2型糖尿病患者CD11b/CD18的表达及活血化瘀药对其的影响

目的：探讨在2型糖尿病(DM)患者中多形核白细胞粘附分子CDllb／CD18的表达及活血化瘀药预防血管病变的可能机制。方法：49例无高血压、无临床肾病的2型DM患者随机分成中药治疗组(26例)和常规治疗组(23例)，治疗3个月。治疗前后观察尿白蛋白排泄率、CDllb／CD18的表达及肿瘤坏死因子-α浓度等指标。结果：与健康对照组比较，2型DM患者的CDllb／CD18表达增高，肿瘤坏死因子-α浓度也明显增高(P＜0．01)。与常规治疗组比较，活血化瘀中药治疗3个月后，2型DM患者的CDllb／CD18表达，尿白蛋白排泄率和肿瘤坏死因子-α明显降低(P＜0．01)，而常规治疗组无类似的变化。相关性分析提示，尿白蛋白排泄率下降与肿瘤坏死因子-α浓度降低和多形核白细胞粘附分子CDllb／CDl8表达的下降呈正相关(r＝0．56，P＜0．01，r＝0．64，P＜0．01)。结论：2型DM患者的多形核白细胞粘附分子CDllb／CD18表达增高；活血化瘀法预防血管病变的机制可能与其抑制CDllb／CD18表达有关。

Effect of Chinese Herbal Medicine for Activating Blood Circulation to Remove Stasis on CDllb/CD18 Expression in Patients with Diabetes Mellitus Type 2

Objective: To explore the expression of polymorphonuclear leucocyte adhesive molecules CD11b/CD18 and to study the possible mechanism of Chinese herbal medicine (TCM) for activating blood circulation to remove stasis in preventing vascular diseases. Methods: Forty-nine patients with diabetes mellitus (DM) but with no complications of hypertension and nephropathy were randomly divided into the treated group (26 patients treated by TCM) and the control group (23 patients treated by conventional treatment) . They were treated for 3 months. The changes of urinary albumin excretion rate (UAER), CD11b/CD18 expression and tumor necrosis factor-a (TNF-a) concentration before and after treatment were observed. Results: The CDllb/CD18 expression and TNF-a concentration in DM patients were higher than those of normal range (P<0.01). After treatment, the UAER, CDllb/CD18 expression and TNF-a concentration lowered significantly in the treated group (P<0.01), but unchanged in the control group. Correlation analysis showed that the lowering of UAER was positively correlated with decreasing of CDllb/CD18 ( r = 0.64, P < 0.01) and TNF-a ( r = 0.56, P < 0.01). Conclusion:Expression of CDllb/CD18 increases in patients with DM type 2. The mechanism of Chinese herbal medicine for activating blood circulation to remove stasis in preventing vascular disease is possibly related with its effect in inhibiting CDllb/CD18 expression.