White crystalline powder
Toddalia asiatica,Citrus aurantium,Citrus maxima,Isatis tinctoria,Zanthoxylum dissitum
HESPERETIN-7-NEOHESPERIDOSIDE/Hesperetin7-neohesperidoside/4H-1-Benzopyran-4-one, 7-[[2-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranosyl]oxy]-2,3-dihydro-5-hydroxy-2-(3-hydroxy-4-methoxyphenyl)-, (2S)-/(2S)-5-Hydroxy-2-(3-hydroxy-4-methoxyphenyl)-4-oxo-3,4-dihydro-2H-chromen-7-yl 2-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranoside/hesperetin 7-O-neohesperoside/Neohesperidin/Neohesperdin/Hesperetin-7-O-neohesperidoside/(S)-4'-Methoxy-3',5,7-trihydroxyflavanone-7-[2-O-(α-L-rhamnopyranosyl)-β-D-glucopyranoside]/4H-1-Benzopyran-4-one, 2,3-dihydro-7-((2-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranosyl)oxy)-5-hydroxy-2-(3-hydroxy-4-methoxyphenyl)-, (S)-/Hesperetin 7-O-neohesperidoside
933.7±65.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:13241-33-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Neohesperidin (NHP), derived from citrus fruits, has attracted considerable interest due to its preventative and therapeutic effects on numerous diseases. However, little progress has been made in determining the exact function of NHP on tumorigenesis. In the current study, we found that NHP inhibited colorectal tumorigenesis in the APC min/+ transgenic mouse model, as well as induced apoptosis and blocked angiogenesis in vivo. Our in-cell study suggested that this tumorigenic preventative effect of NHP is not due to the direct impact on tumor cells. Intriguingly, by utilizing 16 s rRNA gene-based microbiota sequencing, the relative abundance of Bacteroidetes was decreased, while Firmicutes and Proteobacteria were increased in the presence of NHP. Additionally, the fecal microbiota transplantation experiment further revealed that feeding with fecal of NHP-treated mice induced considerable inhibition of tumorigenesis, which indicates that the alteration of gut microbiota is responsible for NHP-mediated prevention of colorectal tumorigenesis. Thus, our study not only suggests the efficacy of NHP as a potent natural product for preventing colorectal cancer but also proposes a compelling model to connect the gut microbiota to the preventative effect of NHP on tumorigenesis.
5-Fluorouracil (PubChem CID: 3385); APC min/+ transgenic mice; Cancer prevention; Colorectal cancer; Gut microbiota; Neohesperidin; Neohesperidin (PubChem CID: 442439); Sorafenib (PubChem CID: 216239).
Neohesperidin Prevents Colorectal Tumorigenesis by Altering the Gut Microbiota
Yanling Gong 1 , Rong Dong 2 , Xiaomeng Gao 1 , Jin Li 1 , Li Jiang 1 , Jiale Zheng 1 , Sunliang Cui 3 , Meidan Ying 1 , Bo Yang 1 , Ji Cao 4 , Qiaojun He 5
A growing body of literature has established a link between the cerebral ischaemic injury and pathological state of Alzheimer’s disease (AD), and this correlation indicated that the preventive agent for ischaemia might improve the pathology of AD. Our previous studies have demonstrated that Neohesperidin (NH) exhibited neuroprotective effects against cerebral ischemia via the down-regulation of Bcl-2, Akt/PI3K and Nrf2 pathways. In the present study, we first confirmed the protective effects of NH on Aβ25-35-induced neurotoxicity on primary cultured hippocampal neurons. We further demonstrated NH attenuated Aβ25-35-induced apoptosis by preventing neurotoxicity associated with lethal UPR and ER stress via blocking S-nitrosylation of protein-disulphide isomerase (PDI). These results suggested that S-nitrosylation of PDI and ER dysfunction might be the synergistic and synchronous pathological process between cerebral ischaemia and AD.
Aβ25-35; ER stress; Neohesperidin; PDI; S-Nitrosylation.
Neohesperidin Prevents Aβ 25-35-Induced Apoptosis in Primary Cultured Hippocampal Neurons by Blocking the S-Nitrosylation of Protein-Disulphide Isomerase
Jijun Wang 1 2 , Yingchun Yuan 2 , Peng Zhang 2 , Huixian Zhang 2 , Xiaomei Liu 2 , Yuelin Zhang 3 4
Idiopathic pulmonary fibrosis (IPF) is a fatal growing problem, with limited therapeutic options. Transforming growth factor beta 1 (TGF-β1) plays a critical role in many pathological processes that characterize pulmonary fibrosis. Effective and well-tolerated antifibrotic agents that interfere with TGF-β1 signaling would be an ideal treatment but no such treatments are available. In this study, we identified that the natural compound, neohesperidin, antagonizes TGF-β1/Smad3 signaling. We found that neohesperidin not only inhibited the TGF-β1-induced injury to alveolar epithelial cells but also decreased the TGF-β1-induced myofibroblast differentiation, extracellular matrix production, and fibroblast migration. Furthermore, we obtained in vivo evidence that neohesperidin treatment inhibited bleomycin-induced lung injuries and even attenuated established pulmonary fibrosis in mice. Our data suggest that neohesperidin can target the critical signaling pathway and profibrogenic responses in progressive pulmonary fibrosis and may have a potential use in treatment.
Fibroblast; Neohesperidin; Pulmonary fibrosis; TGF-β1.
Neohesperidin Inhibits TGF-β1/Smad3 Signaling and Alleviates Bleomycin-Induced Pulmonary Fibrosis in Mice
Jiasen Guo 1 , Yinshan Fang 1 , Fangxin Jiang 1 , Lian Li 2 , Honggang Zhou 3 , Xiaojun Xu 4 , Wen Ning 5
2019 Dec 1