Ren De Cheng, Du Guan Hua, Zhang Jun Tian
Institute of Materia Medica, Chinese Academy of Medical Sciences, Beijing.
Jpn J Pharmacol. 2002 Nov;90(3):276-80. doi: 10.1254/jjp.90.276.
The effect of the water-soluble extract (WSE) of Salvia miltiorrhiza on neutrophil-endothelial cell adhesion was investigated. Cell adhesion was evaluated by testing neutrophil myeloperoxidase activity: expression of adhesion molecules in human umbilical vein endothelial cells (HUVEC) was measured by ELISA: the neutrophil activation rate induced by N-formyl-methionyl-leucyl-phenylalanine (fMLP) was tested by the method of nitroblue tetrazolium (NBT) reduction. The results showed that the adhesion rate of neutrophils to unstimulated HUVEC was very low. TNFalpha (50 - 800 U/ml) increased the adhesion of neutrophils to TNFalpha-stimulated HUVEC in a concentration- and time-dependent manner. The WSE of Salvia miltiorrhiza (0.01 - 1 mg/ml) dose-dependently inhibited the adhesion of neutrophils. The inhibitory rate of the WSE of Salvia miltiorrhiza at 0.01, 0.1 and 1 mg/ml was 6.2%, 17.0% and 28.0%, respectively. fMLP (10(-9) - 10(-5) M) increased the activation rate of neutrophils concentration-dependently. The WSE of Salvia miltiorrhiza also concentration-dependently inhibited the adhesion of fMLP-activated neutrophils to HUVEC. The inhibitory rate of the WSE of Salvia miltiorrhiza at 0.001, 0.01 and 0.1 mg/ml was 5.3%, 26.3% and 28.9%, respectively. Moreover, TNFalpha upregulated expression of adhesion molecule E-selectin, ICAM-1 and VCAM-1. The WSE of Salvia miltiorrhiza had an inhibitory effect on TNF alpha-induced expression of these molecules. These results indicated that the WSE of Salvia miltiorrhiza inhibited neutrophil-endothelial adhesion. The action mechanism of the WSE of Salvia miltiorrhiza was partly related to suppressing the expression of adhesion molecules.
研究了丹参水溶性提取物（WSE）对中性粒细胞与内皮细胞黏附的影响。通过检测中性粒细胞髓过氧化物酶活性来评估细胞黏附：采用酶联免疫吸附测定法（ELISA）检测人脐静脉内皮细胞（HUVEC）中黏附分子的表达；通过硝基蓝四氮唑（NBT）还原法检测N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸（fMLP）诱导的中性粒细胞活化率。结果显示，中性粒细胞与未刺激的HUVEC的黏附率很低。肿瘤坏死因子α（TNFα，50 - 800 U/ml）以浓度和时间依赖性方式增加中性粒细胞与经TNFα刺激的HUVEC的黏附。丹参水溶性提取物（0.01 - 1 mg/ml）剂量依赖性地抑制中性粒细胞的黏附。丹参水溶性提取物在0.01、0.1和1 mg/ml时的抑制率分别为6.2%、17.0%和28.0%。fMLP（10(-9) - 10(-5) M）浓度依赖性地增加中性粒细胞的活化率。丹参水溶性提取物也浓度依赖性地抑制fMLP激活的中性粒细胞与HUVEC的黏附。丹参水溶性提取物在0.001、0.01和0.1 mg/ml时的抑制率分别为5.3%、26.3%和28.9%。此外，TNFα上调黏附分子E-选择素、细胞间黏附分子-1（ICAM-1）和血管细胞黏附分子-1（VCAM-1）的表达。丹参水溶性提取物对TNFα诱导的这些分子的表达有抑制作用。这些结果表明，丹参水溶性提取物抑制中性粒细胞与内皮细胞的黏附。丹参水溶性提取物的作用机制部分与抑制黏附分子的表达有关。
