was not changed by pretreatment of IFN-alpha (10,000 U/ml) with the isolated aorta rings for 2 h. CONCLUSION: The vasorelaxation induced by IFN-alpha in rat aorta rings is endothelium-dependent and is possibly mediated by inducible nitric oxide synthase. Chronic treatment of IFN-alpha may impair the endothelium or NO-sGC pathway.