Corilagin, geraniin, and the bioaccessible fraction, combined with the enriched polysaccharide fraction, demonstrated substantial anti-hyperglycemic activity, resulting in approximately 39-62% glucose-6-phosphatase inhibition.
For the first time, the species was found to contain caffeoylglucaric acid isomers, tannin acalyphidin M1, and lignan demethyleneniranthin. In vitro gastrointestinal digestion led to a modification of the extract's chemical constituents. The dialyzed fraction exhibited a potent inhibitory effect on glucose-6-phosphatase activity.
Initial reports of caffeoylglucaric acid isomers, tannin acalyphidin M1, and lignan demethyleneniranthin are documented in this species. The composition of the extract changed following the simulated in vitro gastrointestinal process. Following dialysis, the fraction displayed a robust inhibition of glucose-6-phosphatase activity.
For the treatment of gynaecological diseases, safflower is a traditional Chinese medicinal remedy. However, the physical constituents and the mechanism of operation for treating endometritis brought on by incomplete abortion are still shrouded in ambiguity.
This study sought to uncover the underlying material basis and mechanism of action behind safflower's efficacy in treating endometritis stemming from incomplete abortion, employing a multifaceted approach encompassing network pharmacology and 16S rDNA sequencing analyses.
Using network pharmacology and molecular docking, the primary active constituents and potential mechanisms of action of safflower in treating endometritis, a consequence of incomplete abortion in rats, were identified. A rat model of endometrial inflammation, resulting from incomplete abortion, was established. Rats were treated with safflower total flavonoids (STF) predicated on forecasting data; then, serum levels of inflammatory cytokines were determined. To understand the active ingredient's impact and the treatment's mechanism, immunohistochemistry, Western blot analyses, and 16S rDNA sequencing were undertaken.
Safflower's active compounds, as predicted by network pharmacology, totalled 20 and interacted with 260 targets. The investigation indicated that endometritis, often caused by incomplete abortion, involved 1007 targets. Importantly, the study uncovered 114 overlapping targets between drugs and the disease, key ones being TNF, IL6, TP53, AKT1, JUN, VEGFA, CASP3 and others. This points to a possible significant role for PI3K/AKT and MAPK signaling pathways in the relationship between incomplete abortion and endometritis. STF's efficacy in significantly repairing uterine damage and lessening the amount of bleeding was confirmed by the results of the animal study. STF treatment, compared with the model group, led to a significant reduction in the expression levels of pro-inflammatory factors, including IL-6, IL-1, NO, TNF-, and the proteins JNK, ASK1, Bax, caspase-3, and caspase-11. The levels of anti-inflammatory factors, TGF- and PGE2, and the protein expression of ER, PI3K, AKT, and Bcl2 were elevated in parallel. Analysis revealed notable distinctions in the intestinal flora between the normal and model groups, and STF treatment brought the rats' intestinal flora closer to the normal group's profile.
The multifaceted treatment of endometritis, stemming from incomplete abortion, employed STF through multiple, interwoven pathways. The gut microbiota's composition and ratio, potentially affecting the activation of the ER/PI3K/AKT signaling pathway, could be central to the mechanism.
The STF treatment strategy for endometritis, arising from an incomplete abortion, showcased a multi-pronged, multi-pathway intervention, impacting various biological processes. bio-inspired propulsion The mechanism's action may involve influencing the composition and ratio of gut microbiota, thereby activating the ER/PI3K/AKT signaling pathway.
Rheum rhaponticum L. and R. rhabarbarum L. treatments in traditional medicine target more than thirty conditions, encompassing cardiovascular issues like cardiac pain, pericardium discomfort, nasal bleeding, and diverse types of bleeding, alongside blood purification and venous circulation disorders.
This study explored, for the first time, the effects of extracts obtained from the petioles and roots of R. rhaponticum and R. rhabarbarum, along with the stilbene compounds rhapontigenin and rhaponticin, on the haemostatic properties of endothelial cells and the operational capacity of blood plasma components in the haemostatic system.
The study leveraged three primary experimental modules, focusing on the activity of proteins within the human blood plasma's coagulation cascade and fibrinolytic system, coupled with examinations of the hemostatic function of human vascular endothelial cells. Moreover, the constituent components of rhubarb extracts engage with key serine proteases of the coagulation and fibrinolysis cascades, exemplified by (but not restricted to) these. A computational approach was used to analyze thrombin, coagulation factor Xa, and plasmin.
