中国临床药理学杂志
中國臨床藥理學雜誌
중국림상약이학잡지
THE CHINESE JOURNAL OF CLINICAL PHARMACOLOGY
2014年
4期
340-343
,共4页
张红兵%李强%冯靖%狄柯坪
張紅兵%李彊%馮靖%狄柯坪
장홍병%리강%풍정%적가평
川芎嗪%血管平滑肌细胞%炎症%黏附
川芎嗪%血管平滑肌細胞%炎癥%黏附
천궁진%혈관평활기세포%염증%점부
tetramethylpyrazine%vascular smooth muscle cells%inflammation%adhesion
目的：观察川芎嗪对内皮损伤诱导的新生内膜形成的影响。方法用贴块法，培养血管平滑肌细胞（ VSMCs），建立血小板源性生长因子（ PDGF）诱导的细胞增殖模型。用细胞计数法观察4个浓度（0，20，40，80μmol· L-1）川芎嗪对VSMCs增殖的影响；用Western blot分析各组细胞中反式作用因子激活蛋白-1（AP-1）、增殖细胞核抗原（PCNA）、环氧合酶-2（COX-2）、细胞间黏附分子-1（ICAM-1）和整合素连接激酶（ILK）等的表达变化；用球囊剥脱法观察对内皮损伤诱导的新生内膜形成的影响。结果川芎嗪呈剂量依赖性地抑制PDGF诱导的细胞增生以及AP-1、PCNA、COX-2、ICAM-1等相关基因的表达，有效阻断黏附分子ILK信号。川芎嗪可预防球囊损伤诱导的血管新生内膜肥厚，明显降低内膜/中膜面积（ I/M）比值。结论川芎嗪通过抑制增殖和炎性基因表达、阻断黏附分子信号传递等形式发挥抗血管内膜异常增殖的作用。
目的：觀察川芎嗪對內皮損傷誘導的新生內膜形成的影響。方法用貼塊法，培養血管平滑肌細胞（ VSMCs），建立血小闆源性生長因子（ PDGF）誘導的細胞增殖模型。用細胞計數法觀察4箇濃度（0，20，40，80μmol· L-1）川芎嗪對VSMCs增殖的影響；用Western blot分析各組細胞中反式作用因子激活蛋白-1（AP-1）、增殖細胞覈抗原（PCNA）、環氧閤酶-2（COX-2）、細胞間黏附分子-1（ICAM-1）和整閤素連接激酶（ILK）等的錶達變化；用毬囊剝脫法觀察對內皮損傷誘導的新生內膜形成的影響。結果川芎嗪呈劑量依賴性地抑製PDGF誘導的細胞增生以及AP-1、PCNA、COX-2、ICAM-1等相關基因的錶達，有效阻斷黏附分子ILK信號。川芎嗪可預防毬囊損傷誘導的血管新生內膜肥厚，明顯降低內膜/中膜麵積（ I/M）比值。結論川芎嗪通過抑製增殖和炎性基因錶達、阻斷黏附分子信號傳遞等形式髮揮抗血管內膜異常增殖的作用。
목적：관찰천궁진대내피손상유도적신생내막형성적영향。방법용첩괴법，배양혈관평활기세포（ VSMCs），건립혈소판원성생장인자（ PDGF）유도적세포증식모형。용세포계수법관찰4개농도（0，20，40，80μmol· L-1）천궁진대VSMCs증식적영향；용Western blot분석각조세포중반식작용인자격활단백-1（AP-1）、증식세포핵항원（PCNA）、배양합매-2（COX-2）、세포간점부분자-1（ICAM-1）화정합소련접격매（ILK）등적표체변화；용구낭박탈법관찰대내피손상유도적신생내막형성적영향。결과천궁진정제량의뢰성지억제PDGF유도적세포증생이급AP-1、PCNA、COX-2、ICAM-1등상관기인적표체，유효조단점부분자ILK신호。천궁진가예방구낭손상유도적혈관신생내막비후，명현강저내막/중막면적（ I/M）비치。결론천궁진통과억제증식화염성기인표체、조단점부분자신호전체등형식발휘항혈관내막이상증식적작용。
Objective To investigate the effect of tetramethylpyrazine ( TMP) on neointimal hyperplasia induced by balloon injury.Methods VSMCs were cultured by tissue explants adherent method and VSMCs proliferation models induced by platelet -derived growth factor ( PDGF) were established.Cell counting analysis was adopted to evaluate the in-hibitory effects of TMP in a dose of 0, 20, 40 and 80 μmol · L-1 on VSMCs.Western blot analysis was performed to analyze the effect of TMP on the activator protein -1 ( AP-1 ) , proliferating cell nuclear antigen ( PCNA ) , cyclooxygenase ( COX-2 ) , intercellular adhesion molecular ( ICAM -1 ) , and integrin -linked kinase ( ILK ) expressions in VSMCs.Hemetoxylin and Eosin ( HE) staining was performed to investi-gate the effects of TMP on the neointimal hyperplasia induced by balloon injury.Results TMP inhibited cell proliferation induced by PDGF ( 20μg· L-1 ) in a dose-dependent (0, 20, 40, 80 μmol· L-1 ) manner.Remarkable decreases of AP -1, PCNA, COX-2, ICAM-1 and ILK expression were demonstrated in the TMP group compared with the model group in VSMCs.TMP inhibited the neointimal thickening induced by ballon injury , with a significantly lower ratio of intima -to-media area ( l/M) in the TMP group.Conclusion TMP plays a role in preventing neointimal hyperplasia through inhibiting or blocking proliferation , expressions of inflammatory genes and adhesion molecules.
