Present ten unique, structurally diverse, rephrased versions of the input sentence. Mongholicus (Beg) Hsiao and Astragalus membranaceus (Fisch.) Bge. serve as both medicinal and culinary assets. Hyperuricemia treatment in traditional Chinese medicine sometimes employs AR, yet concrete evidence of this effect and the precise mechanisms involved remain largely undisclosed.
Examining the uric acid (UA)-lowering properties and the underlying mechanisms of AR and its representative compounds, utilizing a constructed hyperuricemia mouse model and cellular models.
Employing UHPLC-QE-MS, this study analyzed AR's chemical profile and concurrently studied AR's mechanism of action, focusing on its effect on hyperuricemia, using well-established mouse and cellular models.
Among the key compounds present in AR were terpenoids, flavonoids, and alkaloids. In the mice group receiving the highest AR dosage, serum uric acid levels (2089 mol/L) were markedly lower than those of the control group (31711 mol/L), with statistical significance indicated by a p-value less than 0.00001. Furthermore, UA levels in urine and feces displayed a dose-proportional increase. Mice liver xanthine oxidase, serum creatinine, and blood urea nitrogen levels all decreased (p<0.05) in every case, implying that AR could mitigate acute hyperuricemia. AR administration resulted in reduced expression of UA reabsorption proteins URAT1 and GLUT9, but an elevated expression of the secretory protein ABCG2. This may indicate that AR aids UA excretion by regulating UA transporters through the PI3K/Akt signalling cascade.
The activity and mechanism of action of AR in mitigating UA levels were validated in this study, providing a strong empirical and clinical basis for its use in hyperuricemia treatment.
By demonstrating the effectiveness and clarifying the methodology of AR's UA-lowering activity, this study established a critical experimental and clinical foundation for the treatment of hyperuricemia with AR.

IPF, a persistent and worsening lung disease, suffers from a dearth of effective treatment options. The Renshen Pingfei Formula (RPFF), a traditional Chinese medicine derivative, has demonstrated therapeutic efficacy against idiopathic pulmonary fibrosis (IPF).
This study investigated the anti-pulmonary fibrosis mechanism of RPFF using a three-pronged approach comprising network pharmacology, clinical plasma metabolomics analysis, and in vitro experiments.
Network pharmacology served as the methodology to study the overarching pharmacological processes of RPFF in treating IPF. Pulmonary infection Untargeted metabolomics analysis uncovered the unique plasma metabolites associated with RPFF treatment outcomes in individuals with IPF. Through a combined metabolomics and network pharmacology approach, the therapeutic targets of RPFF in IPF, along with their corresponding herbal components, were discovered. The orthogonal design facilitated in vitro analysis of how kaempferol and luteolin, crucial components within the formula, modulated the adenosine monophosphate (AMP)-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor (PPAR-) pathway.
The investigation into the treatment of IPF with RPFF yielded a total of ninety-two potential targets. Analysis of the Drug-Ingredients-Disease Target network indicated a significant relationship between herbal ingredients and the drug targets PTGS2, ESR1, SCN5A, PPAR-, and PRSS1. Within the protein-protein interaction (PPI) network, key targets of RPFF in IPF treatment were determined to be IL6, VEGFA, PTGS2, PPAR-, and STAT3. The Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated the principal enriched pathways that involved PPAR, significantly within the context of the AMPK signaling pathway among various other signaling cascades. Untargeted metabolomic profiling of plasma samples from patients with IPF distinguished them from healthy controls and showed modifications in metabolite profiles before and after treatment with RPFF in patients with IPF. Six distinct plasma metabolites were explored as potential indicators of RPFF treatment effectiveness within the context of IPF. By integrating network pharmacology, researchers determined PPAR-γ as a key therapeutic target and the accompanying herbal constituents from RPFF for treating Idiopathic Pulmonary Fibrosis (IPF). Kaempferol and luteolin, as revealed by experiments using an orthogonal design, were found to decrease the mRNA and protein levels of -smooth muscle actin (-SMA). Moreover, their combined application at lower doses suppressed -SMA mRNA and protein expression by enhancing the AMPK/PPAR- pathway in TGF-β1-treated MRC-5 cells.
The study highlights the multifaceted nature of RPFF's therapeutic effects, resulting from multiple ingredients targeting multiple pathways; PPAR-, a critical target in IPF, is further shown to participate in the AMPK signaling pathway. Kaempferol and luteolin, two key components of RPFF, effectively inhibit fibroblast proliferation and the myofibroblast differentiation induced by TGF-1, showcasing a synergistic impact through the activation of the AMPK/PPAR- pathway.
This study's exploration of RPFF's therapeutic mechanism in IPF revealed the presence of multiple ingredients, acting on multiple targets and pathways. PPAR-γ, a key therapeutic target, functions within the AMPK signaling cascade. In RPFF, kaempferol and luteolin collaboratively inhibit both fibroblast proliferation and the differentiation of myofibroblasts, triggered by TGF-1, via AMPK/PPAR- pathway activation.

