Effect of shuxuetong in preventing restenosis after intracoronary stenting / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To evaluate the effect of shuxuetong (SXT) in preventing restenosis after intracoronary stenting.</p><p><b>METHODS</b>Sixty-eight patients, accepted intracoronary stenting, were divided into two groups, the SXT group and the control group, both of them were treated with conventional treatment, and to the SXT group, SXT was given additionally. The condition of treated coronary artery restenosis in the two groups was compared by way of quantitative coronary angiography and a 6-month follow-up study was adopted.</p><p><b>RESULTS</b>Follow-up study was completed in 43 patients (23 cases in the SXT group, and 20 in the control group). The angina recurrence rate in the SXT group (3 cases, 13%) was significantly lower than that in the control group (7 cases, 35%, P < 0.05). Quantitative coronary angiography showed the restenosis degree of operated artery in the SXT group was significantly milder than that in the control group, with the last lumen losing and index in the SXT group (0.46 +/- 0.25 mm, 24.26 +/- 8.64%) less than those in the control group (0.75 +/- 0.33 mm, 31.25 +/- 11.03%). The net gain lumen and the net gain index in the SXT group (1.23 +/- 0.30 mm, 58.96 +/- 24.68%) were greater than those in the control group (0.98 +/- 0.33 mm, 42.68 +/- 29.51%), all P < 0.05. But the restenosis rate in the two groups was insignificantly different (P > 0.05).</p><p><b>CONCLUSION</b>SXT might has some definite effect in preventing restenosis after intracoronary stenting.</p>

ROS-mediated ERK activation in delayed protection from anoxic preconditioning in neonatal rat cardiomyocytes / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The activation of extracellular signal-regulated kinase1/2 (ERK1/2) has been shown to be important signaling pathway in the ischemic preconditioning (IPC) response. Recently, some studies suggest a key role for the mitochondrial ATP-sensitive potassium channel (mKATP) as both a trigger and an end effector of acute and delayed protection of IPC. Hence, this study was undertaken to elucidate the relationship between mKATP and ERK1/2 in the delayed protection mechanism of anoxic preconditioning (APC).</p><p><b>METHODS</b>An APC model was established using cultured neonatal rat cardiomyocytes. Pharmacological agents [diazoxide, 5-hydroxydecanoate (5-HD), 2-mercaptopropionylglycine (MPG), and PD98059] were used to modulate mKATP and ERK1/2 activation. Cellular injury was evaluated by measuring cellular superoxide dismutase (SOD) activity, cell viability, and lactate dehydrogenase (LDH) release. The generation of cellular reactive oxygen species (ROS) and the activation of ERK1/2 were determined at different time points starting from the beginning of preconditioning with anoxia or diazoxide (an mKATP opener).</p><p><b>RESULTS</b>Cell viability and SOD activity in the APC [(81.9 +/- 11.4)%, (13.6 +/- 3.7) U/L] and diazoxide [(79.2 +/- 12.4)%, (16.5 +/- 4.6) U/L] groups were significantly higher than in the anoxia/reoxygenation (A/R) [(42.2 +/- 7.3)%, (8.8 +/- 2.8) U/L] group (all P < 0.01). LDH activity in the APC group [(101.9 +/- 18.9) U/L] and diazoxide group [(97.5 +/- 17.7) U/L] was significantly lower than in the A/R group [(250.5 +/- 43.6) U/L] (all P < 0.01). Both APC and diazoxide simultaneously facilitated intracellular ROS generation and rapid ERK1/2 activation. But the effects of APC and diazoxide were remarkedly attenuated by 5-HP (an mKATP blocker) and by MPG (a free radical scavenger). In addition, the ERK1/2 inhibitor PD98059 also abolished the cellular protective effects induced by diazoxide.</p><p><b>CONCLUSION</b>mKATP may mediate ERK1/2 activation during anoxia preconditioning by generating ROS, which then triggers the delayed protection of APC in rat cardiomyocytes.</p>

Different roles of ERK(1/2) and p38 MAPK(alpha/beta) in cellular signaling during cardiomyocyte anoxia preconditioning / 生理学报

Preconditioning (PC) exhibits earlier and delayed protection. But the mechanism of cellular signaling in delayed protection of PC remains unclear. We explored the roles of ERK(1/2) and p38 MAPK(alpha/beta) (p38(alpha/beta)) in delayed protection of anoxia preconditioning (APC). The anoxia/reoxygenation (A/R) injury and APC models were established in cultured neonatal rat cardiomyocytes. An ERK(1/2) inhibitor (PD98059) and a p38(alpha/beta) blocker (SB203580) were applied and their effects on A/R and APC models were observed. The cellular contents of MDA, SOD, cell viability and LDH release was measured at the end of the study. ERK(1/2) and p38 MAPK total activity was measured by in-gel myelin basic protein phosphorylation assay at different points during sustained anoxia. The results obtained are as follows: (1) PD98059 (but not SB203580), administered in preconditioning anoxia phase in APC group, abolished completely the delayed protection of APC; (2) SB203580 administered in sustained anoxia phase in A/R group could relieve cell injury induced by anoxia, but not by PD98059; (3) the highest activity of ERK(1/2) and p38 MAPK induced by anoxia appeared at 4 h after the beginning of sustained anoxia. APC inhibited the over activation of both ERK(1/2) and p38 during the following sustained anoxia. These results suggest that ERK(1/2) activation during preconditioning may be an important link of cell signal transduction in the mechanism of APC delayed protection. p38(alpha/beta) activation at the preconditioning stage dose not participate in signaling of APC delayed protection. The excessive activation of p38(alpha/beta) is possibly a key factor in mediating cell injury induced by sustained anoxia. The inhibition of p38(alpha/beta) excessive activation during subsequent sustained anoxia might play a role in delayed protection mechanism of APC.