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PLOS Pathogens:研究发现他汀类药物有抗疟疾功效

  1. 他汀类药物
  2. 疟疾

来源:生物谷 2012-12-28 13:22

2012年12月28日讯 /生物谷BIOON/ --近日,研究人员发现,一种广泛使用的降胆固醇药物洛伐他汀具有抗疟药治疗功效,能降低发炎反应,防止脑型疟疾小鼠模型的认知功能障碍。 虽然脑型疟疾小鼠模型与人类疾病之间有差异,但这些新发现证实他汀类药物值得考虑开展脑型疟疾的临床试验,相关研究论文发表在12月27日的PLOS Pathogens杂志上。

2012年12月28日讯 /生物谷BIOON/ --近日,研究人员发现,一种广泛使用的降胆固醇药物洛伐他汀具有抗疟药治疗功效,能降低发炎反应,防止脑型疟疾小鼠模型的认知功能障碍。

虽然脑型疟疾小鼠模型与人类疾病之间有差异,但这些新发现证实他汀类药物值得考虑开展脑型疟疾的临床试验,相关研究论文发表在12月27日的PLOS Pathogens杂志上。

脑型疟疾是一种恶性疟原虫感染的严重潜在致命性的神经系统并发症。儿童脑型疟疾研究发现,在许多幸存者被治愈后认知功能障碍如记忆力减退,学习,语言和数学能力减退长期存在。

他汀类药物,一类降低胆固醇的药物,也被证明在调节各种免疫系统反应是积极的。在新研究中,Zimmerman和他的同事评估了他汀类药物在脑型疟疾的小鼠模型的功效。研究人员发现,一种药物洛伐他汀能防止脑型疟疾感染小鼠认知功能障碍。

他们发现洛伐他汀除了降低白血细胞的积累和大脑血管泄漏外,洛伐他汀也减少了破坏性含氧分子和其他促进炎症因素的生成。虽然引起脑型疟疾和随后引发的认知功能障碍分子机制尚不清楚,然而事实表明他汀类药物治疗可以降低有害血管炎症和认知功能障碍。

Zimmerman和他的同事们还研究了洛伐他汀对细菌性败血症实验模型中的作用,该模型特征是严重的全身炎症状态,也可导致认知功能障碍。他们发现洛伐他汀也能防止细菌性败血症引发的认知功能障碍。研究人员相信,该研究是首次提供了实验证据支持使用他汀类药物以减少危重病人认知功能障碍的可能性。(生物谷:Bioon.com)

Statins Decrease Neuroinflammation and Prevent Cognitive Impairment after Cerebral Malaria

Patricia A. Reis,et al.

Cerebral malaria (CM) is the most severe manifestation of Plasmodium falciparum infection in children and non-immune adults. Previous work has documented a persistent cognitive impairment in children who survive an episode of CM that is mimicked in animal models of the disease. Potential therapeutic interventions for this complication have not been investigated, and are urgently needed. HMG-CoA reductase inhibitors (statins) are widely prescribed for cardiovascular diseases. In addition to their effects on the inhibition of cholesterol synthesis, statins have pleiotropic immunomodulatory activities. Here we tested if statins would prevent cognitive impairment in a murine model of cerebral malaria. Six days after infection with Plasmodium berghei ANKA (PbA) mice displayed clear signs of CM and were treated with chloroquine, or chloroquine and lovastatin. Intravital examination of pial vessels of infected animals demonstrated a decrease in functional capillary density and an increase in rolling and adhesion of leukocytes to inflamed endothelium that were reversed by treatment with lovastatin. In addition, oedema, ICAM-1, and CD11b mRNA levels were reduced in lovastatin-treated PbA-infected mice brains. Moreover, HMOX-1 mRNA levels are enhanced in lovastatin-treated healthy and infected brains. Oxidative stress and key inflammatory chemokines and cytokines were reduced to non-infected control levels in animals treated with lovastatin. Fifteen days post-infection cognitive dysfunction was detected by a battery of cognition tests in animals rescued from CM by chloroquine treatment. In contrast, it was absent in animals treated with lovastatin and chloroquine. The outcome was similar in experimental bacterial sepsis, suggesting that statins have neuroprotective effects in severe infectious syndromes in addition to CM. Statin treatment prevents neuroinflammation and blood brain barrier dysfunction in experimental CM and related conditions that are associated with cognitive sequelae, and may be a valuable adjuvant therapeutic agent for prevention of cognitive impairment in patients surviving an episode of CM.

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