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This study aimed to explore the effect and mechanism of polyphyllin Ⅱ in improving di(2-ethylhexyl)phthalate(DEHP)-induced learning and memory impairment. In the experiment, male C57BL/6 mice were randomly divided into five groups: a control group, a model group(exposed to 5 mg·kg~(-1) DEHP), and polyphyllin Ⅱ groups(5 mg·kg~(-1) DEHP + 0.5 mg·kg~(-1) polyphyllin Ⅱ, DEHP + 1 mg·kg~(-1) polyphyllin Ⅱ, and DEHP + 2 mg·kg~(-1) polyphyllin Ⅱ). The learning and memory function of mice was tested using the Morris water maze. The hippocampal neuron structure was detected by Nissl staining. The expression of casein kinase Ⅱ subunit beta(CK2b), protein kinase B(Akt)-cAMP response element binding protein(CREB) pathway-related proteins, as well as postsynaptic density protein 95(PSD95) and synapsin 1 was determined by immunofluorescence and Western blot. The brain-derived neurotrophic factor(BDNF) expression was measured by enzyme-linked immunosorbent assay(ELISA). The results showed that compared with the control group, DEHP induced learning and memory impairment, as well as hippocampal neuronal apoptosis in mice. Additionally, DEHP downregulated CK2b, inhibited the Akt-CREB pathway, and downregulated the PSD95, synapsin1, and BDNF expression. After polyphyllin Ⅱ administration, DEHP-induced learning and memory impairment was significantly improved, with inhibited hippocampal neuronal apoptosis, restored CK2b expression, reactivated Akt-CREB pathway, as well as restored expression of PSD95, synapsin1, and BDNF. Furthermore, the surface plasmon resonance(SPR) experiment of N2a cells demonstrated that polyphyllin Ⅱ targeted CK2b and stabilized its expression. After using siRNA to inhibit CK2b, the neuroprotective effect of polyphyllin Ⅱ was also significantly inhibited, and neuronal apoptosis was reinduced. In conclusion, polyphyllin Ⅱ can ameliorate DEHP-induced learning and memory impairment, with its potential mechanism involving the Akt-CREB pathway activation via CK2b upregulation, which leads to restored PSD95 and synapsin1 expression, and synaptic plasticity, as well as inhibited neuronal apoptosis, ultimately exerting a neuroprotective effect. This study suggests that polyphyllin Ⅱ possesses a neuroprotective effect and has potential application value in improving cognitive impairment. Show less

This study aimed to investigate the effects of L-borneol on the molecular, biochemical, and histological damage caused by acrylamide (ACR) in the hippocampus of adult male Wistar rats. It also examined the impact of L-borneol on spatial memory and anxiety-like behaviors in these animals. Animals were divided into four groups: control, L-borneol, ACR, and ACR + L-borneol. ACR (25 mg/kg) and L-borneol (50 mg/kg) were administered orally for 21 consecutive days. L-borneol reduced levels of malondialdehyde and nitric oxide, increased glutathione content, and enhanced superoxide dismutase activity in the hippocampus of rats treated with ACR. In addition, L-borneol lowered the expression of pro-inflammatory markers, nuclear factor-κB, and inducible nitric oxide synthase in the hippocampus. It effectively prevented changes in the expression of apoptosis-related genes, which are associated with decreased neuronal death in the cornus ammonis 1 and dentate gyrus regions. Moreover, L-borneol increased the expression of sirtuin 1 (SIRT1), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1), brain-derived neurotrophic factor, and alpha 7-nicotinic acetylcholine receptors, while reducing the expression and activity of acetylcholinesterase. Finally, L-borneol improved spatial memory and reduced anxiety-like behaviors. In conclusion, L-borneol enhances behavioral performance in ACR-exposed animals by decreasing oxidative and nitrosative stress, as well as inhibiting inflammation and apoptosis. It appears that the upregulation of the SIRT1/Nrf2/HO-1 signaling pathway and the stimulation of acetylcholine signaling are crucial for mitigating ACR-induced neurotoxicity. Show less

Lilium brownii is a plant that can be used for medicinal and food purposes. 1-O-p-coumaroyl-3-O-feruloyl glycerol (CF) is a phenolic acid glycerol dimer isolated from Lilium brownii. This study aims to evaluate the neuroprotective effects of CF and elucidate the possible molecular mechanisms underlying its neuroprotective effects through in vivo and in vitro models of Parkinson's disease. 1-methyl-4-phenylpyridinium ions (MPP Following CF administration, the apoptosis rate and reactive oxygen species (ROS) levels in PC12 cells were significantly reduced. CF markedly upregulated the expression of proteins including dopamine, tyrosine hydroxylase, brain-derived neurotrophic factor (BDNF), while simultaneously downregulating the expression of proteins such as α-synuclein. Molecular docking results demonstrated favorable affinity between CF and proteins including p62. This compound not only ameliorated motor and cognitive impairments in Parkinson's disease mice but also markedly increased neuronal numbers within the substantia nigra region of these animals. CF exerts a neuroprotective effect in Parkinson's disease by modulating the p62-Keap1-Nrf2 signalling pathway. Show less

