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Abstract Title:

Myricitrin attenuates memory impairment in a rat model of sepsis-associated encephalopathy via the NLRP3/Bax/Bcl pathway.

Abstract Source:

Folia Neuropathol. 2019 ;57(4):327-334. PMID: 32337945

Abstract Author(s):

Junzuo Gong, Shu Luo, Shiqiao Zhao, Songlin Yin, Xiaofeng Li, Tianyi Mou

Article Affiliation:

Junzuo Gong

Abstract:

INTRODUCTION: The present investigation determined the protective effect of myricitrin against sepsis-associated encephalopathy in rats.

MATERIAL AND METHODS: Sepsis was induced by cecal ligation and puncture (CLP); rats were treated with 30 or 100 mg/kg of myricitrin for 5 days prior to the induction of CLP. The effect of myricitrin was observed by determining the neurological function using the open field test and step-down inhibitory avoidance test. Cerebral oedema and the levels of inflammatory and oxidative stress mediators were determined in brain tissues. Moreover, the expression levels of Bcl-2, Bax, IκB-α, nuclear factor κB (NF-κB), caspase-3 and NLRP3 were estimated in brain tissues by Western blotting and the mRNA expression of NF-κB, caspase-3 and NLRP3 in brain tissues was estimated by real-time polymerase chain reaction. An immunofluorescence assay was performed to estimate inflammasome activity.

RESULTS: The results suggest that treatment with myricitrin protects neuronal function in rats with CLP-induced sepsis. Decreases in inflammation and oxidative stress mediators were observed in the brain tissues of the myricitrin-treated group compared to the CLP group. Moreover, treatment with myricitrin ameliorated the altered Bcl-2, Bax, IκB-α, NF-κB, caspase-3 and NLRP3 protein and mRNA expression levels in the brain tissues of septic rats.

CONCLUSIONS: The data reveal that myricitrin ameliorated neuroinflammation and improved memory in rats with CLP-induced sepsis by regulating the NLRP3/Bax/Bcl signalling pathway.

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