Herbal complement inhibitors in the treatment of neuroinflammation - Future strategy for neuroprotection

Herbal complement inhibitors in the treatment of neuroinflammation - Future strategy for neuroprotection
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DOI:
10.1196/annals.1352.020
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发表时间:
2005-01-01
期刊:
NATURAL PRODUCTS AND MOLECULAR THERAPY
影响因子:
--
通讯作者:
Kotwal, GJ
Kotwal, GJ
中科院分区:
其他
文献类型:
--
作者:
Kulkarni, AP;Kellaway, LA;Kotwal, GJ

文献摘要

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补体系统的上调在中枢神经系统(CNS)疾病中起着破坏性的作用。经典途径和交替途径是阿尔茨海默病、多发性硬化症、创伤性脑损伤、脊髓损伤、HIV相关性痴呆、帕金森氏病和疯牛病等神经炎性疾病中激活的两条主要途径。现有的抗炎药,特别是环氧合酶抑制剂,在中枢神经系统疾病的大规模流行病学临床试验中未能提供显著的神经保护作用,这表明迫切需要开发新的神经保护剂。补体调节分子,如痘苗病毒补体控制蛋白治疗中枢神经系统疾病的临床前阳性结果提示,将补体抑制分子用作神经保护剂的可能性。几种草药来源的活性成分被发现具有补体抑制活性。这些草药成分与其他抗炎作用一起,可能对治疗与中枢神经系统疾病相关的神经炎症有用。根据补体抑制活性成分的化学性质和对激活补体系统的主要途径的特异性,对中草药来源的活性成分进行了总结和分类。文中还讨论了一些具体实例的构效关系。这些信息可能有助于研制出一种天然的灵丹妙药来对抗补体介导的神经炎症。
The upregulated complement system plays a damaging role in disorders of the central nervous system (CNS). The classical and alternate pathways are two major pathways activated in neuroinflammatory disorders such as Alzheimer's disease, multiple sclerosis, traumatic brain injury, spinal cord injury, HIV-associated dementia, Parkinson's disease, and mad cow disease. Failure of currently available anti-inflammatory agents, especially cycloxygenase inhibitors, in offering significant neuroprotection in large epidemiologic clinical trials of CNS disorders suggests an urgent need for the development of new neuroprotective agents. The positive preclinical outcomes in treating CNS disorders by complement regulatory molecules, such as vaccinia virus complement control protein, suggest the possibility of using complement-inhibitory molecules as neuroprotective agents. Several active ingredients of herbal origin are found to have complement-inhibitory activity. These herbal ingredients along with other anti-inflammatory roles might be useful in treating neuroinflammation associated with CNS disorders. Active ingredients of herbal origin with complement inhibitory ingredients are summarized and classified according to their chemical nature and specificity towards the major pathways activating the complement system. The structure activity relationship of some specific examples is also discussed in this report. This information might be helpful in formulating a natural panacea against complement-mediated neuroinflammation.