Dehydroevodiamine ameliorates neurological dysfunction after traumatic brain injury in mice via regulating the SIRT1/FOXO3a/Bim pathway

Xu, Min; Zhao, Yalin; Gong, Mingjie; He, Ziyang; Wang, Wenhua; Li, Yunjuan; Zhai, Weiwei; Yu, Zhengquan

doi:10.1016/j.phymed.2023.155321

Cited by 3 publications

(1 citation statement)

References 40 publications

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“…In animal models of traumatic brain TBI, the augmentation in Foxo-positive neuronal populations displays a temporal dependency ( Liu et al, 2021 ). Mechanistically, acetylated Foxo3a was identified as a mediator driving Bim upregulation within traumatized cerebral tissue ( Xu et al, 2024 ). Foxo3a was further delineated to directly stimulate Aquaporin 4 (AQP4) transcription, thereby promoting cytotoxic edema post-TBI and consequent memory deficits ( Kapoor et al, 2013 ).…”

Section: Role Of Foxo3a In Cognitive Disordersmentioning

confidence: 99%

The role of Foxo3a in neuron-mediated cognitive impairment

Liu,

Wu,

Wang

et al. 2024

Front. Mol. Neurosci.

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Cognitive impairment (COI) is a prevalent complication across a spectrum of brain disorders, underpinned by intricate mechanisms yet to be fully elucidated. Neurons, the principal cell population of the nervous system, orchestrate cognitive processes and govern cognitive balance. Extensive inquiry has spotlighted the involvement of Foxo3a in COI. The regulatory cascade of Foxo3a transactivation implicates multiple downstream signaling pathways encompassing mitochondrial function, oxidative stress, autophagy, and apoptosis, collectively affecting neuronal activity. Notably, the expression and activity profile of neuronal Foxo3a are subject to modulation via various modalities, including methylation of promoter, phosphorylation and acetylation of protein. Furthermore, upstream pathways such as PI3K/AKT, the SIRT family, and diverse micro-RNAs intricately interface with Foxo3a, engendering alterations in neuronal function. Through several downstream routes, Foxo3a regulates neuronal dynamics, thereby modulating the onset or amelioration of COI in Alzheimer’s disease, stroke, ischemic brain injury, Parkinson’s disease, and traumatic brain injury. Foxo3a is a potential therapeutic cognitive target, and clinical drugs or multiple small molecules have been preliminarily shown to have cognitive-enhancing effects that indirectly affect Foxo3a. Particularly noteworthy are multiple randomized, controlled, placebo clinical trials illustrating the significant cognitive enhancement achievable through autophagy modulation. Here, we discussed the role of Foxo3a in neuron-mediated COI and common cognitively impaired diseases.

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Section: Role Of Foxo3a In Cognitive Disordersmentioning

confidence: 99%

The role of Foxo3a in neuron-mediated cognitive impairment

Liu,

Wu,

Wang

et al. 2024

Front. Mol. Neurosci.

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Dehydroevodiamine targeting IKKβ to alleviate acute gastric injury via inhibiting the p65/NLRP3 axis

Hu,

Chen,

Zhang

et al. 2024

Phytomedicine

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Dehydroevodiamine Alleviates Ulcerative Colitis by Inhibiting the PI3K/AKT/NF-κB Signaling Pathway via Targeting AKT1 and Regulating Gut Microbes and Serum Metabolism

Ma,

Hu,

Jiang

et al. 2024

Molecules

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Ulcerative colitis (UC) is a typical inflammatory bowel disease (IBD), impairing the quality of life of patients. Dehydroevodiamine (DHE) is an active alkaloid isolated from Tetradium ruticarpum that exerts significant anti-inflammatory effects in gastrointestinal diseases. However, the effect and mechanisms of DHE on UC remain unclear. We performed a DSS-induced experimental UC rat model to reveal the efficacy and potential mechanisms of DHE on UC. HE and AB-PAS staining were used for the evaluation of pathologies, and 16S rRNA sequencing was used to detect changes in gut microbes. Metabolomics was used to detect changes in serum metabolites. Network pharmacology and transcriptomics were conducted to reveal the underlying mechanisms of DHE for UC. HuProt proteome microarrays, molecular docking, and SPR were used to reveal the targets of action of DHE. WB, RT-qPCR, and IHC were used to assess the action effects of DHE. DHE demonstrated significant alleviation of DSS-induced colitis symptoms in rats by suppressing inflammatory and oxidative stress responses, amending colonic barrier injury, and inhibiting apoptosis. In terms of gut microbial modulation, DHE decreased the abundance of Allobaculum, Clostridium, Escherichia, Enterococcus, and Barnesiella and increased the abundance of Lactobacillus, Bifidobacterium, and SMB5. Moreover, metabolomics suggested that the regulation of DHE in DSS-induced UC rats mainly involved aminoacyl-tRNA biosynthesis, vitamin B6 metabolism, phenylalanine, tyrosine, and so on. Mechanically, DHE alleviated UC in rats by targeting AKT1, thereby inhibiting the PI3K/AKT/NF-κB signaling pathway.

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Dehydroevodiamine ameliorates neurological dysfunction after traumatic brain injury in mice via regulating the SIRT1/FOXO3a/Bim pathway

Cited by 3 publications

References 40 publications

The role of Foxo3a in neuron-mediated cognitive impairment

The role of Foxo3a in neuron-mediated cognitive impairment

Dehydroevodiamine targeting IKKβ to alleviate acute gastric injury via inhibiting the p65/NLRP3 axis

Dehydroevodiamine Alleviates Ulcerative Colitis by Inhibiting the PI3K/AKT/NF-κB Signaling Pathway via Targeting AKT1 and Regulating Gut Microbes and Serum Metabolism

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