The microglia-mediated neuroinflammatory response significantly contributes to neuronal damage following ischemic stroke by activating the signal transducer and activator of transcription 3 (STAT3) signal pathway. Rutin has been shown to exhibit STAT3-inhibitory properties, yet the effects of rutin on microglial polarization under ischemic context remain insufficiently understood. Therefore, this study aimed to investigate the effects of rutin on microglial activation and neuroprotection under oxygen-glucose deprivation (OGD) conditions and to elucidate the underlying mechanism.

Neuro-2a cells were subjected to OGD, and the subsequent conditioned medium (CM) was collected, and used to stimulate BV2 cells in vitro. The impact of rutin on microglial activation was assessed by analyzing cytokine profiles and microglial polarization. STAT3 phosphorylation was detected by Western immunoblot analysis, and the potential binding sites of rutin and STAT3 were determined through in silico molecular docking analysis. Neuron-microglia co-culture systems were employed to evaluate neuroprotective effects through viability and apoptosis assays.

Microglia cultured with CM exhibited increased pro-inflammatory cytokines and M1 polarization, which were reversed by rutin treatment. Additionally, rutin significantly promoted anti-inflammatory microglial polarization in a hypoxic condition through a decrease in phosphorylated STAT3 levels. These effects were demonstrated in a dose-dependent manner. Notably, OGD-challenged neurons exhibited enhanced survival and reduced apoptosis when co-cultured with rutin and CM-treated microglia.

Rutin offers neuroprotection by modulating microglial activation towards an anti-inflammatory phenotype, which is associated with the STAT3 pathway, underscoring the potential of rutin as a therapeutic agent for ischemic stroke and related cerebral injury.

Sodium arsenite, a pesticide, is well known to induce cardiotoxicity via myocardial apoptosis. Fisetin, a plant, has antioxidant, anti-inflammatory and anti-apoptotic potential. This study aimed to evaluate the putative mechanism of action of fisetin against sodium arsenite-induced cardiotoxicity in experimental rats.

Cardiotoxicity was induced in male Sprague-Dawley rats (200–230 g, n = 15, in each group) using sodium arsenite (5 mL/kg, p.o., 28 days) and concomitantly treated with either coenzyme Q10 (10 mg/kg) or fisetin (5, 10 and 25 mg/kg, p.o.) orally for 28 days. Various biochemical, molecular, and histopathological analyses were performed to evaluate the efficacy of fisetin against cardiotoxicity. Data were analyzed by one-way Analysis of Variance (ANOVA), while Tukey’s multiple range tests were applied for post hoc analysis.

Chroni carsenite administration promoted a significant (p < 0.001) increase in relative heart weight and alterations in electrocardiographic, hemodynamic, and left ventricular function parameters, which were effectively and dose-dependently attenuated (p < 0.01 and p < 0.001) by fisetin (10 and 25 mg/kg). Moreover, fisetin treatment also markedly decreased elevated serum creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), and lipid levels. Arsenite-induced elevated cardiac oxido-nitrosative stress was also efficiently and dose-dependently decreased (p < 0.01 and p < 0.001) by fisetin. Following arsenite exposure, the mRNA expressions of cardiac nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1) and B-cell lymphoma 2 (Bcl-2) were downregulated, and Bax and Caspase-3 mRNA were up-regulated; these expressions were likewise effectively and dose-dependently (p < 0.01 and p < 0.001) inhibited by fisetin. Histopathological observations of the heart suggested that fisetin attenuated arsenite-induced myocardial aberrations.

Fisetin effectively mitigates sodium arsenite-induced cardiotoxicity in experimental rats. The protective effects of fisetin are associated with antioxidant (Nrf2/HO-1) and apoptotic (Bax/Bcl-2 and caspase-3) pathways in experimental rats. Thus, fisetin can be considered a potential phytoconstituent in managing pesticide-induced cardiotoxicity.

Allergic asthma, a chronic respiratory illness, presents a significant healthcare burden. Honey-processed Chelidonium majus L. (HC), a traditional herbal formula, has shown promise as an anti-asthmatic treatment. However, the underlying mechanisms for these properties remain elusive. Thus, this study aimed to investigate the therapeutic potential and mechanisms of HC in a rat model of ovalbumin (OVA)-induced asthma.

Sprague-Dawley rats were randomly assigned to Control, Model (asthma), Dexamethasone (positive control), low-, medium-, and high-dose HC groups (n = 8). Lung histopathology, serum inflammatory marker (interleukin (IL)-10, IL-13 ,and IL-1β), serum metabolomics, and transcriptomic analyses were employed to assess the effects of HC on airway inflammation, mucus hypersecretion, and related metabolic and gene expression profiles.

