Clinic serum levels of Plin5 is therapeutic target of spinal cord injury and Plin5 reduced inflammation in spinal cord injury via silent information regulator 1 dependent inhibition of NLRP3 inflammasome

Binqiang Wu,Jie Ren,Wei Fan,Bin Zhao,Feng Zhao,Xiao Liang,Chunjiang Li

doi:10.1590/fst.51121

Abstract

The study investigated that clinic significance and molecular mechanism of Plin5 in spinal cord injury (SCI). Serum levels of Plin5 was down-regulated and there is a negative correlation between Plin5 and IL-1β levels in patients with SCI,. Human Plin5 protein could reduce inflammation, and prevented spinal cord injury in rat model of SCI. Over-expression of Plin5 reduced inflammation divisors via activation of SIRT1 and suppression of NLRP3 in vitro model of SCI; down-regulation of Plin5 promoted inflammation divisors via inactivation of SIRT1 and induction of NLRP3 in vitro model of SCI. SIRT1 is important targets of Plin5 in inflammation divisors of SCI. The inhibition of SIRT1 reduced the effects of Plin5 on inflammation divisors of SCI. The activation of NLRP3 also reduced the effects of Plin5 on inflammation divisors of SCI. We concluded that clinic Serum levels of Plin5 is therapeutic target of SCI and Plin5 reduced inflammation in SCI via SIRT1 dependent suppression of NLRP3 Inflammasome.

Highlights

Spinal cord injury (SCI) can be divided into primary injury and secondary injury according to the molecular mechanism of pathogenesis (Gensel & Zhang, 2015)
We assessed the effects of Plin5 in SCI and overexpression of Plin5 in vitro model was used in this study
We found that Plin5 mRNA expression was down-regulated in SCI mice, and human Plin5 protein reduced the water content of spinal cord, increased BBB score and inhibited serum NF-KB p65, TNF-α, IL-1β and IL-6 levels

Summary

Introduction

Spinal cord injury (SCI) can be divided into primary injury and secondary injury according to the molecular mechanism of pathogenesis (Gensel & Zhang, 2015). The functions of SIRT1 is relatively complicated, which can interact with proteins in a variety of signal transduction pathways (Wang et al, 2019). To be specific, it can deacetylate histone, lysine residue, and transcription factors in the organism, and is involved in neuroprotection, cell aging and apoptosis, glycolipid metabolism, insulin secretion, inflammatory oxidative stress response, angiogenesis, thereby regulating gene functions (Yu et al, 2019a)

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Conclusion