Month: October 2022

Rizvi, Syed Arif Hussain; Ling, Siquan; Tian, Fajun; Liu, Jiali; Zeng, Xinnian published the artcile< Interference mechanism of Sophora alopecuroides L. alkaloids extract on host finding and selection of the Asian citrus psyllid Diaphorina citri Kuwayama (Hemiptera: Psyllidae)>, SDS of cas: 6882-68-4, the main research area is Sophora Diaphorina Murraya seedling alkaloid host selection; Alkaloids; Behavioral effect; Botanical pesticides; Diaphorina citri; Host selection; Sophora alopecuroides.

Manipulating insect behavior through the deployment of semiochems. offers a promising opportunity for protecting crops in a sustainable manner. Therefore, there is still a significant opportunity for the development of natural crop protectants as eco-friendly tools in pest management. In this context, the aim of the current investigation is to find a novel prophylactic against the Asian citrus psyllid (ACP) and to gain a better understanding of the host-finding and selection ability of the ACP towards Murraya paniculata seedlings treated with Sophora alopecuroides alkaloids extract (SAAE). Our results indicate that foliar application of SAAE influences the psyllid host-finding and selection process. The behavioral assay with M. paniculata seedlings treated with 15 and 30 mg/mL of SAAE, with masked visual cues, revealed that only 6.6 and 10.4% psyllids were able to locate the host in the vials. The results also indicate that citrus psyllids mainly rely on both visual and olfaction in host-finding and selection. In choice settling experiments, psyllids settled almost completely on control seedlings rather than on seedlings treated with SAAE at a concentration of 30 mg/mL. Chem. analyses of the alkaloids extract revealed the presence of sophocarpine (33.90%), sophoridine (6.23%), anagyrine (2.77%), matrine (2.38%), lupanine (1.68%) aphylline (0.89%), and sophoramine (0.75%). In further behavioral bioassays with the dominant alkaloids sophocarpine and sophoridine, the alkaloids repelled ACP at higher concentrations of 50 and 70 mg/mL as compared to SAAE. Furthermore, the 50 mg/mL (1:1, volume/volume) combination of sophocarpine and sophoridine displayed a synergistic effect and showed the maximum behavioral effect as compared to the individual alkaloid. Based on our results, SAAE makes M. paniculata seedlings unattractive to the psyllids, and therefore, alkaloids could be used in reducing the colonization of citrus plants, subsequently curtailing HLB infection.

Environmental Science and Pollution Researchpublished new progress about Agrochemical sprays. 6882-68-4 belongs to class naphthyridine, and the molecular formula is C15H24N2O, SDS of cas: 6882-68-4.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Li, Wenxuan; Deng, Lijuan; Lei, Yuhe; Liu, Junshan published the artcile< Network-pharmacology and molecular docking-based investigation of mechanism of Sophora flavescens on cancer and inflammation>, Electric Literature of 6882-68-4, the main research area is Sophora network pharmacol mol docking.

Objective: In order to explore the systematical regulatory mechanism of Kushen (Sophora flavescens, SF) on inflammation and cancer, we analyzed inter-mol. interactions between herbal ingredients of SF and human inflammation and cancer through network-pharmacol. and mol. docking-based approaches. Methods: Firstly, ingredients and potential targets were obtained from Traditional Chinese Medicine Systems Pharmacol. Database and Anal. Platform, GeneCards database, Therapeutic Targets Database and Online Mendelian Inheritance in Man database. Then, protein-protein interaction network and medicine-ingredient-target-disease network were established and analyzed via STRING and Cytoscape. Surflex-dock was performed by SybylX-2.0. Finally, functional enrichment and pathway enrichment were achieved by Gene Ontol. database and Kyoto Encyclopedia of Genes and Genomes database. Results: The results showed that 113 components of SF and 53 potential targets were related in the study. Conclusions: The study predicted the mechanism of SF on cancer and inflammation. According to the results, we suggest that the ingredients of SF effect on DNA bingding and transcription in nuclear receptors-like JUN, MYC, RELA, NCOA, PPARG. the receptors trigger several pathways including NF-κB pathway, the Bcl-2/Bax pathway and others. Eventually, it regulats inflammatory factors and cell proliferation, senescence and apoptosis.

TMR Modern Herbal Medicinepublished new progress about Aging, animal. 6882-68-4 belongs to class naphthyridine, and the molecular formula is C15H24N2O, Electric Literature of 6882-68-4.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Yu, Pan; Cao, Weiya; Yang, Shilong; Wang, Yuan; Xia, Aixin; Tan, Xinlan; Wang, Luyi published the artcile< Design, synthesis and antitumor evaluation of novel quinazoline analogs in hepatocellular carcinoma cell>, HPLC of Formula: 1223001-51-1, the main research area is quinazoline preparation antitumor activity mol docking protein kinase inhibitor.

In this paper, five quinazoline analogs I (R = Cl, 1H-indol-5-yl, 4-chlorophenyl, pyridin-3-yl, 4-aminophenyl) were preliminary designed through scaffold shopping from mTOR inhibitors and synthesized in four steps. Five compounds I exhibited potent antitumor activity against the HepG2 cell line by MTT assay. Compound I (R = 1H-indol-5-yl) (II) (IC50 = 4.06μM) was found as the most potent analog and showed better antiproliferative ability than sorafenib (IC50 = 6.14μM). The result of the wound healing assay and transwell migration assay indicated II strong potential to suppress HepG2 cell migration in a dose- and time-dependent manner. The underlying mechanism of its cytotoxicity was also investigated and the results of western blotting confirmed that compound II exposure could block the cell cycle, promote apoptosis and inhibit AKT and mTOR phosphorylation in HepG2 cells. Mol. docking further supported that compound II showed a high affinity to mTOR kinase. The results favored rational design intention and hinted that the new quinazolines I might be helpful in the further explorations of potent agents.

