目的 :检测α7-烟碱型乙酰胆碱受体(α7-niccotinic acetylcholine receptor,α7-n ACh R)在肺癌组织中的表达,探讨其与临床病理学特征的关系及意义。方法:采用免疫组织化学染色法检测130例肺癌组织及40例癌旁肺组织中α7-nAChR表达,并...目的 :检测α7-烟碱型乙酰胆碱受体(α7-niccotinic acetylcholine receptor,α7-n ACh R)在肺癌组织中的表达,探讨其与临床病理学特征的关系及意义。方法:采用免疫组织化学染色法检测130例肺癌组织及40例癌旁肺组织中α7-nAChR表达,并分析α7-nAChR表达与吸烟、病理分型、分化程度、临床分期、淋巴结转移等关系。结果:肺癌组织α7-nAChR阳性表达率70.77%,癌旁组织阳性率37.50%,肺癌组织中α7-n ACh R阳性表达水平明显高于癌旁组织(P<0.001)。肺癌组织中α7-nAChR的表达水平与肺癌患者吸烟、临床分期、分化程度相关(P<0.05),与患者的性别、年龄、肿瘤大小、病理分型、淋巴结转移之间的关系无统计学意义(P>0.05)。结论:α7-nAChR高表达在肺癌的发生中起一定作用,可为肺癌的α7-nAChR靶向治疗提供一定依据。展开更多
目的:构建α7烟碱型乙酰胆碱受体(α7 nicotine acetylcholine receptor,α7 n AChR)基因敲除小鼠牙髓炎模型,为研究α7 nAChR在牙髓炎发生发展过程中的作用机制提供实验模型。方法:取16只α7 n AChR基因敲除(knock out,KO)小鼠和16只...目的:构建α7烟碱型乙酰胆碱受体(α7 nicotine acetylcholine receptor,α7 n AChR)基因敲除小鼠牙髓炎模型,为研究α7 nAChR在牙髓炎发生发展过程中的作用机制提供实验模型。方法:取16只α7 n AChR基因敲除(knock out,KO)小鼠和16只野生型(wide type,WT)C57BL/6鼠的上颌第一磨牙的牙髓暴露法建立牙髓炎模型,分别在牙髓暴露后1、3、7 d处死小鼠,HE染色、免疫组化检测牙髓组织NOD样受体蛋白3(NOD-like receptor protein 3,NLRP3)表达情况。结果:HE染色结果显示牙髓暴露后1 d,α7 n AChR KO鼠及WT鼠的穿髓孔周围血管充血、组织水肿;牙髓暴露后3 d,炎症细胞聚集,α7 n AChR KO鼠炎症细胞聚集已达冠髓底部,WT鼠的炎症细胞主要聚集在穿髓孔周围的牙髓组织中;牙髓暴露后7 d,α7 nAChR KO鼠的牙髓炎症细胞浸润至根部牙髓,而WT鼠的牙髓炎症细胞仍然主要聚集于冠髓底部。免疫组化染色结果显示,牙髓暴露后,α7 n AChR KO鼠牙髓NLRP3表达高于WT鼠,差异有统计学意义(P <0.05)。结论:成功建立了α7 n AChR基因敲除鼠的牙髓炎模型,而且α7nAChR基因敲除鼠牙髓炎症浸润明显快于WT小鼠。展开更多
Aim Baroreflex dysfunction is associated with a higher rate of sudden death after myocardial infarction （MI）. Ketanserin enhances baroreflex function in rats. The present work was designed to examine whether ketan- ...Aim Baroreflex dysfunction is associated with a higher rate of sudden death after myocardial infarction （MI）. Ketanserin enhances baroreflex function in rats. The present work was designed to examine whether ketan- serin improves the post-MI cardiac function and to explore the possible mechanism involved. Methods Spontane- ously hypertensive rats （SHR） were treated with ketanserin （0.3 mg · kg^-1 · d^-l）. Two weeks later, blood pres- sure and baroreflex function were measured, followed by a ligation of the left coronary artery. The expressions of ve- sicular acetylcholine transporter （VAChT） and α7 nicotinic acetylcholine receptor （α7-nAChR） in ischemic myo- cardium, angiogenesis, cardiac function, and left ventricular （LV） remodeling were evaluated subsequently. Re- sults Ketanserin significantly improved baroreflex sensitivity （0.62 ± 0. 21 vs. 0.34 ± 0. 12 ms/mmHg, P 〈 0.01 ） and vagal tonic activity （ heart rate changes in response to atropine, 54.8 ± 16.2 vs. 37.6 ± 13.4 b. p. m. , P 〈 0.01 ） without affecting the blood pressure or basic heart rate in SHR. Treatment of SHR with ketanserin promi- nently improved cardiac function and alleviated LV remodeling, as reflected by increases in the ejection fraction, fractional shortening, and LV systolic pressure as well as decreases in LV internal diameter and LV relative weight. The capillary density, vascular endothelial growth factor expression, and blood flow in the ischemic myocardium were significantly higher in the ketanserin-treated group. In addition, ketanserin markedly increased the expression of VAChT and α7-nAChR in ischemic myocardium. Conclusion Ketanserin improved post-MI cardiac function and angiogenesis in ischemic myocardium. The findings provide a mechanistic basis for restoring baroreflex function using ketanserin in the treatment of MI.展开更多
