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with the rapid development of the economy and society , the incidence of tbi in china is rising year by year , and its mortality and morbidity rates remain high , making it a great burden for the patients families both mentally and economically .
it has been revealed that tbi can be divided into two phases : the initial injury caused by violence , which is inevitable , and the secondary injury within hours or days after initial injury , caused by the inflammatory response , oxidative stress , calcium overload , and a series of other pathological processes , which is the major target of current interventions .
previous studies have demonstrated the effectiveness of hyperbaric oxygen therapy in treatments for secondary brain damage after trauma , but the mechanism has not been fully clarified . in this study , we investigated the efficacy of hyperbaric oxygen for secondary brain injury after trauma , with a focus on the tlr4/nf-b signaling pathway , in an effort to clarify the mechanism of its protective effect and to provide guidance for the safer and more efficient clinical use of hyperbaric oxygen .
sixty healthy adult male sd rats were randomly divided into 3 groups : the sham group , the untreated tbi group , and the hyperbaric oxygen - treated tbi group . a rat model of tbi
the rats were anesthetized using chloral hydrate at 4 mg / kg and fixed on a bracket . after skin preparation ,
a 5 mm opening was made with an orthopedic drill at 3 mm to the right of the coronal suture and 3 mm behind the sagittal suture , keeping the dura intact .
then , a 40 g object was dropped from 15 cm high and vertically crashed into the exposed dura to make a 3 mm deep and 4 mm diameter hole .
all of the experimental program and operation procedures in this study were approved by the experimental animal ethics committee .
the rats were placed into the animal chamber , which was purged with pure oxygen for 10 min to ensure that the oxygen fraction in the chamber was > 95% .
the sham control group and untreated tbi group were also placed in the same chambers and were subjected to the same experimental procedures , only without the hyperbaric oxygen treatment . at 24 h after injury , the rats were anesthetized , and 100 ml of normal saline was infused through the cardiac apex .
protein concentration was determined by bradford assay , and 1/4 volume of 5 loading buffer was added , followed by a boiling water bath for 20 min for denaturation .
a sample consisting of 35 g of protein was loaded , separated by electrophoresis , transferred to membrane , blocked , and incubated with antibodies to tlr4 , ib , p65 , cleaved caspase-3 , gapdh , or h3 ( 1:200 , purchased from santa cruz , usa ) at 4c on a shaker overnight , then washed , incubated with the corresponding hrp - conjugated secondary antibody , and washed again .
finally , ecl solution was added to reveal the bands , whose gray value was analyzed by image j software .
elisa assay kits for tnf- , il-6 and il-1 were all purchased from unitech biotechnology , and experiments were conducted according to the manufacturer s instructions .
paraffin - embedded brain tissue was cut into 4 m sections and analyzed by the tunel assay to determine apoptosis of the neurons .
the tunel assay kit was purchased from roche , usa , and the experiment was conducted strictly according to the manufacturer s instructions . the tunel assay result for the tissue around the trauma
was observed under an optical microscope , and 10 random visual sections under 400 magnification were evaluated for the percentage of tunel - positive cells .
the neurological function of the rats was evaluated by the neurological severity scores ( nss ) , including motor function , sensory function , balance ability , physiological reflex defect , and abnormal movement .
for each of the 18 projects , the inability to complete a task or lack of corresponding response was scored 1 point .
cases with scores of 1318 points in total are regarded as severe injury , 712 points as moderate injury , and 16 points as mild injury .
the spss 15.0 software was used for statistical analysis , and the data are presented as means  standard deviation ( xs ) .
the neurological function scores were compared by the kruskal - wallis test , and comparisons among multiple groups were performed using one - way analysis of variation .
sixty healthy adult male sd rats were randomly divided into 3 groups : the sham group , the untreated tbi group , and the hyperbaric oxygen - treated tbi group . a rat model of tbi
the rats were anesthetized using chloral hydrate at 4 mg / kg and fixed on a bracket . after skin preparation ,
a 5 mm opening was made with an orthopedic drill at 3 mm to the right of the coronal suture and 3 mm behind the sagittal suture , keeping the dura intact .
then , a 40 g object was dropped from 15 cm high and vertically crashed into the exposed dura to make a 3 mm deep and 4 mm diameter hole .
all of the experimental program and operation procedures in this study were approved by the experimental animal ethics committee .
the rats were placed into the animal chamber , which was purged with pure oxygen for 10 min to ensure that the oxygen fraction in the chamber was > 95% .
the sham control group and untreated tbi group were also placed in the same chambers and were subjected to the same experimental procedures , only without the hyperbaric oxygen treatment .
at 24 h after injury , the rats were anesthetized , and 100 ml of normal saline was infused through the cardiac apex .
protein concentration was determined by bradford assay , and 1/4 volume of 5 loading buffer was added , followed by a boiling water bath for 20 min for denaturation .