Postoperative complications are common issues that may arise from anesthetic drugs or surgical procedures. This study aimed to investigate the protective and therapeutic effects of ginsenosides on anesthesia-associated side effects and postoperative complications. This study was conducted following the PRISMA 2020 guidelines. A comprehensive search was conducted across PubMed/MEDLINE, Scopus, Web of Science, Embase, and the Cochrane Library to identify relevant studies published prior to October 13, 2024. Predefined inclusion and exclusion criteria were applied, and duplicates were removed. Ginsenosides inhibit oxidative stress and enhance cognitive function by activating pathways such as phosphoinositide 3-kinase (PI3K)/Protein kinase B (PKB) (AKT)/glycogen synthase kinase-3 beta (GSK-3β), promoting neuroplasticity, alleviating oxidative stress, and modulating neuroinflammatory markers, as well as microglia and astrocytes. They help to maintain mitochondrial integrity, thereby reducing apoptosis and neurotoxicity caused by anesthetic agents. Ginsenosides also alleviate postoperative pain by modulating N-methyl-D-aspartate (NMDA) and suppressing inflammatory cytokines. They also improved neuropsychological problems by increasing Nerve Growth Factor (NGF) and Brain-Derived Neurotrophic Factor (BDNF). The anti-fatigue properties of ginsenosides are attributed to enhanced antioxidant activity, improved skeletal muscle metabolic function, and increased Adenosine Triphosphate (ATP) production. These results are consistent with prior studies demonstrating the neuroprotective effects of ginsenosides. Despite promising outcomes, the prevalence of animal studies and the absence of clinical data underscore the necessity for clinical validation and safety profiling in future research. Preclinical evidence shows ginsenosides, particularly Rg1, Rb1, and Rg3, demonstrate promising protective and therapeutic effects against anesthesia-associated adverse effects and postoperative complications. Show less

Despite available therapies for depression, many patients do not achieve adequate improvement, illustrating the need for innovative treatment strategies. Nutritional psychiatry is an emerging area, with increasing evidence that microbially derived butyrate contributes to the beneficial effects of dietary, pre-, pro- and synbiotics interventions - raising the exciting possibility that direct butyrate administration might alleviate depressive symptoms. The main objective was to systematically review the effects of butyrate on depressive symptoms in humans and depressive-like behavior in animals (PROSPERO; CRD42023g0739). A search was conducted in MEDLINE, Embase, PsycINFO, and Web of Science, ICTPR and ClinicalTrials.gov up to October 2025. Studies were included if they examined depressive symptoms in humans or relevant behaviors in animal models of depression/anxiety, involved treatment with butyrate formulations, included a control or pre-post comparison, and reported behavioral or clinical outcomes. Eligible designs included case-control, cohort, (randomized) controlled trials, experimental, or in vivo studies published in English or Dutch. Studies were excluded if depression was not the primary focus or if butyrate was combined with another treatment. Risk of bias was assessed with SYRCLE for animal studies and RoB 2 for the human studies. Of the two randomized controlled trials, one found no measurable effect of 1-week oral butyrate in healthy males, whereas the other found reductions in depressive and anxiety symptoms in patients with ulcerative colitis after 12-weeks oral butyrate. Thirty-two animal studies showed that butyrate generally modulated depressive- and anxiety-like phenotypes in rodents, potentially via anti-inflammatory, neuroplastic, epigenetic and gut-mediated mechanisms. Preclinical findings support the therapeutic promise of butyrate as a novel intervention for depression, warranting further clinical investigation. BDNF, Brain-derived neurotrophic factor; CRS, Chronic restraint stress; CSD, Chronic social defeat; CUMS, Chronic unpredictable mild stress; DASS, Depression, anxiety, Stress Scales; EPM, Elevated plus maze; FMT, Fecal microbiota transplant; FST, Forced swim test; HDAC, Histone deacetylase; HFD, High-fat diet; HPA, Hypothalamic-pituitary-adrenal; ICTRP International Clinical Trials Registry Platform; IL, Interleukin; LDB, Light-dark box; LEIDS-R, Leiden Index of Depression Severity-Revised; LPS, Lipopolysaccharide; MD, Maternal deprivation; MDD, Major depressive disorder; MGBA, Microbiota-gut-brain axis; NORT, Novel object recognition test; OFT, Open field test; PFC, Prefrontal cortex; PRISMA Preferred reporting items for systematic reviews and meta-analyses; SCFA, Short-chain fatty acid; SPT, Sucrose preference test; SYRCLE, Systematic Review Centre for Laboratory Animal Experimentation; TCA, Tricarboxylic acid; TNF, Tumor necrosis factor; TST, Tail suspension test; ZO-1, Zonulin-1. Show less