Bicyclol protects rat thoracic aorta from superoxide anion-induced inhibition of vascular relaxation / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the effect of bicyclol on vascular oxidative stress injury induced by superoxide anion.</p><p><b>METHODS</b>Rat thoracic aortic rings were isolated for isometric tension recording using organ bath technique. Superoxide arterial injury was induced by pyrogallol exposure, and the effect of bicyclol on endothelium-dependent relaxation was evaluated.</p><p><b>RESULTS</b>Bicyclol (10(-8) - 10(-5) mol/L) relaxed endothelium-intact aortic rings precontracted by phenylephrine. This effect was abolished by L-NAME, an inhibitor of nitric oxide synthase and indomethacin, an inhibitor of cyclooxygenase. Exposure to pyrogallol (500 micromol/L) resulted in decrease of acetylcholine(ACh)-induced endothelium-dependent relaxation in aortic rings, and pre-incubation of bicyclol (10(-5) mol/L) for 45 min improved the relaxation attenuated by pyrogallol. In aortic rings pre-treated with indomethacin, bicyclol increased the ACh-induced relaxation that was inhibited by pyrogallol (500 micromol/L). This effect was not found in aortic rings pre-treated with L-NAME.</p><p><b>CONCLUSION</b>Bicyclol has endothelium-dependent vasodilating effect on rat thoracic aorta and improves vascular function by attenuating oxidative stress. Nitric oxide from endothelium is involved in the anti-oxidative effect of bicyclol.</p>

Electrophysiological effect of atorvastatin on isolated rat hearts injured by ischemia/reperfusion / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the myocardial electrophysiological effect and its underlying mechanisms of atorvastatin (Ator) on isolated rat hearts injured by ischemia/reperfusion (I/R).</p><p><b>METHODS</b>Isolated SD rat hearts were mounted on Langendorff system, and a local I/R was induced by ligation (30 min) and release (15 min) of the left anterior descending artery. During the reperfusion period, the effect of Ator on diastolic excitation threshold (DET), effective refractory period (ERP) and ventricular fibrillation threshold (VFT) on rat heart were measured.</p><p><b>RESULT</b>Compared with the control group, medium concentration of Ator prolonged the ERP in normal rat hearts; low, medium and high concentration of Ator significantly inhibited the decrease of DET, ERP and VFT induced by I/R. However, pretreatment with L-NAME cancelled these cardiac electrophysiological effects of Ator.</p><p><b>CONCLUSION</b>Ator reduced electrophysiological alteration induced by I/R in isolated rat hearts, which may be mediated by activating nitric oxide pathway to enhance the myocardial electrophysiological stability.</p>

Expression of FANCD2 in Sporadic Breast Cancer and Clinicopathological Analysis / 华中科技大学学报（医学）（英德文版）

FANCD2 is involved in DNA damage repair and maintenance of chromosome stability.The purpose of this study was to investigate the expression of FANCD2 in sporadic breast cancer tissues and its association with clinicopathological features.A total of 162 Chinese women with invasive breast carcinoma who had no family history in first-degree relatives and 12 normal breast tissues were examined.The expression of FANCD2 was detected by immunohistochemical staining based on a tissue microarray technique.SAS system was used to analyze the data.Twenty-one out of the 162 invasive breast cancers(13%)were negative for FANCD2.The mean percentage of FANCD2 positive cells was significantly lower in breast cancers than in controls(P＜0.05).FANCD2 expression was significantly inversely associated with histological grade and TNM stage(P＜0.05),but not with axillary lymph node status or other conventional prognostic markers such as ER,PR,Her-2 and PCNA(P＞0.05).It was suggested that FANCD2 may play a critical role in breast carcinogenesis.It may become a valuable and independent marker for identifying women with sporadic breast cancer and evaluating the prognosis.

Vasodilating effect and its mechanism of ethanol on isolated rat thoracic aorta at different resting tension / 中国应用生理学杂志

<p><b>AIM</b>To investigate the vasodilating effect and its mechanism of ethanol on isolated rat thoracic aorta at different resting tension.</p><p><b>METHODS</b>The tension of the isolated Sprague-Dawley rat thoracic aorta rings perfused with different concentrations of ethanol was measured using organ bath technique.</p><p><b>RESULTS</b>At different resting tension (1.0, 1.5, 2.0, 2.5, 3.0, 3.5 and 4.0 g), ethanol (0.1-7.0 per thousand) caused a concentration-dependent relaxation on endothelium-denuded aortic rings precontracted with KCl (6 x 10(-2)mol/L) or phenylephrine (PE, 10(-6) mol/L), and the vasodilating effect was the most potent when the aortic rings were at the resting tension of 3 g. Ethanol had much less vasodilating effect on endothelium-intact aortic rings. Ethanol at 3 per thousand (the maximum-effect concentration) inhibited the CaCl2 induced contraction and downward shifted concentration-response curve of endothelium-denuded aortic rings pre-contracted with KCI or PE at the resting tension of 3 g. Incubation of aorta with ruthenium red (10(-5) mol/L) or heparin (50 mg/L) decreased the vasodilating effect of ethanol (3.0 per thousand) on endothelium-denuded aorta precontracted with PE at the resting tension of 3 g.</p><p><b>CONCLUSION</b>Ethanol induces endothelium-independent relaxation on rat thoracic aorta, which is concerned with the resting tension. This effect of ethanol may be mediated by the inhibition of voltage-dependent and receptor-operated Ca2+ channels in the vascular smooth muscle cells. The inhibition of the ryanodine receptor and trisphosphate inositol (IP3) pathway may also contribute to this effect.</p>