Search

Objective: Metabolomics based on ultra-high performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q/TOF-MS) was applied to explore the metabolic changes in the urine of mice with Alzheimer’s disease (AD) after intervention with camellia oil. Methods: Mice were randomly divided into four groups: normal control, AD model, positive drug and camellia oil treatment. In all mice except for those in the control group, AD was induced by amyloid β-protein (Aβ) 25-35 peptide, and urine samples were collected from each group for UPLC-Q/TOF-MS analysis after protein precipitation. The obtain urine metabolite data were analyzed by the SIMCA-P14.1 software with principal component analysis (PCA) and orthogonal partial least squares-discriminant analysis (OPLS-DA). Using the online databases of HMBD, MassBank, MetaboAnalyst and Kyoto Encyclopedia of Genes and Genomes (KEGG), biomarker identification, pathway enrichment analysis, and metabolic network construction were conducted. Results: In the PCA score plots, the camellia oil group was clearly separated from the model group and closer to the normal group. Totally 48 biomarkers were identified and the major pathways involved were taurine and hypotaurine metabolism, arginine and proline metabolism, cysteine and methionine metabolism, alanine, aspartate and glutamate metabolism. Conclusion: Camellia oil can improve the metabolism of AD mice by regulating energy metabolism, amino acid metabolism and other pathways, which provides a reference for further study of camellia oil intervention against AD.

Seven new alkaloids [1, (±)-2, (±)-3, 4, and 5] and one new natural product (6), along with eight known analogues, were isolated from the tubers of Pinellia pedatisecta Schott. Their structures were determined by a comprehensive analysis of spectroscopic data, including HRESIMS, and electronic circular dichroism (ECD). In addition, the results of the bioactivity evaluation showed that compounds (±)-3, 6, and 9 exhibited significantly protective effects against Aβ25-35-induced PC-12 cell injury and ameliorated cell viabilities by decreasing the levels of the reactive oxidative species (ROS) and mitochondrial membrane potential (MMP). [ABSTRACT FROM AUTHOR]

Gardeniae fructus (GF) is known for its various beneficial effects on cholestatic liver injury (CLI). However, the biological mechanisms through which GF regulates CLI have not been fully elucidated. This study aimed to explore the potential mechanisms of GF against α‐naphthylisothiocyanate (ANIT)‐induced CLI. First, HPLC technology was used to analyze the chemical profile of the GF extract. Second, the effects of GF on serum biochemical indicators and liver histopathology were examined. Lastly, metabolomics was utilized to study the changes in liver metabolites and clarify the associated metabolic pathways. In chemical analysis, 10 components were identified in the GF extract. GF treatment regulated serum biochemical indicators in ANIT‐induced CLI model rats and alleviated liver histological damage. Metabolomics identified 26 endogenous metabolites as biomarkers of ANIT‐induced CLI, with 23 biomarkers returning to normal levels, particularly involving primary bile acid biosynthesis, glycerophospholipid metabolism, tryptophan metabolism, and arachidonic acid metabolism. GF shows promise in alleviating ANIT‐induced CLI by modulating multiple pathways. [ABSTRACT FROM AUTHOR]

Background: Alzheimer's disease (AD) is a common chronic neurodegenerative disease in older people, and there is no specific treatment that can stop or reverse its progression. Neobavaisoflavone (NBIF) is a flavonoid that has been shown to have neuroprotective effects, but its role in AD has not been revealed. The present study investigated the role and mechanism of NBIF on Aβ25‐35‐induced brain injury. Methods: In this experiment, the AD mouse model was established by injection of Aβ25‐35 peptides (200 μM, icv), and Donepezil (Don, 10 mg/kg/days), NBIF‐L (15 mg/kg/days), and NBIF‐H (30 mg/kg/days) were administered orally for 4 weeks. Learning memory, hippocampal pathological changes, pathological markers, apoptosis, oxidative stress, inflammation, immune cells were measured in mice. Network pharmacology combined with the GEO database led to the identification of SIRT1, a key target for NBIF intervention in AD, and levels of SIRT1, p‐STAT3 and FOXO1 were measured. In addition, the antagonistic activity of SIRT1 transfection silencing against NBIF in Aβ25‐35‐induced in N9 cells and N2a‐APP69 cells was investigated to assess whether the effects caused by NBIF were mediated by SIRT1. Results: The results showed that NBIF ameliorated learning memory and hippocampal neuronal damage, reduced pathological markers, apoptosis, oxidative stress and neuroinflammation, and modulated immune cells. SIRT1 is a key target for NBIF intervention in AD, and NBIF upregulates SIRT1 and reduces the expression levels of p‐STAT3 and FOXO1. Furthermore, silencing SIRT1 effectively reduced the protective effect of NBIF on Aβ25‐35‐induced N9 cells and N2a‐APP69 cells, which indicated that the protective effect of NBIF on AD is related to SIRT1. Conclusions: NBIF ameliorated Aβ25‐35‐induced brain injury by inhibiting apoptosis, oxidative stress, and neuroinflammation, which may be mediated through SIRT1 signaling. These findings provide a rationale for NBIF in the treatment of AD and help facilitate the development of clinical therapeutic agents for AD. [ABSTRACT FROM AUTHOR]