Guo Jinfeng, Li Zhengjie, Yao Yun, Fang Lei, Yu Mingdi, Wang Zuhui
The Nursing Department of Anhui College of Traditional Chinese Medicine, Wuhu, Anhui, China.
The Outpatient and Emergency Department of Wuhu Hospital of Traditional Chinese Medicine, Wuhu, Anhui, China.
Front Neurol. 2024 May 10;15:1380353. doi: 10.3389/fneur.2024.1380353. eCollection 2024.
Traumatic brain injury (TBI), a leading cause of high morbidity and mortality, represents a significant global public health challenge. Currently, no effective treatment for TBI exists. Curcumin, an active compound extracted from the root of , has demonstrated neuroprotective properties both and . Notably, it has shown potential in reducing oxidative stress and inflammation and enhancing redox balance. This paper conducts a systematic review and meta-analysis to explore curcumin's role in TBI animal models extensively. The findings offer valuable insights for future human clinical trials evaluating curcumin as a therapeutic supplement or nutraceutical in TBI management.
Comprehensive literature searches were conducted across MEDLINE, Embase, Cochrane, Web of Science, and Google Scholar databases. These searches aimed to identify relevant manuscripts in all languages, utilizing the keywords "curcumin" and "traumatic brain injury."
The final quantitative analysis included 18 eligible articles corresponding to animal studies. The analysis revealed that curcumin significantly reduced inflammatory cytokines, including IL-1β ( = 0.000), IL-6 ( = 0.002), and TNF-α ( = 0.000), across various concentrations, time points, and administration routes. Additionally, curcumin markedly enhanced the activity of oxidative stress markers such as SOD ( = 0.000), Sir2 ( = 0.000), GPx ( = 0.000), and Nrf2 ( = 0.000), while reducing MDA ( = 0.000), 4-HNE ( = 0.001), and oxyprotein levels ( = 0.024). Furthermore, curcumin improved cerebral edema ( = 0.000) and upregulated neuroprotective factors like synapsin I ( = 0.019), BDNF ( = 0.000), and CREB ( = 0.000), without reducing mNSS ( = 0.144). About autophagy and apoptosis, curcumin increased the activity of Beclin-1 ( = 0.000) and Bcl-2 ( = 0.000), while decreasing caspase-3 ( = 0.000), the apoptosis index ( = 0.000), and P62 ( = 0.002).
Curcumin supplementation positively affects traumatic brain injury (TBI) by alleviating oxidative stress and inflammatory responses and promoting neuroprotection. It holds potential as a therapeutic agent for human TBI. However, this conclusion necessitates further substantiation through high-quality literature and additional randomized controlled trials (RCTs).
https://www.crd.york.ac.uk/prospero/. The registration number of PROSPERO: CRD42023452685.
创伤性脑损伤(TBI)是导致高发病率和死亡率的主要原因,是一项重大的全球公共卫生挑战。目前,尚无针对TBI的有效治疗方法。姜黄素是从姜黄根中提取的一种活性化合物,在体内和体外均已显示出神经保护特性。值得注意的是,它在减轻氧化应激和炎症以及增强氧化还原平衡方面已显示出潜力。本文进行了一项系统综述和荟萃分析,以广泛探讨姜黄素在TBI动物模型中的作用。这些发现为未来评估姜黄素作为TBI治疗补充剂或营养保健品的人体临床试验提供了有价值的见解。
在MEDLINE、Embase、Cochrane、科学网和谷歌学术数据库中进行了全面的文献检索。这些检索旨在利用关键词“姜黄素”和“创伤性脑损伤”识别所有语言的相关手稿。
最终的定量分析包括18篇符合动物研究的合格文章。分析表明,在不同浓度、时间点和给药途径下,姜黄素显著降低了炎性细胞因子,包括白细胞介素-1β(P = 0.000)、白细胞介素-6(P = 0.002)和肿瘤坏死因子-α(P = 0.000)。此外,姜黄素显著增强了超氧化物歧化酶(P = 0.000)、沉默信息调节因子2(P = 0.000)、谷胱甘肽过氧化物酶(P = 0.000)和核因子E2相关因子2(P = 0.000)等氧化应激标志物的活性,同时降低了丙二醛(P = 0.000)、4-羟基壬烯醛(P = 0.001)和氧化蛋白水平(P = 0.024)。此外,姜黄素改善了脑水肿(P = 0.000),并上调了突触素I(P = 0.019)、脑源性神经营养因子(P = 0.000)和环磷腺苷效应元件结合蛋白(P = 0.000)等神经保护因子,而未降低改良神经功能缺损评分(P = 0.144)。关于自噬和凋亡,姜黄素增加了Beclin-1(P = 0.000)和Bcl-2(P = 0.000)的活性,同时降低了半胱天冬酶-3(P = 0.000)、凋亡指数(P = 0.000)和P62(P = 0.002)。
补充姜黄素通过减轻氧化应激和炎症反应以及促进神经保护,对创伤性脑损伤(TBI)产生积极影响。它有望成为人类TBI的治疗药物。然而,这一结论需要通过高质量的文献和更多的随机对照试验(RCT)进一步证实。
https://www.crd.york.ac.uk/prospero/。PROSPERO注册号:CRD42023452685。