Methane-rich saline restores brain SOD activity and alleviates cognitive impairment in rats with traumatic brain injury

Jie Li,Rui Chen,Xu Zhai,Fei-Di Wang,Fang Wang

doi:10.1590/fst.54921

Abstract

Clinically, methane is an anti-inflammatory gas used to treat organ damage. There is no extensive research on methane's repair of traumatic brain injury (TBI), so this study aims to investigate the role of methane and its potential mechanism. A rat TBI model was established by mechanical impact. SD rats were divided into four groups, including sham group, TBI group, 2 or 20 mL/kg methane-rich saline (MS) group. Morris water maze test revealed that MS improved cognitive function in TBI rats. HE and Nissl staining showed that MS reduced the blurring of brain tissues boundary, the number of necrotic plaques and neurons in TBI rats. In addition, ELISA revealed that MS restored the oxidative stress of TBI rats and reversed the inflammatory effect of TBI on brain cells, and TUNEL staining detected that MS inhibited cell apoptosis. Western blotting showed that MS downregulated Caspase-3 and Bax protein levels and upregulated Bcl-2 level. And MS inhibited phosphorylated expressions of Janus kinase 1 (JAK1), signal transducer and activator of the transcription (STAT1) and NF-κb-p65. In conclusion, MS improved cognitive function, reduced inflammatory response and oxidative stress and inhibited cell apoptosis to relieve rat TBI by blocking the activation of the JAK1/STAT1/NF-κb-p65 pathway.

Highlights

Traumatic brain injury (TBI) is one of the common severe diseases in neurosurgery, with high mortality and morbidity
We investigated whether the Janus kinase 1 (JAK1)/STAT1/NF-κB-p65 pathway plays an important role in the treatment of TBI rats
Our results indicated that TBI treatment promoted the levels of phosphorylated JAK1, STAT1 and NF-κB p65 proteins, while methane-rich saline (MS) treatment reversed the activation of the JAK1/STAT1/NF-κB-p65 signal pathway induced by TBI and inhibited the phosphorylation of JAK1, STAT1 and NF-κB-p65 proteins (Figure 5e, f)

Summary

Introduction

Traumatic brain injury (TBI) is one of the common severe diseases in neurosurgery, with high mortality and morbidity. According to a research report, in the United States, TBI patients have an increased risk of death (Harrison-Felix et al, 2015), and about 30% of patients with TBI are permanently disabled (Faul et al, 2010). All of these clinical studies remind us that it’s necessary to explore a powerful treatment for TBI based on its pathophysiological mechanism. Liu et al.reported that TBI induced the intestinal mucosa damage and epithelial barrier dysfunction (Liu et al, 2017b) These studies indicated that TBI affected various systems with complex mechanism. TBI treatment urgently needs drugs that have positive effects on most systems

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