广东医学
廣東醫學
엄동의학
GUNAGDONG MEDICAL JOURNAL
2010年
5期
564-565
,共2页
廖欣鑫%廖彩仙%黄勇平%秦安成%袁杰%赖勇强%龚祖元
廖訢鑫%廖綵仙%黃勇平%秦安成%袁傑%賴勇彊%龔祖元
료흔흠%료채선%황용평%진안성%원걸%뢰용강%공조원
肝纤维化%肝硬化%CXCL13%CXCL16%趋化因子
肝纖維化%肝硬化%CXCL13%CXCL16%趨化因子
간섬유화%간경화%CXCL13%CXCL16%추화인자
fibrosis%cirrhosis%liver%CXCL13/BCA-1%CXCL16%chemokine
目的 观察肝纤维化与肝硬化患者肝组织中趋化因子CXCL13和CXCL16的表达变化.方法 用ELISA方法分别检测9例正常人和10例肝纤维化、11例肝硬化患者肝组织中的CXCL13和CXCL16含量.结果 正常对照组、肝纤维化组、肝硬化组的CXCL13浓度分别为(2.34±2.05)ng/g、(6.04±2.97)ng/g和(12.10±10.38)ng/g;肝硬化组的浓度显著高于正常对照组和肝纤维化组,正常对照组与肝纤维化组的CXCL13浓度差异无统计学意义.正常对照组、肝纤维化组、肝硬化组的CXCL16浓度分别为(1.32±0.91)ng/g、(3.34±1.81)ng/g和(3.49±1.90)ng/g;肝硬化组和肝纤维化组浓度均显著高于正常对照组浓度,肝硬化组和肝纤维化组的CXCL16浓度差异无统计学意义.结论 肝脏发生纤维化损伤时,肝脏表达CXCL13和CXCL16的数量都显著增多.但两者的变化规律不同.肝内CXCL13水平在肝纤维化阶段开始升高,至肝硬化阶段升高到显著水平.肝内CXCL16水平在肝纤维化阶段就已经升高到显著水平,至肝硬化阶段仍维持在高水平状态.
目的 觀察肝纖維化與肝硬化患者肝組織中趨化因子CXCL13和CXCL16的錶達變化.方法 用ELISA方法分彆檢測9例正常人和10例肝纖維化、11例肝硬化患者肝組織中的CXCL13和CXCL16含量.結果 正常對照組、肝纖維化組、肝硬化組的CXCL13濃度分彆為(2.34±2.05)ng/g、(6.04±2.97)ng/g和(12.10±10.38)ng/g;肝硬化組的濃度顯著高于正常對照組和肝纖維化組,正常對照組與肝纖維化組的CXCL13濃度差異無統計學意義.正常對照組、肝纖維化組、肝硬化組的CXCL16濃度分彆為(1.32±0.91)ng/g、(3.34±1.81)ng/g和(3.49±1.90)ng/g;肝硬化組和肝纖維化組濃度均顯著高于正常對照組濃度,肝硬化組和肝纖維化組的CXCL16濃度差異無統計學意義.結論 肝髒髮生纖維化損傷時,肝髒錶達CXCL13和CXCL16的數量都顯著增多.但兩者的變化規律不同.肝內CXCL13水平在肝纖維化階段開始升高,至肝硬化階段升高到顯著水平.肝內CXCL16水平在肝纖維化階段就已經升高到顯著水平,至肝硬化階段仍維持在高水平狀態.
목적 관찰간섬유화여간경화환자간조직중추화인자CXCL13화CXCL16적표체변화.방법 용ELISA방법분별검측9례정상인화10례간섬유화、11례간경화환자간조직중적CXCL13화CXCL16함량.결과 정상대조조、간섬유화조、간경화조적CXCL13농도분별위(2.34±2.05)ng/g、(6.04±2.97)ng/g화(12.10±10.38)ng/g;간경화조적농도현저고우정상대조조화간섬유화조,정상대조조여간섬유화조적CXCL13농도차이무통계학의의.정상대조조、간섬유화조、간경화조적CXCL16농도분별위(1.32±0.91)ng/g、(3.34±1.81)ng/g화(3.49±1.90)ng/g;간경화조화간섬유화조농도균현저고우정상대조조농도,간경화조화간섬유화조적CXCL16농도차이무통계학의의.결론 간장발생섬유화손상시,간장표체CXCL13화CXCL16적수량도현저증다.단량자적변화규률불동.간내CXCL13수평재간섬유화계단개시승고,지간경화계단승고도현저수평.간내CXCL16수평재간섬유화계단취이경승고도현저수평,지간경화계단잉유지재고수평상태.
Objective To investigate the expression of chemotactic factors (CXCL13 and CXCL16) in the liver of patients with hepatic fibrosis and cirrhosis and in normal controls. Methods Hepatic tissues were obtained in surgery from 9 normal persons, 10 patients with hepatic fibrosis, and 11 patients with cirrhosis. Expression of CXCL13 and CXCL16 in hepatic tissues was quantified by ELISA. Results The concentrations of CXCL13 were 2.34±2.05, 6.04±.97 and 12.10±10.38 ng/g in normal, hepatic fibrosis and hepatic cirrhosis group, respectively. CXCL13 in sclerotic liver was higher than that in normal controls and fibrotic liver, but there was no significant difference. The concentrations of CXCL16 were 1.32±0.91, 3.34±1.81 and 3.49±1.90 ng/g in normal, hepatic fibrosis and hepatic cirrhosis group. CXCL16 in fibrotic liver and sclerotic liver were higher than that in normal liver, but there was still no significant difference. Conclusion With the aggravation of hepatic fibrous degeneration, hepatic levels of CXCL13 and CXCL16 increase, but follow a different way. CXCL13 begins to rise in the stage of liver fibrosis and has a significant increase in cirrhosis stage. CXCL16 increases to significant level in the stage of liver fibrosis, and remains in a high state in liver cirrhosis stage.