Journal of Molecular Structurepublished new progress about Antitumor agents. 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, HPLC of Formula: 1223001-51-1.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Tamir, Tigist Y.; Bowman, Brittany M.; Agajanian, Megan J.; Goldfarb, Dennis; Schrank, Travis P.; Stohrer, Trent; Hale, Andrew E.; Siesser, Priscila F.; Weir, Seth J.; Murphy, Ryan M.; LaPak, Kyle M.; Weissman, Bernard E.; Moorman, Nathaniel J.; Ben Major, M. published the artcile< Gain-of-function genetic screen of the kinome reveals BRSK2 as an inhibitor of the NRF2 transcription factor>, Quality Control of 1223001-51-1, the main research area is nuclear erythroid transcription factor brain specific kinase human disease; AMPK; BRSK1; BRSK2; Functional genomics; Kinase; NRF2; Oxidative stress response; Phosphoproteomics; mTOR.

Nuclear factor erythroid 2-related factor 2 (NFE2L2, also known as NRF2) is a transcription factor and master regulator of cellular antioxidant response. Aberrantly high NRF2-dependent transcription is recurrent in human cancer, but conversely NRF2 activity diminishes with age and in neurodegenerative and metabolic disorders. Although NRF2-activating drugs are clin. beneficial, NRF2 inhibitors do not yet exist. Here, we describe use of a gain-of-function genetic screen of the kinome to identify new druggable regulators of NRF2 signaling. We found that the under-studied protein kinase brain-specific kinase 2 (BRSK2) and the related BRSK1 kinases suppress NRF2-dependent transcription and NRF2 protein levels in an activity-dependent manner. Integrated phosphoproteomics and RNAseq studies revealed that BRSK2 drives 5′-AMP-activated protein kinase α2 (AMPK) signaling and suppresses the mTOR pathway. As a result, BRSK2 kinase activation suppresses ribosome-RNA complexes, global protein synthesis and NRF2 protein levels. Collectively, our data illuminate the BRSK2 and BRSK1 kinases, in part by functionally connecting them to NRF2 signaling and mTOR. This signaling axis might prove useful for therapeutically targeting NRF2 in human disease.

Journal of Cell Sciencepublished new progress about Activating transcription factor 3 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 1223001-51-1 belongs to class naphthyridine, and the molecular formula is C24H15F3N4O, Quality Control of 1223001-51-1.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem

Peng, Zhiyang; Guan, Qing; Luo, Jianfei; Deng, Wenhong; Liu, Jiasheng; Yan, Ruicheng; Wang, Weixing published the artcile< Sophoridine exerts tumor-suppressive activities via promoting ESRRG-mediated β-catenin degradation in gastric cancer>, COA of Formula: C15H24N2O, the main research area is sophoridine tumor suppressive activity ESRRG catenin degradation gastric cancer; ESRRG; Gastric cancer; Sophoridine; β-Catenin.

As a natural alkaloid product isolated from Sophora alopecuroides. L, Sophoridine reshapes gastric cancer immune microenvironment via inhibiting chemotaxis and M2 polarization of tumor-associated macrophages (TAMs). However, the exact effects and underlying mechanism of Sophoridine on gastric cancer cells remains poorly known. The potential anti-tumor effects of Sophoridine on gastric cancer cell lines, including AGS and SGC7901 cells, were detected by CCK-8, EDU and colony forming assay, immunofluorescence, transwell assay, and flow cytometry. Mol. mechanisms of Sophoridine were investigated by siRNA transfection, nuclear/cytoplasmic extraction and western blot. The synergistic effects of Sophoridine with cisplatin on gastric cancer cells were further investigated in in vitro functional studies. Sophoridine exhibited potent tumor-suppressive activities in gastric cancer cells, including inhibition of proliferation, colony formulation, migration and invasion, as well as induction of apoptosis. In addition, we further showed that Sophoridine induced G2/M cell cycle arrest via inhibiting double-stranded DNA breaks repair and enhanced the efficacy of cisplatin in gastric cancer cells. Mol. studies further revealed that Sophoridine promoted β-catenin degradation by enhancing Estrogen-related receptor gamma (ESRRG) expression, but not depended on ubiquitination-proteasome pathway, either TRIM33-mediated (GSK3β-independent) or altered GSK3β activity, and thus exerted potent tumor-suppressive activities. Sophoridine depends on targeting ESRRG/β-catenin pathway to exert tumor-suppressive activities in gastric cancer cells and enhances the anti-tumor effect of cisplatin. Our study provided the promising preclin. anti-tumor evidence for the potential application of Sophoridine against gastric cancer.

BMC Cancerpublished new progress about Animal gene, Bcl-2 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 6882-68-4 belongs to class naphthyridine, and the molecular formula is C15H24N2O, COA of Formula: C15H24N2O.

Referemce:
1,8-Naphthyridine – Wikipedia,
1,8-Naphthyridine | C8H6N2 – PubChem