Dong Wei-Guo, Liu Shao-Ping, Zhu Hai-Hang, Luo He-Sheng, Yu Jie-Ping
Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan 430060, Hubei Province, China.
World J Gastroenterol. 2004 Feb 15;10(4):606-9. doi: 10.3748/wjg.v10.i4.606.
To explore the abnormal function of platelets and the role of angelica sinensis injection (ASI) in patients with ulcerative colitis (UC).
In 39 patients with active UC, 25 patients with remissive UC and 30 healthy people, alpha-granule membrane protein (GMP-140) and thromboxane B(2) (TXB(2)) were detected by means of ELISA, 6-keto-PGF(1a) was detected by radioimmunoassay, platelet count (PC) and 1 min platelet aggregation rate (1 min PAR) were detected by blood automatic tester and platelet aggregation tester respectively, and von Willebrand factor related antigen (vWF:Ag) was detected by the means of monoclonal -ELISA. The 64 patients with UC were divided into two therapy groups. After routine treatment and angelica sinensis injection (ASI) + routine treatment respectively for 3 weeks, all these parameters were also detected.
The PC, 1 min PAR and levels of GMP-140, TXB(2), and vWF:Ag in active UC were significantly higher than those in remissive UC and normal controls (P<0.05-0.01).Meanwhile, 1 min PAR and levels of GMP-140, TXB(2), and vWF:Ag in remissive UC were still significantly higher than those in normal controls (P<0.05). Furthermore, 6-keto-PGF(1a) level in active and remissive UC was remarkably lower than that in normal control (P<0.05-0.01). These parameters except 6-keto-PGF(1a) were significantly improved after the treatment in ASI therapy group (P<0.05-0.01), whereas they all were little changed in routine therapy group (P>0.05).
Platelets can be significantly activated in UC, which might be related with vascular endothelium injury and imbalance between TXB(2) and 6-keto-PGF(1a) in blood. ASI can significantly inhibit platelet activation, relieve vascular endothelial cell injury, and improve microcirculation in UC.
探讨溃疡性结肠炎(UC)患者血小板功能异常及当归注射液(ASI)的作用。
采用酶联免疫吸附测定法(ELISA)检测39例活动期UC患者、25例缓解期UC患者及30例健康对照者的α-颗粒膜蛋白(GMP-140)和血栓素B2(TXB2);采用放射免疫分析法检测6-酮-前列腺素F1α(6-keto-PGF1α);分别用血液自动分析仪和血小板聚集仪检测血小板计数(PC)及1分钟血小板聚集率(1分钟PAR);采用单克隆ELISA法检测血管性血友病因子相关抗原(vWF:Ag)。将64例UC患者分为两组,分别给予常规治疗和ASI+常规治疗3周后,再次检测上述各项指标。
活动期UC患者的PC、1分钟PAR及GMP-140、TXB2、vWF:Ag水平均显著高于缓解期UC患者及正常对照组(P<0.05-0.01)。同时,缓解期UC患者的1分钟PAR及GMP-140、TXB2、vWF:Ag水平仍显著高于正常对照组(P<0.05)。此外,活动期和缓解期UC患者的6-keto-PGF1α水平均显著低于正常对照组(P<0.05-0.01)。ASI治疗组治疗后,除6-keto-PGF1α外,其余各项指标均显著改善(P<0.05-0.01),而常规治疗组各项指标变化均不明显(P>0.05)。
UC患者血小板可被显著激活,这可能与血管内皮损伤及血液中TXB2与6-keto-PGF1α失衡有关。ASI可显著抑制血小板激活,减轻血管内皮细胞损伤,改善UC患者的微循环。