Liaoning University of Traditional Chinese Medicine

About: Liaoning University of Traditional Chinese Medicine is a education organization based out in Shenyang, China. It is known for research contribution in the topics: Randomized controlled trial & Acupuncture. The organization has 2040 authors who have published 1326 publications receiving 14664 citations.

Receptor for Advanced Glycation End-Products (RAGE) Blockade Do Damage to Neuronal Survival via Disrupting Wnt/β-Catenin Signaling in Spinal Cord Injury

Abstract: Wnt signaling are recognized key factors in neuronal development, cell proliferation and axonal guidance. However, RAGE effect on wnt signaling after spinal cord injury (SCI) are poorly understood. Our study aims to explore RAGE blockade effect on wnt signaling after SCI. We constructed Allen SCI model and micro-injected with RAGE neutralizing antibody or IgG after injury. We determined β-catenin, wnt3a and its receptor frizzled-5 via Western blot. We determined β-catenin/NeuN expression at 2 weeks after SCI via immunofluorescence (IF). We found that β-catenin, wnt3a and wnt receptor frizzled5 expression were activated after SCI at 3 days after injury. However, RAGE blockade inhibit β-catenin, wnt3a and frizzled5 expression. We found that β-catenin accumulation in NeuN cells were activated after SCI via IF, however, RAGE blockade reduced β-catenin and NeuN positive cells. RAGE blockade attenuated number of survived neurons and decreased area of spared white matter around the epicenter. RAGE signaling may involved in disrupting wnt signaling to aids neuronal recovery after SCI.

HPLC method for the simultaneous determination of four compounds in rat plasma after intravenous administration of Portulaca oleracea L. extract

Abstract: The objective of the present study was to develop a simple and selective HPLC method for the simultaneous determination of hesperidin (HP), caffeic acid (CA), ferulic acid (FA) and p-coumaric acid (p-CA) in rat plasma after intravenous administration of Portulaca oleracea L. extract (POE). With the hyperoside as the internal standard, the sample pretreatment procedure involved simple single-step extraction with methanol of 0.2 mL plasma. The mobile phase consisted of methanol-acetonitrile-tetrahydrofuran-0.5% glacial acetic acid (5:3:18:74, v/v/v/v). The calibration curves were linear over the range of 0.1-25 µg mL-1, 0.1-25 µg mL-1, 0.1-25 µg mL-1and 0.015-3 µg mL-1 for HP, CA, FA and p-CA, respectively. The method developed was suitable for the pharmacokinetic study of HP, CA, FA and p-CA in rats after intravenous administration of POE.

Lentinan Attenuated the PM2.5 Exposure-Induced Inflammatory Response, Epithelial-Mesenchymal Transition and Migration by Inhibiting the PVT1/miR-199a-5p/caveolin1 Pathway in Lung Cancer.

Abstract: PM2.5 plays an important role in the physiological and pathological progression of lung cancer. Lentinan exerts antitumor activity in many kinds of human cancers. Plasmacytoma variant translocation 1 (PVT1) exerts antitumor activity in many kinds of human cancers. However, the role and underlying molecular mechanism of PVT1 in the role of lentinan in PM2.5-exposed lung cancer are still largely unknown. Our study confirmed that PM2.5 exposure induced the production of inflammatory factors, epithelial-mesenchymal transition (EMT) and migration of lung cancer cells. Lentinan exerted antitumor effects by inhibiting the production of inflammatory factors, EMT, and migration of lung cancer cells. Lentinan suppressed PM2.5 exposure-induced cellular progression by inhibiting the PM2.5 exposure-induced elevation of PVT1 expression. PVT1 absorbed miR-199a, and miR-199a inhibited caveolin1 expression and thus formed the PVT1/miR-199a/caveolin1 signaling pathway in lung cancer cells. Our study revealed that silencing of the PVT1/miR-199a/caveolin1 signaling pathway affected the role of lentinan in PM2.5-exposed lung cancer cells. Thus, this study first investigated the role of lentinan in PM2.5-exposed lung cancer cells and further displayed the underlying molecular mechanism, providing a potential treatment for PM2.5-exposed lung cancer.