文摘目的 :检测α7-烟碱型乙酰胆碱受体(α7-niccotinic acetylcholine receptor,α7-n ACh R)在肺癌组织中的表达,探讨其与临床病理学特征的关系及意义。方法:采用免疫组织化学染色法检测130例肺癌组织及40例癌旁肺组织中α7-nAChR表达,并分析α7-nAChR表达与吸烟、病理分型、分化程度、临床分期、淋巴结转移等关系。结果:肺癌组织α7-nAChR阳性表达率70.77%,癌旁组织阳性率37.50%,肺癌组织中α7-n ACh R阳性表达水平明显高于癌旁组织(P<0.001)。肺癌组织中α7-nAChR的表达水平与肺癌患者吸烟、临床分期、分化程度相关(P<0.05),与患者的性别、年龄、肿瘤大小、病理分型、淋巴结转移之间的关系无统计学意义(P>0.05)。结论:α7-nAChR高表达在肺癌的发生中起一定作用,可为肺癌的α7-nAChR靶向治疗提供一定依据。
文摘目的:构建α7烟碱型乙酰胆碱受体(α7 nicotine acetylcholine receptor,α7 n AChR)基因敲除小鼠牙髓炎模型,为研究α7 nAChR在牙髓炎发生发展过程中的作用机制提供实验模型。方法:取16只α7 n AChR基因敲除(knock out,KO)小鼠和16只野生型(wide type,WT)C57BL/6鼠的上颌第一磨牙的牙髓暴露法建立牙髓炎模型,分别在牙髓暴露后1、3、7 d处死小鼠,HE染色、免疫组化检测牙髓组织NOD样受体蛋白3(NOD-like receptor protein 3,NLRP3)表达情况。结果:HE染色结果显示牙髓暴露后1 d,α7 n AChR KO鼠及WT鼠的穿髓孔周围血管充血、组织水肿;牙髓暴露后3 d,炎症细胞聚集,α7 n AChR KO鼠炎症细胞聚集已达冠髓底部,WT鼠的炎症细胞主要聚集在穿髓孔周围的牙髓组织中;牙髓暴露后7 d,α7 nAChR KO鼠的牙髓炎症细胞浸润至根部牙髓,而WT鼠的牙髓炎症细胞仍然主要聚集于冠髓底部。免疫组化染色结果显示,牙髓暴露后,α7 n AChR KO鼠牙髓NLRP3表达高于WT鼠,差异有统计学意义(P <0.05)。结论:成功建立了α7 n AChR基因敲除鼠的牙髓炎模型,而且α7nAChR基因敲除鼠牙髓炎症浸润明显快于WT小鼠。
文摘Aim Baroreflex dysfunction is associated with a higher rate of sudden death after myocardial infarction （MI）. Ketanserin enhances baroreflex function in rats. The present work was designed to examine whether ketan- serin improves the post-MI cardiac function and to explore the possible mechanism involved. Methods Spontane- ously hypertensive rats （SHR） were treated with ketanserin （0.3 mg · kg^-1 · d^-l）. Two weeks later, blood pres- sure and baroreflex function were measured, followed by a ligation of the left coronary artery. The expressions of ve- sicular acetylcholine transporter （VAChT） and α7 nicotinic acetylcholine receptor （α7-nAChR） in ischemic myo- cardium, angiogenesis, cardiac function, and left ventricular （LV） remodeling were evaluated subsequently. Re- sults Ketanserin significantly improved baroreflex sensitivity （0.62 ± 0. 21 vs. 0.34 ± 0. 12 ms/mmHg, P 〈 0.01 ） and vagal tonic activity （ heart rate changes in response to atropine, 54.8 ± 16.2 vs. 37.6 ± 13.4 b. p. m. , P 〈 0.01 ） without affecting the blood pressure or basic heart rate in SHR. Treatment of SHR with ketanserin promi- nently improved cardiac function and alleviated LV remodeling, as reflected by increases in the ejection fraction, fractional shortening, and LV systolic pressure as well as decreases in LV internal diameter and LV relative weight. The capillary density, vascular endothelial growth factor expression, and blood flow in the ischemic myocardium were significantly higher in the ketanserin-treated group. In addition, ketanserin markedly increased the expression of VAChT and α7-nAChR in ischemic myocardium. Conclusion Ketanserin improved post-MI cardiac function and angiogenesis in ischemic myocardium. The findings provide a mechanistic basis for restoring baroreflex function using ketanserin in the treatment of MI.
