4/2020
vol. 58
abstract:
Original paper
Antcin C ameliorates neuronal inflammation due to cerebral
haemorrhage by inhibiting the TLR-4 pathway
1.
Department of Surgery, Hebei Medical University, Shijiazhuang, Hebei, China
2.
Department of Neurosurgery, Weifang People’s Hospital, Weifang, China
3.
Department of Neurosurgery, Tangshan GongrenHospital, Tangshan, Hebei, China
4.
School of Basic Medical Science, North China University of Science and Technology, Tangshan,Hebei, China
5.
Hebei Key Laboratory for Chronic Diseases, Tangshan Key Laboratory for Preclinical and Basic Research on Chronic Diseases, Tangshan, China
Folia Neuropathol 2020; 58 (4): 317-323
Online publish date: 2021/01/11
Introduction This study investigated the protective effects of antcin C against cerebral haemorrhage injury.
Material and methods Cerebral haemorrhage was treated with antcin C 100 mg/kg i.p. at 60 min after the induction of cerebral injury. Neurological scores and volumes of cerebral injury were assessed to determine the effects of antcin C, based on oxidative stress and serum mediators of inflammation by ELISA. qRT-PCR was used to estimate the mRNA expression of Toll-like receptor 4 (TLR-4) and interleukin-1 receptor-associated kinase 4 (IRAK4) proteins in the cerebral tissue of rats with cerebral haemorrhage. Western blot assay and histopathology were also performed.
Results The findings suggest that treatment with antcin C reduced the neurological scores and volumes of cerebral injury in cerebral injured rats. Parameters of oxidative stress and cytokine levels were reduced in the serum of the antcin C-treated group compared with the negative control group. Treatment with antcin C ameliorated the expression of TLR-4, IRAK4, and zonula occludens-1 (ZO-1) proteins in the cerebral tissue of cerebral injured rats.
Conclusions The results revealed that treatment with antcin C protected against cerebral haemorrhage damage by controlling microglia inflammation through the TLR-4 pathway.
keywords:
antcin C, cerebral haemorrhage, inflammation, oxidative stress, neuronal injury
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