姜黄素
神经炎症
创伤性脑损伤
PI3K/AKT/mTOR通路
医学
蛋白激酶B
药理学
神经营养因子
信号转导
神经保护
原肌球蛋白受体激酶B
神经科学
生物
受体
免疫学
炎症
内科学
细胞生物学
精神科
作者
Danial Khayatan,Seyed Mehrad Razavi,Zahra Najafi Arab,Amir Hossein Niknejad,Kiana Nouri,Saeideh Momtaz,Eric Gumpricht,Tannaz Jamialahmadi,Amir Hossein Abdolghaffari,George E. Barreto,Amirhossein Sahebkar
标识
DOI:10.1016/j.biopha.2022.113621
摘要
Neuroinflammation is a key pathophysiological mechanism implicated in the neurodegenerative condition. One such condition implicating neuroinflammation is traumatic brain injury (TBI). Over the past decades, various alternative natural compounds, such as curcumin, have been investigated as novel therapeutic options to mitigate the pathophysiological pathways and clinical sequelae involved in TBI. As the main component of turmeric (Curcuma longa), curcumin has a broad range of clinical properties due to its considerable antioxidative and anti-inflammatory actions. This review discusses the pleiotropic mechanisms, the side effects, curcumin's delivery to the central nervous system (CNS), and its immunomodulatory and protective effects on TBI. Clinical trials, in vivo, and in vitro studies were extracted from different scientific databases, including PubMed, Scopus, and Google Scholar, to assess the effects of curcumin or its derivatives in TBI. Findings reveal that curcumin exhibited some protective effects on TBI via modulation of cell signaling pathways including toll-like receptor-4 (TLR-4), nuclear factor kappa B (NF-κB), and Nod-like receptor family proteins (NLRPs). Moreover, curcumin upregulates the brain-derived Neurotrophic Factor/Tropomyosin receptor kinase B (BDNF/TrkB) signaling pathway, phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT), nuclear factor erythroid 2-related factor 2 (Nrf2), which have crucial functions in modulation of TBI pathophysiological-mediated pathways. Curcumin displays beneficial immunomodulatory functions and protective capacities in different TBI models, although more clinical experiments are required to clarify curcumin's precise mechanisms and function in TBI.
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