HC treatment alleviated histological lung injury in asthmatic rats, downregulated the levels of proinflammatory cytokines (IL-13 and IL-1β), while upregulating the anti-inflammatory cytokine IL-10. Metabolomic analysis revealed 46 metabolic biomarkers while the transcriptome analysis identified 754 differentially expressed genes (DEGs) between the Model and Control groups. Moreover, 35 metabolites were reversed and 273 DEGs were identified following high-dose HC treatment. Integration analysis manifested that 7 DEGs and 11 metabolites were associated with several enriched metabolic pathways, including amino acid metabolism, fatty acid metabolism, glycometabolism, organic acid metabolism, and nucleotide metabolism.

HC treatment ameliorates OVA-induced asthma in rats by regulating the expression of specific genes to restore metabolic homeostasis and suppress inflammation. This study provides valuable insights into the therapeutic potential and mechanisms of HC for asthma treatment.

Sleep is essential for human physiological functions; however, the prevalence of sleep disorders has increased in recent years. Traditional Chinese Medicine has gained widespread attention owing to the reduced observed side effects and significant efficacy following administration. Thus, this study aimed to provide a new treatment option for sleep disorders using a drug pairing of Radix Ginseng and Semen Ziziphi Spinosae Drug pair (R–S).

A total of 60 mice were randomly divided into six groups. An enzyme-linked immunosorbent assay (ELISA) was used to measure the SS (somatostatin), SP (substance P), np-y (neuropeptide Y), 5-HTR4 (5-hydroxytryptamine (serotonin) receptor 4) and 5-HTR3 (5-hydroxytryptamine (serotonin) receptor 3) levels in the small intestine tissues of the mice. Real-time quantitative PCR (RT-qPCR) was employed to assess the Piezo1 and Piezo2 mRNA expression levels. Hematoxylin and eosin (H&E) staining was used to observe cell morphology, and immunohistochemistry was employed to detect brain-derived neurotrophic factor (BDNF) and glial fibrillary acidic protein (GFAP) expression in the small intestine. Data were analyzed using SPSS 27.0 software. A p-value < 0.05 was considered statistically significant.

The treatment groups presented higher levels of np-y (p < 0.01) and lower levels of SS, SP, np-y, 5-HTR4 and 5-HTR3 (p < 0.01) compared to the model group. Meanwhile, the treatment groups showed a decreasing trend in Piezo1 and Piezo 2 mRNA expression, an elevated positive expression of BDNF, and a reduced positive expression of GFAP proteins (p < 0.05, p < 0.01).

R–S treatment can regulate 5-HTR/Piezo/BDNF/GFAP to improve the sleep of mice with PCPA (para-chlorophenylalanine)-induced insomnia mice, which provides experimental evidence for studying R–S in the treatment of insomnia.

Doxorubicin (DOX) use can promote neurobehavioral changes and neurodegeneration, which have been attributed to oxidative stress. Thus, this study aimed to examine the effect of Hippophae rhamnoides L., fruit extract (HRe), against possible oxidative brain damage and behavioral disorders in rats caused by DOX.

A total of 24 male Sprague-Dawley rats were utilized in this study and were divided randomly into four groups (n = 6 in each groups): CG, healthy control; HRe, 50 mg/kg HRe; DOX, 5 mg/kg i.p., in a single intraperitoneal dose of DOX; Hre + DOX, 50 mg/kg HRe + 5 mg/kg DOX. HRe was administered orally once a day for two weeks, while DOX was administered intraperitoneally twice a week for two weeks. Subsequently, behavioral tests were performed—the sucrose preference test (SPT) and pole test—to assess depression-like behaviors and motor function, respectively. Then, the level of oxidative stress was biochemically evaluated in the brain tissues of the rats. One-way analysis of variance (ANOVA) was conducted, followed by a post hoc Tukey’s test for the statistical analysis. A p-value < 0.05 was considered statistically significant.

The HRe treatment markedly reduced DOX-induced depression-like behaviors and improved motor dysfunction. The HRe treatment also restored the impaired antioxidant response by inhibiting the DOX-related malondialdehyde increase and reducing the decrease in total glutathione levels, as well as superoxide dismutase and catalase activities.

The present study indicates that HRe treatment has beneficial effects on motor dysfunction as well as depression-like behavior associated with neurodegeneration following DOX-induced brain damage. Possible mechanisms underlying these beneficial effects include lipid peroxidation inhibition and restoration of antioxidant defense mechanisms by HRe.