Xueping Huo

Area of research

Complementary and alternative medicine · Biomaterials

Research interest

Research topics from publications: Hydroxy‐Safflower Yellow A inhibits the TNFR1‐Mediated Classical NF‐κB Pathway by Inducing Shedding of TNFR1; Astragaloside III activates TACE/ADAM17‐dependent anti‐inflammatory and growth factor signaling in endothelial cells in a p38‐dependent fashion; Polyhedral magnetic nanoparticles induce apoptosis in gastric cancer stem cells and suppressing tumor growth through magnetic force generation; Syntenin regulates melanogenesis via the p38 MAPK pathway; Lipopolysaccharide reduces melanin synthesis in vitiligo melanocytes by regulating autophagy; An effective disease diagnostic model related to pyroptosis in ischemic cardiomyopathy; A Comparative Study on Inhibition of Total Astragalus Saponins and Astragaloside IV on TNFR1-Mediated Signaling Pathways in Arterial Endothelial Cells; Strategies for the Isolation and Identification of Gastric Cancer Stem Cells; ADAM17 participates in the protective effect of paeoniflorin on mouse brain microvascular endothelial cells; Identification and verification of a glycolysis-related gene signature for gastric cancer. Representative work: Hydroxy-safflower yellow A (HSYA) is the major active component of safflower, a traditional Asia herbal medicine well known for its cardiovascular protective activities. The purpose of this study was to investigate the effect of HSYA on TNF-α-induced inflammatory responses in arterial endothelial cells (AECs) and to explore the mechanisms involved. The results showed that HSYA suppressed the up-regulation of ICAM-1 expression in TNF-α-stimulated AECs in a dose-dependent manner. High concentration (120 μM) HSYA significantly inhibited the TNF-α-induced adhesion of RAW264.7 cells to AECs. HSYA blocked the TNFR1-mediated phosphorylation and degradation of IκBα and also prevented the nuclear tra Astragaloside III (AS-III) is a triterpenoid saponin contained in Astragali Radix and has potent anti-inflammatory effects on vascular endothelial cells; however, underlying mechanisms are unclear. In this study, we provided the first piece of evidence that AS-III induced phosphorylation of TNF-α converting enzyme (TACE) at Thr735 and enhanced its sheddase activity. As a result, AS-III reduced surface TNFR1 level and increased content of sTNFR1 in the culture media, leading to the inhibition of NF-κB signaling pathway and attenuation of downstream cytokine gene expre

Looking for a research collaborator?

Search millions of scientists by field, institution, impact, and funding status — see their work, find their email, and reach out directly.