中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2001年
1期
29-31
,共3页
余路%邱鸿鑫%王亚平%司良毅%吴珊%祝继华
餘路%邱鴻鑫%王亞平%司良毅%吳珊%祝繼華
여로%구홍흠%왕아평%사량의%오산%축계화
糖基化终产物,高级%细胞粘着分子%内皮%细胞%自由基
糖基化終產物,高級%細胞粘著分子%內皮%細胞%自由基
당기화종산물,고급%세포점착분자%내피%세포%자유기
目的:探讨糖基化终产物(AGEs)致内皮细胞表达细胞间粘附分子-1(ICAM-1)与自由基产生之间的关系。方法:内皮细胞(EC)用抗AGEs抗体、抗IL-1β多抗、N-乙酰半胱氨酸(NAC)预处理1h后AGEs作用6h,测定IL-1β、超氧化物歧化酶(SOD)、ICAM-1、内皮细胞-中性粒细胞粘附率。结果:AGEs刺激后ICAM-1表达增加[吸光度(A)为0.65±0.14vs0.11±0.02]的内皮细胞SOD活性降低[(0.69±0.19)×103U/Lvs(1.71±0.42)×103U/L]。ICAM-1的增加可被抗AGEs抗体[吸光度(A)为(0.12±0.01)]、NAC[吸光度(A)为(0.11±0.05)]和抗ICAM-1抗体[吸光度(A)为(0.10±0.04)]抑制。外源性IL-1β也可刺激内皮细胞表达ICAM-1[吸光度(A)为(0.72±0.23)]。结论:AGEs刺激内皮细胞表达ICAM-1可能与其导致细胞自由基的产生有关;AGEs还可通过刺激其他细胞产生细胞因子间接作用于EC,参与促进ICAM-1表达。
目的:探討糖基化終產物(AGEs)緻內皮細胞錶達細胞間粘附分子-1(ICAM-1)與自由基產生之間的關繫。方法:內皮細胞(EC)用抗AGEs抗體、抗IL-1β多抗、N-乙酰半胱氨痠(NAC)預處理1h後AGEs作用6h,測定IL-1β、超氧化物歧化酶(SOD)、ICAM-1、內皮細胞-中性粒細胞粘附率。結果:AGEs刺激後ICAM-1錶達增加[吸光度(A)為0.65±0.14vs0.11±0.02]的內皮細胞SOD活性降低[(0.69±0.19)×103U/Lvs(1.71±0.42)×103U/L]。ICAM-1的增加可被抗AGEs抗體[吸光度(A)為(0.12±0.01)]、NAC[吸光度(A)為(0.11±0.05)]和抗ICAM-1抗體[吸光度(A)為(0.10±0.04)]抑製。外源性IL-1β也可刺激內皮細胞錶達ICAM-1[吸光度(A)為(0.72±0.23)]。結論:AGEs刺激內皮細胞錶達ICAM-1可能與其導緻細胞自由基的產生有關;AGEs還可通過刺激其他細胞產生細胞因子間接作用于EC,參與促進ICAM-1錶達。
목적:탐토당기화종산물(AGEs)치내피세포표체세포간점부분자-1(ICAM-1)여자유기산생지간적관계。방법:내피세포(EC)용항AGEs항체、항IL-1β다항、N-을선반광안산(NAC)예처리1h후AGEs작용6h,측정IL-1β、초양화물기화매(SOD)、ICAM-1、내피세포-중성립세포점부솔。결과:AGEs자격후ICAM-1표체증가[흡광도(A)위0.65±0.14vs0.11±0.02]적내피세포SOD활성강저[(0.69±0.19)×103U/Lvs(1.71±0.42)×103U/L]。ICAM-1적증가가피항AGEs항체[흡광도(A)위(0.12±0.01)]、NAC[흡광도(A)위(0.11±0.05)]화항ICAM-1항체[흡광도(A)위(0.10±0.04)]억제。외원성IL-1β야가자격내피세포표체ICAM-1[흡광도(A)위(0.72±0.23)]。결론:AGEs자격내피세포표체ICAM-1가능여기도치세포자유기적산생유관;AGEs환가통과자격기타세포산생세포인자간접작용우EC,삼여촉진ICAM-1표체。
AIM: To explore the relationship between intercellular adhesionmolecule-1(ICAM-1)expression in endothelial cells(EC) and advanced glycosylation end products(AGEs) stimulation. METHODS: Murine bone marrow derived ECs was stimulated by AGEs after pretreated with anti-AGEs, anti-IL-1β and N-acetylcysteine(NAC),then SOD activity and ICAM-1 concentration and adhesion rate(AR) were evaluated. RESULTS: ECs which expressed ICAM-1[(0.65±0.14) vs (0.11±0.02)] induced by AGEs showed lower SOD activity [(0.69±0.19)×103 U/L vs (1.71±0.42)×103 U/L]. The ICAM-1 expression as well as the increase of AR caused by AGEs stimulation could be suppressed by anti-AGEs(0.12±0.01) and NAC(0.11±0.05). Anti-IL-1β had no influence on these changes. CONCLUSION: AGEs could induce endothelial cells to express ICAM-1 in vitro, most probably due to the formation of free radicals. Besides, AGEs may stimulate other cells to secrete cytokines resulting in ICAM-1 expression in endothelial cells.