ABSTRACT
Objective To investigate the effect of extracellular signal-regulated kinases (ERKs) on cell cycle regulation after ischemia. Methods Ischemic model was induced by photochemistry method. Animals were divided randomly into cerebral ischemia groups (control and treatment groups) and sham group. Rats in treatment group were subjected to U0126 solution injection at 30 rain pre-ischemia through caudal veins, and animals in control group were subjected to identical volume DMSO solution without U0126. Positive immunostaining for CyclinD1 and CyclinE were detected by immunohistofluorescence method. Expressions of phosphorylated ERK1/2 (pERK1/2), CyclinD1, and CyclinE proteins were examined by Western blot in ischemic slide of brain cortex. Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of transcription factor E2F mRNA in ischemic slide of brain cortex. Results The numbers of CyclinD1 and CyclinE positive cells were highly decreased in the U0126-treated group (P<0.05 vs vehicle-treated group). Expression of pERK1/2 protein in the ischemic group was significantly higher than that in the U0126-treated group, which peaked at 4h, and decreased to the baseline at 12 after ischemia. While the expression levels of CyclinD1 and CyclinE in the U0126-treated group were increased at 6h post injury, peaked at 12 after injury (P<0.05 vs that in vehicle-treated group). In addition, expression of E2F mRNA in the vehicle-treated group was significantly higher than those in the sham-operated group and the U0126-treated group (P<0.05). Conclusions ERK pathway plays a very important role in cerebral ischemia. Inhibiting ERK1/2 phosphorylation post-ischemia reduces the expressions of CyclinD1, CyclinE and E2F, which indicates that ERK can affect cell cycle regulation.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of fluvastatin on blood levels of c-reactive protein (CRP), tumor necrosis factor alpha (TNFalpha) and cardiac troponin I (cTnI) in patients with unstable angina undergoing percutaneous coronary intervention (PCI).</p><p><b>METHODS</b>Sixty patients who underwent PCI from July 2002 to April 2004 in our hospital were randomized into two groups: control group; fluvastatin group (40 mg/d). Serum levels of CRP, TNFalpha and cTnI were measured before and after two weeks treatment (in the early morning of the procedure) and at 24 hours after the procedure.</p><p><b>RESULTS</b>The serum levels of CRP, TNFalpha and cTnI in fluvastatin group were distinctly lower than those in control group before (P < 0.01) and after the procedure (P < 0.01), respectively.</p><p><b>CONCLUSION</b>The result suggested that PCI could lead to a detectable increase in serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could significantly decrease the serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could also decrease the serum levels of CRP, TNFalpha and cTnI in patients with PCI.</p>