The effect of different atmosphere absolute hyperbaric oxygen on the expression of extracellular histones after traumatic brain injury in rats

Abstract

By observing the dynamic changes of extracellular histones H1, H2A, H4, and NF-κB expression in brain tissues after brain injury in rats, we explore the association among the expression of extracellular histones H1, H2A, H4, and NF-κB following traumatic brain injury (TBI), as well as the effect of different atmospheres absolute hyperbaric oxygen (HBO) intervention on the expression and possible mechanisms. A total of 120 SD rats were randomly divided into 4 groups: Sham-operated (SH), TBI (traumatic brain injury) group, traumatic brain injury and hyperbaric oxygen treatment 1.6ATA (TBI + HBO1) group, and traumatic brain injury and hyperbaric oxygen treatment2.2ATA (TBI + HBO2) group, with 30 rats in each group. The rats in each group were then randomly divided into five smaller time-specific sub-groups: 3 h, 6 h, 12 h, 24 h, and 48 h after surgery. TBI models were established, and the brain tissue around the lesion was taken at different time points. On the one hand,we detected the level of local histones H1, H2A, H4, and NF-κB by RT-PCR and Western Blot. On the other hand, we used immunohistochemical methods to detect the expression of NF-κB, while using the TUNEL method to observe the cell apoptosis in experimental groups after brain injury. Extracellular histones H1, H2A, H4, and NF-κB proteins were highly expressed at 3 h, then with a slight fluctuation, reached to peak at 48 h after the injury. HBO can affect the expression of histones H1, H2A, H4, and NF-κB. The decline of each indicator in the 1.6ATA group was significantly lower than that in the 2.2ATA group, especially within 6 h (P < 0. 05). In addition, NF-κB expression was consistent with the pathological changes of apoptosis in experimental groups. Hyperbaric oxygen therapy with relatively low pressure (1.6ATA) at the early stage can significantly inhibit the expression of extracellular histones H1, H2A, H4, and NF-κB around the lesion, reduce the apoptosis of nerve cells, and thus play an important role in alleviating secondary brain injury.

Functional MRI (fMRI) Evaluation of Hyperbaric Oxygen Therapy (HBOT) Efficacy in Chronic Cerebral Stroke: A Small Retrospective Consecutive Case Series

“…The ECHM document is from 2016. In the meantime, many papers [ 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 ] have been published in favour of HBOT, so that its level of evidence may have been increased.…”

“…Although the mechanisms underlying HBOT brain effects have to be clearly defined yet [ 28 ], it seems that many factors are involved: inflammation modulation [ 25 ], strengthening of the antioxidant endogenous system [ 29 , 30 ], neoangiogenesis stimulation in the damaged tissues [ 21 , 31 ] and tissue repair stimulation by bone marrow staminal cells mobilization [ 32 ]. All these mechanisms could account for HBOT ability to stimulate neoangiogenesis and neuroplasticity even years after the brain insult.…”

The Mechanisms of Action of Hyperbaric Oxygen in Restoring Host Homeostasis during Sepsis

“…Studies looking at the impact of HBO 2 on the expression on NF-κB similarly found an increasing effect in a normoxic environment [ 17 , 117 , 160 ] and a decreasing effect in a hypoxic environment [ 161 , 162 ], regardless of the stage of inflammation. In contrast to HIF-1α expression, studies evaluating the effect on NF-κB signaling in conditions of relative hypoxia secondary to inflammatory conditions mostly found a decreasing effect regardless of the inflammatory state or number of HBO 2 sessions [ 46 , 47 , 153 , 154 , 163 , 164 , 165 , 166 , 167 , 168 , 169 , 170 ], with the exception of three studies where 10–30 sessions of HBO 2 were applied to chronic inflammation, which found an increasing effect [ 117 ] or no effect (Part b in Table 1 ) [ 149 , 158 ].…”

Maternal exposure to hyperbaric oxygen at the preimplantation stages increases apoptosis and ectopic Cdx2 expression and decreases Oct4 expression in mouse blastocysts via Nrf2‐Notch1 upregulation and Nf2 downregulation

“…The sizes of the PCR products and sequences of the forward and reverse primers for each gene analyzed in this study are listed in Table 1. Real-time qPCRs of the reversely transcribed cDNAs were performed by the CFX Connect Real-Time PCR Detection System (Bio-Rad Laboratories, Inc., Hercules, CA) and analyzed by the CFX Manager 3.0 software (Bio-Rad Laboratories, Inc.) using GAPDH as the reference housekeeping gene, given that GAPDH has been widely used as the major reference gene in multiple previous studies about the effects of HBO exposures on gene expression, [111][112][113][114] and our microarray analyses revealed less than ±0.2 in the Log2 fold changes and more than 0.5 in the p values in GAPDH gene expression levels in mouse blastocysts under HBO versus normoxic exposures in vivo.…”