Ischemic stroke (IS) is characterized by high recurrence and disability; however, its therapies are very limited. As one of the effective methods of treating acute attacks of IS, intravenous thrombolysis has a clear time window. Quercetin, a flavonoid widely found in vegetables and fruits, inhibits immune cells from secreting inflammatory cytokines, thereby reducing platelet aggregation and limiting inflammatory thrombosis. In pre-clinical studies, it has been shown to exhibit neuroprotective effects in patients with ischemic brain injury. However, its specific mechanism of action remains unknown. Therefore, this review aims to use published data to elucidate the potential value of quercetin in patients with ischemic brain injury. This article also reviews the plant sources, pharmacological effects, and metabolic processes of quercetin in vivo, thus focusing on its mechanism in inhibiting immune cell activation and inflammatory thrombosis as well as promoting neuroprotection against ischemic brain injury.
Objective. The clinical value of intestinal flora balance therapy based on probiotic support in improving cognitive function and symptoms of patients with Alzheimer’s disease was to systematically evaluate, so as to provide evidence-based medicine basis for the promotion and use of this therapy. Methods. The randomized controlled trials (RCTs) were searched for the improvement of cognitive function and symptoms of patients with Alzheimer’s disease by intestinal flora balance therapy supported mainly by probiotics in PubMed, EMBASE, ScienceDirect, Cochrane Library, China Knowledge Network Database (CNKI), China VIP database, Wanfang database, and China Biomedical Literature Database (CBM) online database (RCT). Data were extracted independently by two researchers, and the literature was assessed for risk of bias according to the Cochrane Handbook 5.1.0 criteria. The data were meta-analyzed using RevMan 5.4 statistical software. Results. Finally, 5 randomized controlled trials were included, with a total sample size of 386 cases. The results of meta-analysis showed that Ch i 2 = 13.14 , df = 2 , P = 0.001 , and I 2 = 85 % showed significant heterogeneity in the inclusion of the study data. Probiotic-supported intestinal microflora balance therapy improves cognitive function in patients with Alzheimer’s disease. Through meta-analysis of transient memory scores, it is concluded that intestinal flora balance therapy based on probiotic support can improve transient memory in patients with Alzheimer’s disease. Meta-analysis of ADAS-COG score showed that intestinal flora balance therapy supported by probiotics could improve the cognitive function of patients with Alzheimer’s disease. The ADL score was analyzed by meta, and the heterogeneity test result was Ch i 2 = 0.79 , df = 1 , P = 0.37 > 0.05 , and I 2 = 0 % , indicating that the intestinal flora balance therapy supported by probiotics can improve the ability of daily living of patients with Alzheimer’s disease. Conclusion. Intestinal flora balance therapy based on probiotic support can effectively improve cognitive function, instantaneous memory, and ability of daily life in patients with Alzheimer’s disease. However, more studies and long-term follow-up studies with higher methodological quality are needed to further verify.
Objective. Traditional Chinese medicine formula Kai-Xin-San (KXS) is used to treat psychiatric disorders, especially in anxiety and depression. However, the precise molecular mechanism of action remains unclear. In this study, we investigated the antidepressant effect of KXS on inhibiting inflammation and oxidative stress in corticosterone (CORT)-induced depression. Methods. The therapeutic efficacy of KXS was evaluated in a mouse model of depression induced by CORT. Behavioral tests were conducted to evaluate the effectiveness of KXS in treating depressive-like behavior. Nissl staining and β-galactosidase staining were used to assess the effects of KXS on neuronal injury in depressed mice. To screen key potential therapeutic targets of KXS, transcriptome sequences and data analysis were performed. Then, Iba1 immunofluorescence staining and their relative inflammatory factors mRNA expression were conducted to assess the effect of KXS in inhibiting microglial inflammation activation response. Concurrently, the measurement of 4-Hydroxynonenal (4-HNE) immunohistochemistry staining, malondialdehyde (MDA), superoxide dismutase (SOD), and reactive oxygen species (ROS) were performed to evaluate the effect of KXS on anti-oxidative stress of depression in vivo. Besides, nitric oxide (NO), relative inflammatory factors mRNA expression, JC-1 staining, and ROS were used to evaluate the effect of KXS by lipopolysaccharide (LPS)/interferon-gamma (IFNγ)-induced BV2 cells. Results. KXS significantly relieved the depressive-like symptoms induced by CORT, as well as ameliorating the neuronal damage, which decreased microglia inflammatory activation response of IL-1β, IL-6, and tumor necrosis factor α (TNFα) in vivo or in vitro too. Transcriptome Sequencing and Data Analysis showed that KXS mainly by regulating immune system and transduction pathways decreased CORT-induced depression in mice. And showed that there were 19 Principal components and 10 genes in the main regulatory position with the strongest correlation in depression mice. Meanwhile, KXS effectively decreased senescence, the expression of 4-HNE, MDA content, and the production of ROS, while increasing the SOD activity in CORT-induced mice. Besides, KXS significantly reversed the mitochondrial membrane potential loss and excessive ROS production in LPS/IFNγ-induced BV2 cells. Conclusion. Our research suggested that KXS might protect depressed mice against CORT-induced neuronal injury by inhibiting microglia activation and oxidative stress.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.