The American journal of Chinese medicine
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Parkinson's disease (PD) is a progressive neurodegenerative disorder without a definitive cure. Oriental exercises (OEs) have emerged as a complementary and alternative therapy for PD, but their efficacy in ameliorating non-motor symptoms (NMS) and quality of life (QOL) remains uncertain. This systematic review and meta-analysis actively investigated the efficacy of OEs in addressing NMS and enhancing QOL and sought to offer recommendations for optimal OE regimens for PD patients. ⋯ Specifically, significant improvements were observed in several outcome measures: Parkinson's Disease Questionnaire (PDQ) [MD: [Formula: see text]3.67, 95% CI: [Formula: see text]5.72-[Formula: see text]1.63, [Formula: see text], [Formula: see text]%], Parkinson's Disease Non-Motor Symptom Questionnaire (NMSQ) [MD: [Formula: see text]2.34, 95% CI: [Formula: see text]4.67-[Formula: see text]0.01, [Formula: see text], [Formula: see text]%], Montreal Cognitive Assessment (MoCA) [MD: 1.75, 95% CI: 1.46-2.03, [Formula: see text], [Formula: see text]%], Stroop Color and Word Test (SCWT) [MD: 0.87, 95% CI: 0.49-1.24, [Formula: see text], [Formula: see text]%], Frontal Assessment Battery (FAB) [MD: 1.49, 95% CI: 1.16-1.81, [Formula: see text], [Formula: see text]%], Hamilton Depression Scale (HAMD) [MD: [Formula: see text]4.27, 95% CI: [Formula: see text]6.85-[Formula: see text]1.69, [Formula: see text], [Formula: see text]%], Hamilton Anxiety Scale (HAMA) [MD: [Formula: see text]0.24, 95% CI: [Formula: see text]0.32-[Formula: see text]0.16, [Formula: see text], [Formula: see text]%], and the Symptom Checklist-90 (SCL-90) [MD: [Formula: see text]0.37, 95% CI: [Formula: see text]0.48-[Formula: see text]0.25, [Formula: see text], [Formula: see text]%]. Our findings provide compelling evidence for the potential benefits of OEs in managing NMS and improving QOL in PD patients. To optimize outcomes, we recommend customizing OE regimens based on individual clinical phenotypes, and to validate these results we emphasize the need for rigorous, large-scale studies.
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Myocardial ischemia/reperfusion (I/R) injury is the leading cause of death worldwide. Ginsenoside Rd (GRd) has cardioprotective properties but its efficacy and mechanism of action in myocardial I/R injury have not been clarified. This study investigated GRd as a potent therapeutic agent for myocardial I/R injury. ⋯ GRd also increased PI3K and Akt phosphorylation, suggesting activation of the PI3K/Akt pathway, whereas LY294002, a PI3K inhibitor, blocked the GRd-induced inhibition of OGD/R-induced apoptosis and inflammation in H9c2 cells. The therapeutic effect of GRd in vivo and in vitro against myocardial I/R injury was primarily dependent on PI3K/Akt pathway activation to inhibit inflammation and cardiomyocyte apoptosis. This study provides new evidence for the use of GRd as a cardiovascular drug.
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Review
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.
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Artemisinin (ART) and its derivatives, collectively referred to as artemisinins (ARTs), have been approved for the treatment of malaria for decades. ARTs are converted into dihydroartemisinin (DHA), the only active form, which is reductive in vivo. In this review, we provide a brief overview of the neuroprotective potential of ARTs and the underlying mechanisms on several of the most common neurodegenerative diseases, particularly considering their potential application in those associated with cognitive and motor impairments including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). ⋯ ARTs can also inhibit ferroptosis, activate the Akt/Bcl-2, AMPK, or ERK/CREB pathways to reduce oxidative stress, and maintain mitochondrial homeostasis, protecting neurons from oxidative stress injury. More importantly, ARTs structurally combine with and suppress β-Amyloid (A[Formula: see text]-induced neurotoxicity, reduce P-tau, and maintain O-GlcNAcylation/Phosphorylation balance, leading to relieved pathological changes in neurodegenerative diseases. Collectively, these natural properties endow ARTs with unique potential for application in neurodegenerative diseases.
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Berberine (BBR) is a principal component of Rhizoma coptidis known for its therapeutic potential in treating diseases such as type 2 diabetes mellitus (T2DM) and obesity. Despite the trace levels of BBR in plasma, it's believed that its metabolites play a pivotal role in its biological activities. While BBR is recognized to promote GLP-1 production in intestinal L cells, the cytoprotective effects of its metabolites on these cells are yet to be explored. ⋯ In palmitic acid or TNF[Formula: see text]-treated GLUTag cells, BBB and PMT alleviated cell death, oxidative stress, and mitochondrial dysfunction. Furthermore, they could effectively reverse inflammation-induced inhibition of the Akt signaling pathway. In general, these insights suggest that the beneficial effects of orally administered BBR on GLP-1 secretion are largely attributed to the pharmacological activity of BBB and PMT by their above cytoprotective effects on L cells, which provide important ideas for stimulating GLP-1 secretion and the treatment of T2DM.