Abstract
Plants provide a rich source of lead compounds for a variety of diseases. A novel approach combining phytochemistry and chemotaxis assays was developed and used to identify and study the mechanisms of action of the active compounds in F. japonica, a medicinal herb traditionally used to treat inflammation. Based on a bioactivity-guided purification strategy, two anthranoids, emodin and physcion, were identified from F. japonica. Spectroscopic techniques were used to characterize its crude extract, fractions and phytochemicals. The crude extract, chloroform fraction, and anthranoids of F. japonica significantly inhibited CXCR4-mediated chemotaxis. Mechanistic studies showed that emodin and physcion inhibited chemotaxis via inactivating the MEK/ERK pathway. Moreover, the crude extract and emodin could prevent or treat type 1 diabetes in non-obese diabetic (NOD) mice. This study illustrates the applicability of a combinational approach for the study of anti-inflammatory medicine and shows the potential of F. japonica and its anthranoids for anti-inflammatory therapy.
Highlights
A fundamental feature of inflammation is the migration of leucocytes from blood vessels to inflamed sites
On binding to stromal-derived-factor-1 (SDF-1)/CXCL12, its natural ligand, CXCR4 initiates a signaling cascade which includes the activation of focal adhesion kinase (FAK), phosphatidyl inositol 3-kinase (PI3K), extracellular signal-regulated kinase (ERK), Janus kinase (JAK), tyrosine kinase (TYK), phosphatases, nuclear factor kappa B (NFkB) and signal transducer and activator of transcription (STAT)
A novel combinational chemotaxis assay-guided fractionation and isolation method was used to evaluate the anti-inflammatory properties of the medicinal herb F. japonica (Figure 1) as a means to test the general feasibility of the protocol for the evaluation of the active compounds in medicinal herbs
Summary
A fundamental feature of inflammation is the migration of leucocytes from blood vessels to inflamed sites. This leukocyte migration, termed chemotaxis, is guided by chemokines and their receptors [1]. CXCR4 (fusin) is a CXC chemokine receptor which is expressed in all leukocytes, blastocysts and a variety of cancer cells [3]. On binding to stromal-derived-factor-1 (SDF-1)/CXCL12, its natural ligand, CXCR4 initiates a signaling cascade which includes the activation of focal adhesion kinase (FAK), phosphatidyl inositol 3-kinase (PI3K), extracellular signal-regulated kinase (ERK), Janus kinase (JAK), tyrosine kinase (TYK), phosphatases, nuclear factor kappa B (NFkB) and signal transducer and activator of transcription (STAT). CXCR4 signaling leads to chemotaxis, locomotion, and adhesion [3]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
