endothelin-1 and puerarin

To investigate the effects and possible mechanisms of puerarin on the vascular active factors correlated to cerebral vasospasm (CVS) after aneurysm subarachnoid hemorrhage (aSAH).. Fifty-four patients with aSAH were randomly assigned to the puerarin group (30 cases) and the control group (24 cases) by lot. On the basis of routine treatment, the patients in the puerarin group were intravenously dripped with 0.5 g puerarin by adding in 250 mL glucose injection once daily. The injection was given starting from the 3rd day of the disease course, for 14 successive days. The plasma levels of nitric oxide (NO), endothelin-1 (ET-1), thromboxane B, (TXB2), 6-Keto-prostaglandin F1alpha (6-K-PGF1alpha) were compared between the two groups pre- and post-therapy. The incidence of cerebral vasospasm (CVS) was observed using transcranial Doppler (TCD). The Glasgow outcome scale (GOS) were compared at discharge between the two groups.. Compared with the control group, the plasma levels of NO, ET-1, and 6-K-PGF1alpha increased in the puerarin group (P < 0. 05), the TXB2 level decreased (P < 0.05), the incidence of CVS decreased (P < 0.05), the mean MCA velocity increased (P < 0.05), and the GOS at discharge increased (P < 0.05).. Puerarin is an effective agent for the prophylaxis and treatment of the CVS in patients after aSAH. Moreover, it can improve the prognosis. The mechanism might be correlated with improving the levels of the vascular active factors, i.e., increasing the plasma levels of NO and PGl2, decreasing TXA, in plasma, increasing the cerebral blood flow, and improving cerebral perfusion.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Endothelin-1; Female; Humans; Isoflavones; Male; Middle Aged; Nitric Oxide; Prognosis; Subarachnoid Hemorrhage; Thromboxane B2; Vasospasm, Intracranial

To explore the protective effect and the mechanism of Puerarin Injection (PI) on myocardial ischemia reperfusion in patients with coronary heart disease (CHD) and angina pectoris (AP).. Seventy-eight patients with AP planned to receive the PTCA and stenting treatment were randomly divided and single-blindedly into the conventional group and the PI group. Based on the conventional treatment and pre-operational preparation, the PI group was given 200 ml of PI by intravenous dripping once a day, beginning from one week before operation, but to the conventional group, normal saline was given for instead. The condition of AP attack in balloon dilatatory stage of PTCA was observed and change of ST segment of ECG detected by a 12-lead ECG monitor. The blood levels of von Willebrand factor (vWF:Ag), nitric oxide (NO) and endothelin-1 (ET-1) were also observed before and after treatment.. As compared with those in the conventional group, number of patients having AP attack and ST segment change in PTCA process was lessened in the PI group, with blood levels of vWF:Ag and ET-1 obviously lower, and NO content obviously higher than those in the conventional group,. PI could protect the myocardium in 2-3 days after ischemia reperfusion, one of the possible reasons is that PI can simulate the late phase of ischemic preconditioning, which may be related to its effect in lowering plasma vWF:Ag and ET-1, and increasing the serum NO content.

Topics: Angina Pectoris; Angioplasty, Balloon, Coronary; Antigens; Endothelin-1; Female; Humans; Infusions, Intravenous; Isoflavones; Male; Middle Aged; Myocardial Reperfusion Injury; Nitric Oxide; Stents; von Willebrand Factor

BACKGROUND The aim of this study was to investigate the effects of puerarin on vascular endothelial function and inflammatory factors in coronary artery disease (CAD) patients with stable angina pectoris (SAP). MATERIAL AND METHODS To evaluate the effects of angina pectoris, the differences of scores of the Seattle angina questionnaire (SAQ), vascular endothelial function [endothelial progenitor cells (EPCs), nitric oxide (NO) and endothelin 1 (ET-1)], and inflammatory factors [tumor necrosis factor a (TNF-α), hypersensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6)] in 2 groups were assessed before and after treatment. RESULTS Regarding the curative effect of angina pectoris, the total effective rate of the treatment group was significantly superior to that of the control group (89% vs. 65%, P<0.05). The duration of angina pectoris, the number of abnormal leads, the improvement of the ST segment depression of electrocardiogram, and the scores of SAQ life quality indexes in the treatment group were better than those of the control group (P<0.05). In the 2 groups, EPCs and NO were both elevated, while ET-1 was decreased, and the improvements of the treatment group were superior to those of the control group (P<0.05). After treatment, the average levels of serum TNF-α, hs-CRP and IL-6 in the 2 groups were all decreased, which the treatment group showed a much sharper decrease than in the control group (P<0.05). CONCLUSIONS Puerarin effectively improves clinical symptoms and vascular endothelial function and reduces the levels of inflammatory factors in patients with CAD.

