The American journal of Chinese medicine
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Wilson's disease (WD) is a hereditary condition marked by abnormalities in copper metabolism, which precipitate a spectrum of neurological symptoms and cognitive impairments. Emerging research has highlighted ferroptosis (FPT) as a distinct type of programmed cell death, potentially linked to various cognitive dysfunctions. Nevertheless, the connection between FPT and cognitive impairment in Wilson's disease (WDCI) remains largely enigmatic. ⋯ In addition, Western blot (WB) and quantitative reverse transcription PCR (qRT-PCR) analysis showed that DG significantly upregulated the expression levels of proteins and mRNA such as P38[Formula: see text], GSK3[Formula: see text], P53, GPX4, and PTGS2 in animal and cell models. Furthermore, DG effectively reversed the dysregulated expression of oxidative stress markers, including [Formula: see text], malondialdehyde (MDA), superoxide dismutase (SOD), and reactive oxygen species (ROS). This study elucidates the neuroprotective effect of DG on hippocampal neurons by activating the P38[Formula: see text]-mediated FPT pathway, highlighting its efficacy as a potent monomer in traditional Chinese medicine and illuminating its potential role in the clinical treatment of WDCI.
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Hemorrhagic shock (HS) is a critical condition with high mortality caused by acute blood loss. Cardiac injury and dysfunction induced by HS is a major factor associated with the poor prognosis of affected patients. Schisandrin A (Sch A), a dibenzocyclooctadiene lignan extracted from Fructus schisandrae, exhibits multiple biological activities, including anti-inflammatory, and antioxidant effects. ⋯ The transformation of cytochrome c (Cyto c) induced by HS was also restored by Sch A. Importantly, the activation of the Nrf2 signaling pathway mediated the protective effects of Sch A against cardiac injury induced by HS. In conclusion, it was found that Sch A ameliorated HS-induced cardiac injury and dysfunction through suppressing apoptosis and oxidative stress, as well as alleviating mitochondrial dysfunction via the Nrf2 signaling pathway.
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Luteolin: A Comprehensive and Visualized Analysis of Research Hotspots and its Antitumor Mechanisms.
The aim of this study was to analyze the research hotspots and mechanisms of luteolin in tumor-related fields using bibliometric and bioinformatic approaches to guide future research. We conducted a comprehensive screening of all articles on luteolin and tumors in Web of Science from 2008 to 2023. The extracted words from these publications were visualized using VOSviewer, Scimago Graphica, and CiteSpace. ⋯ A total of 483 overlapping genes between luteolin and tumors were identified, and they were closely associated with the cancer-associated pathways, PI3K-Akt, and MAPK signaling pathways. Luteolin forms a complex network of antitumor-related genes, with TP53, TNF, STAT3, AKT1, JUN, IL6, and SRC playing key roles and showing strong binding affinity to luteolin. Computer technology is becoming increasingly integral to the discipline, and future research will focus on more precise antitumor mechanisms and effective clinical applications.