Expression of the α7 nAChR Subunit Duplicate Form (CHRFAM7A) Was Down-Regulated in Patients with Intracranial Infection and Reduced Inflammation in in vitro Model by p38 MAPK

Hu X.a· Hu K.b· Xu X.c· Zhang W.c· Xu F.c

Author affiliations

aClinical Laboratory of the First Affiliated Hospital of Nanchang University, Nanchang, China
b2019 Graduate Student of Urology, The First Clinical College of Nanchang University Medical College, Nanchang, China
cDepartment of Respiration, The First Affiliated Hospital of Nanchang University, Nanchang, China

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Article / Publication Details

First-Page Preview

Abstract of Research Article

Received: March 01, 2021
Accepted: November 08, 2021
Published online: January 31, 2022

Number of Print Pages: 11
Number of Figures: 6
Number of Tables: 0

ISSN: 1021-7401 (Print)
eISSN: 1423-0216 (Online)

For additional information: https://www.karger.com/NIM

Abstract

Objective: In this study, we investigated that the effects and possible mechanisms of the α7 nAChR subunit duplicate form (CHRFAM7A) affected inflammation in the model of intracranial infection. Methods: Mice of the model group were injected (intracranial injection) with Staphylococcus aureus. Mouse microglial BV2 cell was exposed with 200 ng of LPS for 4 h. Results: CHRFAM7A mRNA expressions were reduced in patients with intracranial infection. CHRFAM7A mRNA and protein expressions were suppressed in mice with intracranial infection in a time-dependent manner. CHRFAM7A reduced inflammation in mice with intracranial infection. The inhibition of CHRFAM7A reduced inflammation in mice with intracranial infection. CHRFAM7A suppressed p38 MAPK in mice with intracranial infection. The inhibition of p38 MAPK shows the effects of CHRFAM7A in intracranial infection. Conclusion: Our data demonstrate that the expression of the CHRFAM7A was down-regulated in patients with intracranial infection and reduced inflammation in in vitro model by p38 MAPK, which suggests the potential role of CHRFAM7A as a diagnostic biomarker for intracranial infection.

© 2022 S. Karger AG, Basel

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First-Page Preview

Abstract of Research Article

Received: March 01, 2021
Accepted: November 08, 2021
Published online: January 31, 2022

Number of Print Pages: 11
Number of Figures: 6
Number of Tables: 0

ISSN: 1021-7401 (Print)
eISSN: 1423-0216 (Online)

For additional information: https://www.karger.com/NIM

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