Department of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Medicinal Plants Research Center, Institute of Medicinal Plants, ACECR, Karaj, Iran; Department of Toxicology and Pharmacology, School of Pharmacy, and Toxicology and Diseases Group, Pharmaceutical Sciences Research Center (PSRC), The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, Tehran, Iran; GI Pharmacology Interest Group (GPIG), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
Biomed Pharmacother. 2022 Oct;154:113621. doi: 10.1016/j.biopha.2022.113621. Epub 2022 Aug 30.
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.
神经炎症是涉及神经退行性疾病的关键病理生理机制之一。涉及神经炎症的一种情况是创伤性脑损伤(TBI)。在过去的几十年中,各种替代天然化合物,如姜黄素,已被研究作为减轻 TBI 涉及的病理生理途径和临床后果的新的治疗选择。作为姜黄(Curcuma longa)的主要成分,姜黄素由于其相当大的抗氧化和抗炎作用,具有广泛的临床特性。这篇综述讨论了姜黄素的多效机制、副作用、向中枢神经系统(CNS)的传递及其对 TBI 的免疫调节和保护作用。从包括 PubMed、Scopus 和 Google Scholar 在内的不同科学数据库中提取了临床试验、体内和体外研究,以评估姜黄素或其衍生物在 TBI 中的作用。研究结果表明,姜黄素通过调节细胞信号通路,包括 Toll 样受体 4(TLR-4)、核因子 kappa B(NF-κB)和 Nod 样受体家族蛋白(NLRPs),对 TBI 表现出一些保护作用。此外,姜黄素上调脑源性神经营养因子/原肌球蛋白受体激酶 B(BDNF/TrkB)信号通路、磷酸肌醇 3-激酶/蛋白激酶 B(PI3K/AKT)、核因子红细胞 2 相关因子 2(Nrf2),这些通路在调节 TBI 病理生理介导的途径中具有重要作用。姜黄素在不同的 TBI 模型中显示出有益的免疫调节功能和保护能力,尽管需要更多的临床实验来阐明姜黄素在 TBI 中的确切机制和功能。