Honey-processed licorice (HPL) is the end product of the roasting of licorice root. Licorice, when processed with honey, exhibits enhanced heart protection, according to the Shang Han Lun. Nonetheless, investigations into its cardioprotective properties and the in vivo distribution of HPL remain constrained.
Investigating the cardio-protective effects of HPL, while simultaneously exploring the in vivo distribution of its ten primary components under physiological and pathological conditions, aims to reveal the pharmacological basis of HPL's anti-arrhythmic therapy.
The establishment of the adult zebrafish arrhythmia model relied on doxorubicin (DOX). Zebrafish heart rate variations were detected via the utilization of an electrocardiogram (ECG). Oxidative stress levels in the myocardium were measured via the application of SOD and MDA assays. The morphological transformation of myocardial tissues subsequent to HPL treatment was visualized via HE staining. Ten critical HPL components within heart, liver, intestine, and brain samples were measured using an adapted UPLC-MS/MS technique, taking into account normal and heart-injury situations.
DOX administration produced a reduction in the heart rate of zebrafish, a reduction in superoxide dismutase activity, and an increase in malondialdehyde content within the myocardial tissue. D609 DOX exposure led to the detection of tissue vacuolation and inflammatory cell infiltration in the zebrafish myocardium. The heart injury and bradycardia resulting from DOX exposure could be partially improved by HPL, due to an increase in superoxide dismutase activity and a reduction in malondialdehyde levels. The tissue distribution study demonstrated a higher concentration of liquiritin, isoliquiritin, and isoliquiritigenin in the heart when arrhythmias occurred in contrast to healthy cases. Translation Due to pathological exposure to these three components, the heart might exhibit anti-arrhythmic effects, stemming from regulated immunity and oxidation.
The HPL demonstrates a protective role against DOX-induced heart injury, a consequence of its impact on alleviating oxidative stress and tissue damage. Possible cardioprotection offered by HPL under diseased states might be related to the extensive distribution of liquiritin, isoliquiritin, and isoliquiritigenin in cardiac tissue. Experimental methodology in this study provides insight into the cardioprotective effects and tissue distribution of HPL.
HPL demonstrates a protective role against heart injury induced by DOX, with this protection attributed to its ability to alleviate oxidative stress and tissue injury. The cardioprotective influence of HPL, when conditions are pathological, might be linked to the high presence of liquiritin, isoliquiritin, and isoliquiritigenin in heart tissue. This study utilizes experimentation to demonstrate the cardioprotective impact and tissue distribution patterns of HPL.

Known for its potent effects on blood circulation and the clearing of blood stasis, Aralia taibaiensis is also recognized for its ability to energize meridians and alleviate arthralgia. Aralia taibaiensis (sAT) saponins' active components are frequently used in the management of cardiovascular and cerebrovascular diseases. Although the potential exists, the benefit of sAT in improving ischemic stroke (IS) through its role in promoting angiogenesis has not been observed or reported.
Employing both in vivo and in vitro methodologies, this study probed sAT's role in promoting post-ischemic angiogenesis in murine models.
A study was undertaken to create a live mouse model for middle cerebral artery occlusion (MCAO). Our initial assessment focused on neurological function, brain infarct size, and brain swelling in MCAO mice. We also documented pathological changes in brain tissue, ultrastructural alterations in blood vessels and neurons, and the level of vascular neovascularization. We further developed an in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) model employing human umbilical vein endothelial cells (HUVECs) to assess the survival, proliferation, migration and tubulogenesis of the OGD/R-treated HUVECs. In conclusion, we ascertained the regulatory mechanism of Src and PLC1 siRNA on sAT-promoted angiogenesis by employing a cellular transfection method.
In cerebral ischemia-reperfusion mice, sAT displayed a notable improvement in cerebral infarct volume, brain swelling degree, neurological impairments, and brain histological structure, thus combating the impact of cerebral ischemia/reperfusion injury. An augmentation in the double-positive expression of BrdU and CD31 in brain tissue was observed, coupled with an elevation in VEGF and NO release, and a decrease in NSE and LDH release.