Objective To investigate the effect and possible mechanism of tetramethylpyrazine involved in regulating vascular calcification. Methods Angiosteosis in rats was induced by vitamin D3 intramuscular injection and nicotine intragastric administration. Calcification of vascular smooth muscle cells (VSMC) was induced by β-glycerophosphate. The Ca2+ contents in aorta and VSMCs were measured by an atom absorptive spectrophotography. Ca2+ deposition in aorta and VSMCs was evaluated by the 45CaCl2 absorption and Von Kossa staining. The alkaline phosphatase (ALP) activity was detected by a chemical colorimetric method. The mRNA level of osteopontin ( OPN) was determined by reverse transcription PCR. Results ALT activity, Ca 2+ contents and 45 Ca2+ deposition were significantly increased, but osteopontin mRNA expression was significantly decreased in calcified vessel and VSMC. After treatment with tetramethylpyrazine (40 mg · kg-1 in vivo and 200 mg · L-1 in vitro) , the Ca2+ content, 45Ca2+-deposition and ALP activity were decreased, while osteopontin mRNA expression was increased in plasma, aorta and VSMCs, respectively. Conclusion Our results indicated that tetramethylpyrazine significantly protects the aorta against calcification partly through the activation of the endogenous anti-calcification system in local aorta tissues.%目的 探讨川芎嗪调节血管钙化的作用及可能机制.方法 建立肌内注射维生素D3和口服尼古丁诱导大鼠血管钙化以及β-甘油磷酸盐诱导血管平滑肌细胞钙化模型,并给予川芎嗪干预.采用原子吸收分光光度法测定主动脉和细胞钙含量、45 CaCl2摄入法和Von Kossa染色评价钙沉积、化学比色法测定碱性磷酸酶活性、逆转录聚合酶链反应测定骨桥蛋白mRNA的表达水平.结果 钙化大鼠血管和血管平滑肌细胞碱性磷酸酶活性、钙含量和钙沉积明显增强,骨桥蛋白表达水平显著降低.川芎嗪40 mg·kg-1治疗大鼠、200 mg· L-1处理钙化血管平滑肌细胞,均可有效抑制血管钙化、明显上调骨桥蛋白mRNA的表达.结论 川芎嗪可能部分通过上调血管组织局部的内源性钙化拮抗系统而产生抑制血管组织和血管平滑肌细胞钙化的作用.
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