Combinatorial chemistry & high throughput screening最新文献

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Since the authors are not responding to the editor’s requests to fulfill the editorial requirement, therefore, the article has been withdrawn.

Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused.

The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php

Bentham science disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

Background: Rheumatoid Arthritis (RA), a chronic inflammatory autoimmune illness, is characterized by synovitis, progressive joint damage, and bone erosion. Even though the potent drugs available contain biologics, several patients fail to react to them or cause hostile effects.

Objectives: Betanin (BTN), the betacyanin present in the red beetroot, has antioxidant, antiinflammatory, and apoptotic properties. In this study, we assessed the anti-inflammatory and apoptotic effect of BTN on collagen-induced arthritis (CIA).

Materials and methods: The rats were arbitrarily separated into four sets: Normal, CIA, CIA+BTN (25 mg/kg bw), and CIA+BTN (50 mg/kg bw). The hematological, biochemical markers, cytokines, inflammatory enzymes, histopathology of the ankle joint, and protein expression of inflammatory and apoptotic proteins were studied.

Results: Inflammatory enzymes, histopathological variations, cytokines generation, and joint inflammation were strongly alleviated, and apoptosis was augmented by BTN in a concentrationdependent manner. Bcl-2 and MAPK/NF-κB proteins were reduced, while the caspase-3, caspase- 9, and Bax were intensified. The anti-rheumatic action of BTN was correlated to the attenuation of the MAPK/NF-κB pathway, which suppresses cytokine production, inflammation, and reduced cartilage impairments.

Conclusion: These outcomes recommend that BTN can be employed as a strong healing alternative for RA management.

Introduction: The traditional Chinese medicine formula, Bushen Daozhuo Granules (BSDZG), is used to treat chronic non-bacterial prostatitis (CNP) clinically. However, its mechanism of action is unclear. The aim of our study was to determine the effect of BSDZG on CNP and its underlying mechanisms.

Methods: Male Wistar rats were randomly assigned to control, CNP, and BSDZG groups. CNP was induced using purified prostaglandin solution and Freund's complete adjuvant, after which the BSDZG group received 1.54 g/kg/d of BSDZG for 30 days. Prostate tissues were used to determine apoptosis and inflammatory cytokines. The herb-composition-target network and functional signaling pathways were built using a network pharmacology approach, which was also confirmed in vivo.

Results: Treatment with BSDZG significantly alleviated the histopathological lesions, inflammation, and apoptosis in the prostate of CNP rats. The herb-composition-target network comprising 42 active compounds and 32 targets of 11 herbs was illustrated, and KEGG pathways analysis identified the Akt and MAPK pathways as related to the effects of BSDZG. Phosphorylation of p38 MAPK, NF-кB, and Bax expression was significantly enhanced and phosphorylated Akt and Bcl-2 levels were decreased in CNP rats, which could be reversed by BSDZG.

Conclusion: This study presented for the first time that BSDZG effectively alleviated CNP symptoms in rats and elucidated the underlying mechanisms mediated by the Akt and MAPK pathways, providing the theoretical basis for the clinical use and promotion of BSDZG.

Since the authors are not responding to the editor’s requests to fulfill the editorial requirement, therefore, the article has been withdrawn.

Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused.

The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php

Bentham science disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

Since the authors are not responding to the editor’s requests to fulfill the editorial requirement, therefore, the article has been withdrawn.

Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused.

The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php

Bentham science disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

Since the authors are not responding to the editor’s requests to fulfill the editorial requirement, therefore, the article has been withdrawn.

Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused.

The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php

Bentham science disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

Introduction: Qilong capsule (QC) has been used clinically to treat ischemic stroke in China. This study evaluated the therapeutic effects of QC on myocardial ischemia-reperfusion injury (MIRI) and its potential mechanisms.

Method: The components and candidate targets of QC against MIRI were predicted by network pharmacology via relevant databases such as TCMSP, BATMAN-TCM, GeneCards. The potential mechanisms were predicted by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses and verified by enzyme-linked immunosorbent assay (ELISA) and Western blot.

