About this Biochemistry, Genetics and Molecular Biology article

Icaritin inhibits neuroinflammation in a rat cerebral ischemia model by regulating microglial polarization through the GPER–ERK–NF-κB signaling pathway by Zining Yu; Guangjun Su; Limei Zhang; Gaigai Liu; Yonggang Zhou; Shicai Fang; Qian Zhang; Tianyun Wang; Cheng Huang; Zhihua Huang; Liangdong Li is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

## Abstract ## Background Activated microglia play a key role in initiating the inflammatory cascade following ischemic stroke and exert proinflammatory or anti-inflammatory effects, depending on whether they are polarized toward the M1 or M2 phenotype. The present study investigated the regulatory effect of icaritin (ICT) on microglial polarization in rats after cerebral ischemia/reperfusion injury (CI/RI) and explored the possible anti-inflammatory mechanisms of ICT. ## Methods A rat model of transient middle cerebral artery occlusion (tMCAO) was established. Following treatment with ICT, a G protein-coupled estrogen receptor (GPER) inhibitor or an extracellular signal-regulated kinase (ERK) inhibitor, the Garcia scale and rotarod test were used to assess neurological and locomotor function. 2,3,5-Triphenyltetrazolium chloride (TTC) and Fluoro-Jade C (FJC) staining were used to evaluate the infarct volume and neuronal death. The levels of inflammatory factors in the ischemic penumbra were evaluated using enzyme-linked immunosorbent assays (ELISAs). In addition, western blotting, immunofluorescence staining and quantitative PCR (qPCR) were performed to measure the expression level

Author

Zining Yu; Guangjun Su; Limei Zhang; Gaigai Liu; Yonggang Zhou; Shicai Fang; Qian Zhang; Tianyun Wang; Cheng Huang; Zhihua Huang; Liangdong Li

Publisher

Springer Science and Business Media LLC

Published

2022

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)