阿托伐他汀可预防恶性疟原虫的细胞黏附和内皮损伤。
Atorvastatin prevents Plasmodium falciparum cytoadherence and endothelial damage.
机构信息
INSERM, UMR S945, Université Pierre et Marie Curie-Paris 6, CHU-Pitié-Salpêtrière, 91 bd de l'Hôpital, 75013 Paris, France.
出版信息
Malar J. 2011 Feb 28;10:52. doi: 10.1186/1475-2875-10-52.
BACKGROUND
The adhesion of Plasmodium falciparum parasitized red blood cell (PRBC) to human endothelial cells (EC) induces inflammatory processes, coagulation cascades, oxidative stress and apoptosis. These pathological processes are suspected to be responsible for the blood-brain-barrier and other organs' endothelial dysfunctions observed in fatal cases of malaria. Atorvastatin, a drug that belongs to the lowering cholesterol molecule family of statins, has been shown to ameliorate endothelial functions and is widely used in patients with cardiovascular disorders.
METHODS
The effect of this compound on PRBC induced endothelial impairments was assessed using endothelial co-culture models.
RESULTS
Atorvastatin pre-treatment of EC was found to reduce the expression of adhesion molecules and P. falciparum cytoadherence, to protect cells against PRBC-induced apoptosis and to enhance endothelial monolayer integrity during co-incubation with parasites.
CONCLUSIONS
These results might suggest a potential interest use of atorvastatin as a protective treatment to interfere with the pathophysiological cascades leading to severe malaria.
背景
恶性疟原虫寄生的红细胞（PRBC）与人类内皮细胞（EC）的黏附会诱导炎症过程、凝血级联反应、氧化应激和细胞凋亡。这些病理过程可能是导致致命性疟疾中观察到的血脑屏障和其他器官内皮功能障碍的原因。阿托伐他汀是一种属于降低胆固醇分子他汀类药物家族的药物，已被证明可改善内皮功能，广泛用于心血管疾病患者。
方法
使用内皮细胞共培养模型评估该化合物对 PRBC 诱导的内皮损伤的影响。
结果
发现阿托伐他汀预处理 EC 可降低黏附分子的表达和恶性疟原虫的细胞黏附，可保护细胞免受 PRBC 诱导的凋亡，并增强与寄生虫共孵育期间内皮单层的完整性。
结论
这些结果可能提示阿托伐他汀作为一种保护性治疗的潜在应用，以干扰导致严重疟疾的病理生理级联反应。
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