The tested extracts displayed a noteworthy anticoagulant effect, substantially reducing (by about 40%) the clotting of human blood plasma induced by tissue factor. The tested extracts exhibited inhibitory actions against both thrombin and coagulation factor Xa (FXa). With regard to the selected passages, the IC
The g/ml readings displayed a considerable range, from 2026g/ml up to 4811g/ml. Endothelial cell haemostatic responses, including von Willebrand factor, tissue-type plasminogen activator, and plasminogen activator inhibitor-1 release, have also exhibited modulatory effects.
We report, for the first time, that the examined Rheum extracts had an impact on the haemostatic properties of blood plasma proteins and endothelial cells, with a clear dominance of the anticoagulant effect. The investigated extracts' anticoagulant impact potentially results in part from their hindrance of FXa and thrombin, the vital serine proteases within the blood coagulation sequence.
For the first time, our results demonstrated that the Rheum extracts under investigation altered the haemostatic properties of blood plasma proteins and endothelial cells, with anticoagulation being the prominent effect. The extracts' ability to inhibit blood clotting might be partially attributed to their suppression of the FXa and thrombin enzymes, the key serine proteases in the cascade of blood coagulation.
Rhodiola granules (RG), a traditional Tibetan medicine, are prescribed for ameliorating the symptoms of ischemia and hypoxia associated with cardiovascular and cerebrovascular ailments. Its application in alleviating myocardial ischemia/reperfusion (I/R) injury is not reported, and the identity of its active components and the mechanism underlying its effect on myocardial ischemia/reperfusion (I/R) injury remain undisclosed.
This investigation sought to comprehensively identify the bioactive compounds and pharmacological pathways through which RG could ameliorate myocardial injury resulting from ischemia/reperfusion.
UPLC-Q-Exactive Orbitrap/MS technology was applied to analyze the chemical makeup of RG, and the potential bioactive components and corresponding targets were predicted through the use of the SwissADME and SwissTargetPrediction databases. The protein-protein interaction (PPI) network approach was used to predict the core targets, complementing Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis to determine the functions and pathways. Epigenetics inhibitor Experimental validation encompassed the molecular docking and ligation procedures applied to the anterior descending coronary artery-induced rat I/R models.
A total of 37 ingredients were found in RG, featuring nine flavones, ten flavonoid glycosides, one glycoside, eight organic acids, four amides, two nucleosides, one amino acid, and two other components. The presence of salidroside, morin, diosmetin, and gallic acid, along with 13 other chemical constituents, was established as being key active components within the group. From the construction of a protein-protein interaction network comprising 124 common potential targets, ten core targets were distinguished, prominently including AKT1, VEGF, PTGS2, and STAT3. These potential targets were found to be integral components of the regulatory mechanisms governing oxidative stress and the HIF-1/VEGF/PI3K-Akt signaling pathways. Additionally, the molecular docking process confirmed that the bioactive substances within RG have favorable binding interactions with AKT1, VEGFA, PTGS2, STAT3, and HIF-1 proteins. Animal experiments using I/R rats treated with RG indicated notable enhancements in cardiac function, a reduction in myocardial infarct size, improved myocardial architecture, and a decrease in myocardial fibrosis, inflammatory cell infiltration, and myocardial apoptosis rates. Our results, in addition, showed that RG treatment led to a decrease in the levels of AGE, Ox-LDL, MDA, MPO, XOD, SDH, and Ca ions.
Elevated concentrations of Trx, TrxR1, SOD, T-AOC, NO, ATP, Na, and ROS.
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Calcium ion fluxes are frequently regulated by ATPase activity.
Involved in the process, ATPase and CCO. Furthermore, RG exhibited a noteworthy suppression of Bax, Cleaved-caspase3, HIF-1, and PTGS2 expression levels, concurrently increasing the expression of Bcl-2, VEGFA, p-AKT1, and p-STAT3.
Our comprehensive research approach, for the first time, elucidated the active ingredients and mechanisms by which RG potentially treats myocardial I/R injury. prognostic biomarker RG's potential to mitigate myocardial ischemia-reperfusion (I/R) injury could result from a combined effect on inflammation, energy metabolism, and oxidative stress. This synergistic effect may lead to the improvement of I/R-induced myocardial apoptosis, potentially through modulation of the HIF-1/VEGF/PI3K-Akt signaling pathway. Our investigation into RG's clinical application yields new insights, and serves as a valuable resource for future studies on the development and mechanisms of other Tibetan medicinal compound preparations.
Our comprehensive research strategy, for the first time, uncovers the active components and mechanisms of RG in treating myocardial I/R injury.