Topics: Aged; Angina Pectoris; Angina, Stable; C-Reactive Protein; China; Coronary Artery Disease; Endothelial Cells; Endothelial Progenitor Cells; Endothelin-1; Female; Humans; Inflammation; Interleukin-6; Isoflavones; Male; Middle Aged; Nitric Oxide; Treatment Outcome; Tumor Necrosis Factor-alpha

Fine particulate matter (PM2.5) is a major risk factor for the development and progression of atherosclerosis. Proliferation and infiltration of vascular smooth muscle cells (VSMCs) from the blood vessel media into the intima is a crucial step in the pathophysiology of atherosclerosis. Puerarin, a natural extract from Radix Puerariae, possesses significant anti-atherosclerosis properties. However, the underlying molecular mechanisms responsible for the effect of puerarin on the VSMCs proliferation induced by PM2.5 remain unclear. The present study was designed to examine the effect of puerarin on PM2.5-induced VSMCs proliferation, and to explore the p38 mitogen-activated protein kinase (p38 MAPK) signal mechanism involved.. VSMCs viability was measured by CCK-8 assay, VSMCs proliferation was assessed by BrdU immunofluorescence, the levels of superoxide dismutase (SOD) and malonaldehyde (MDA) were assayed by colorimetric assay kits, the levels of nitric oxide (NO) and endothelin-1 (ET-1) were determined by nitrate reductase method and radioimmunoassay, the levels of vascular cell adhesion molecule-1 (VCAM-1), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were measured by ELISA. The protein expressions of phospho-p38 MAPK (p-p38 MAPK) and proliferating cell nuclear antigen (PCNA) in the VSMCs were subjected by Western blot.. Compared to the PM2.5-treated cells, in addition to inhibiting the PM2.5-induced VSMCs proliferation, puerarin also down-regulated the protein expressions of p-p38 MAPK and PCNA, decreased the levels of ET-1, VCAM-1, IL-6, TNF-α and MDA, increased the levels of NO and SOD. Moreover, the anti-proliferative effects of puerarin were significantly enhanced by the co-incubation of puerarin with SB203580, a selective inhibitor of p38 MAPK, as compared to the puerarin-treated cells.. These results suggest that puerarin might suppress the PM2.5-induced VSMCs proliferation via the inhibition of the p38 MAPK signaling pathway.

Topics: Aorta; Cell Proliferation; Cells, Cultured; Endothelin-1; Humans; Isoflavones; Muscle, Smooth, Vascular; Nitric Oxide; p38 Mitogen-Activated Protein Kinases; Particulate Matter; Vascular Cell Adhesion Molecule-1

The aim of this study was to explore the mechanism of 3-methoxy puerarin on decreasing the cerebral ischemia-reperfusion injury in rats. Before the model of cerebral ischemia-reperfusion injury was made, the rats in one group (3-methoxy puerarin group, 3-MP group) were pretreated with 3-methoxy puerarin (100 mg/kg) by gavageing two times per day for seven days. At an hour before operation, the rats in the 3-MP group were additionally given 3-methoxy puerarin by gavageing once. The level of prostacyclin (PGI2) and the expression of endothelin-1 (ET-1) mRNA in cerebral tissue, the activity of plasma tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) were measured. Cerebral tissue pathologic changes were also observed. The levels of PGI2 in cerebral tissue and the activity of plasma t-PA in 3-MP group were significantly higher than those in the group of cerebral ischemia-reperfusion injury (CIRI group) (p<0.01). The activity of plasma PAI and the expression of ET-1 mRNA in cerebral tissue in 3-MP group were significantly lower than those in CIRI group (p<0.01). The cerebral tissue pathologic changes were significant in CIRI group, which were significantly ameliorated in the 3-MP group. The study showed, in the rat model of cerebral ischemia-reperfusion injury, 3-methoxy puerarin can not only increase the level of PGI2 in cerebral tissue and the activity of plasma t-PA, but also inhibit the activity of plasma PAI and the expression of ET-1 mRNA in cerebral tissue. Those findings might be the mechanisms behind the protecting effects of 3-methoxy puerarin on the cerebral ischemia-reperfusion injury.

Topics: Animals; Brain; Disease Models, Animal; Endothelin-1; Epoprostenol; Isoflavones; Male; Plasminogen Activator Inhibitor 1; Random Allocation; Rats; Rats, Sprague-Dawley; Reperfusion; Reperfusion Injury; RNA, Messenger; Tissue Plasminogen Activator; Vasodilator Agents