Results: Network pharmacology analysis indicated that the cardioprotective effect of QC against MIRI was associated with inflammatory pathways. We further confirmed that QC effectively decreased the levels of inflammatory factors, including hs-CRP and MCP-1, and suppressed the expression of TNF-α and the phosphorylation of STAT3.

Conclusion: This study provides evidence for further clinical applications of QC for MIRI therapy.

Background: Dental root canal failure is a disease caused by gram-positive bacteria, Enterococcus faecalis. The disease is caused by the bacterial cell wall consisting of a peptidoglycan layer that protects the bacteria from internal osmotic pressure. Peptidoglycan biosynthesis includes many enzymes, such as MurA, Penicillin-binding protein (PBP), and SrtA. Herbal plants are a source of bioactive compounds, including antibacterial agents. There is information that red betel leaves, also known as Piper crocatum, contain active substances such as flavonoids, terpenoids, and steroids. However, there is no additional information on the antibacterial properties of P. crocatum and the molecular mechanisms that affect the cell wall of E. faecalis ATCC 29212 bacteria.

Objective: This study aims to determine the antibacterial activity of the extract in vitro, screen and study the antibacterial compounds of red betel leaves against oral pathogenic bacteria, namely E.faecalis ATCC 29212 through molecular docking.

Methods: The n-hexan:ea (9:1) fraction of P. crocatum extract was tested for inhibition zones against E. faecalis ATCC 29212 bacteria, fractions that had positive results were then identified using the LC-MS method. The LC-MS resulting compounds were tested using In Silico.

Results: Antibacterial in the n-hexane: ethyl acetate (9:1) fraction of Red Betel Leaf has the best concentration of 10% with a moderate inhibition zone category. LC-MS test results identified compounds including Longicamphenylone, m/z 207, Nootkatone m/z 219, and Tridecanal m/z 221. Molecular interactions between these compounds with target proteins, namely MurA, PBP, and SrtA, show lower binding affinity values than natural ligands and positive controls for each protein.

Conclusion: Nootkatone compounds demonstrated potential as MurA and PBP inhibitors, while Longicamphenylone compounds showed potential as SrtA inhibitors. Both compounds have the potential to inhibit peptidoglycan biosynthesis and bacterial cell wall formation through docking simulations.

Introduction: In recent years, there has been a rise in the incidence of renal cell carcinoma (RCC), with metastatic RCC being a prevalent and significant contributor to mortality. While a regulatory role for microRNAs (miRNAs) in the development and progression of RCC has been recognized, their precise functions, molecular mechanisms, and potential clinical implications remain inadequately elucidated. Hence, this study aimed to explore the role of miR-507 in RCC and identify STEAP3 as a downstream target of miR-507.

Methods: Bioinformatics analysis was used to analyze the expression of miR-507 and STEAP3 in RCC specimens. CCK-8, Transwell, and flow cytometry assays were used to assess the function of miR-507 in RCC cells. The connection between miR-507 and STEAP3 was confirmed through a luciferase reporter assay. The expression level of STEAP3, p53, and xCT was analyzed by western blotting.

Results: Bioinformatics analysis showed that miR-507 was expressed at low levels in RCC tissues and was linked to poor overall survival. STEAP3 was found to be significantly upregulated in RCC. Further, STEAP3 was shown to be targeted by miR-507. High levels of miR-507 reduced the expression of STEAP3, leading to stagnant cell viability, apoptosis, and migrative capacity. Whereas miR-507 knockdown reverted such a tendency. The study also discovered that miR-507 exerted its inhibitory effect through the op53/xCT pathway.

Conclusion: Within RCC, miR-507 modulates the expression of SETAP3/p53/xCT axis, exhibiting a tumor suppressive effect. These discoveries offer present prospective biomarkers for both surveillance and treatment of RCC.