a sample consisting of 35 g of protein was loaded , separated by electrophoresis , transferred to membrane , blocked , and incubated with antibodies to tlr4 , ib , p65 , cleaved caspase-3 , gapdh , or h3 ( 1:200 , purchased from santa cruz , usa ) at 4c on a shaker overnight , then washed , incubated with the corresponding hrp - conjugated secondary antibody , and washed again .
finally , ecl solution was added to reveal the bands , whose gray value was analyzed by image j software .
elisa assay kits for tnf- , il-6 and il-1 were all purchased from unitech biotechnology , and experiments were conducted according to the manufacturer s instructions .
paraffin - embedded brain tissue was cut into 4 m sections and analyzed by the tunel assay to determine apoptosis of the neurons .
the tunel assay kit was purchased from roche , usa , and the experiment was conducted strictly according to the manufacturer s instructions . the tunel assay result for the tissue around the trauma
was observed under an optical microscope , and 10 random visual sections under 400 magnification were evaluated for the percentage of tunel - positive cells .
the neurological function of the rats was evaluated by the neurological severity scores ( nss ) , including motor function , sensory function , balance ability , physiological reflex defect , and abnormal movement . for each of the 18 projects , the inability to complete a task or lack of corresponding response
cases with scores of 1318 points in total are regarded as severe injury , 712 points as moderate injury , and 16 points as mild injury .
the spss 15.0 software was used for statistical analysis , and the data are presented as means  standard deviation ( xs ) . the neurological function scores were compared by the kruskal - wallis test , and comparisons among multiple groups were performed using one - way analysis of variation .
compared to the sham group ( figures 1 , 2 ; table 1 ) , the tlr4 , p65 , and cleaved caspase-3 levels in peri - trauma tissue in the untreated tbi group were significantly elevated ( p<0.05 ) , while hyperbaric oxygen significantly inhibited the expression of tlr4 , p65 , and cleaved caspase-3 ( p<0.05 ) ; in addition , hyperbaric oxygen significantly inhibited the degradation of ib after tbi ( p<0.05 ) . compared to the sham group ,
the levels of tnf- , il-6 and il-1 in the untreated tbi group were significantly increased ( table 2 , p<0.05 ) , while hyperbaric oxygen significantly inhibited expression of tnf- , il-6 and il-1 ( table 2 , p<0.05 ) .
apoptotic neurons with condensed nuclei were stained brown in the tunel assay ( figure 3 ) , while normal cells were large , round , and not stained . in the sham group , few apoptotic neurons were observed ; in the untreated tbi group , significantly more apoptotic neurons were observed ( figure 3 , table 2 , p<0.05 ) ; and after hyperbaric therapy , the number of peri - trauma apoptotic neurons was significantly reduced ( p<0.05 ) . compared with the sham group ,
the neurological function of rats of the tbi group decreased significantly ( table 3 , p<0.05 ) , whereas hyperbaric oxygen significantly improved the neurological function of the rats after tbi ( table 3 , p<0.05 ) .
compared to the sham group ( figures 1 , 2 ; table 1 ) , the tlr4 , p65 , and cleaved caspase-3 levels in peri - trauma tissue in the untreated tbi group were significantly elevated ( p<0.05 ) , while hyperbaric oxygen significantly inhibited the expression of tlr4 , p65 , and cleaved caspase-3 ( p<0.05 ) ; in addition , hyperbaric oxygen significantly inhibited the degradation of ib after tbi ( p<0.05 ) .
compared to the sham group , the levels of tnf- , il-6 and il-1 in the untreated tbi group were significantly increased ( table 2 , p<0.05 ) , while hyperbaric oxygen significantly inhibited expression of tnf- , il-6 and il-1 ( table 2 , p<0.05 ) .
apoptotic neurons with condensed nuclei were stained brown in the tunel assay ( figure 3 ) , while normal cells were large , round , and not stained . in the sham group , few apoptotic neurons were observed ; in the untreated tbi group , significantly more apoptotic neurons were observed ( figure 3 , table 2 , p<0.05 ) ; and after hyperbaric therapy , the number of peri - trauma apoptotic neurons was significantly reduced ( p<0.05 ) .
compared with the sham group , the neurological function of rats of the tbi group decreased significantly ( table 3 , p<0.05 ) , whereas hyperbaric oxygen significantly improved the neurological function of the rats after tbi ( table 3 , p<0.05 ) .
numerous studies have shown that hyperbaric oxygen can increase oxygen concentration , increase oxygen diffusion distance , and induce a variety of mechanisms to correct the acidosis neuroprotective effect .
this study showed that hyperbaric oxygen can significantly reduce the rate of neuronal apoptosis after traumatic brain injury , significantly improving neurological function in rats , which is consistent with previous studies .
recent studies have also found that hyperbaric oxygen could suppress the inflammatory response after traumatic brain injury to exert neuroprotective effects .
tlr4 is an important member of the tlr family , a group of type i transmembrane molecules , consisting of an extracellular segment , a transmembrane segment and an intracellular tir segment .
it plays an important role in hypoxic - ischemic brain injury , cerebral hemorrhage , spinal cord injury , and other acute injury of the central nervous system [ 68 ] .
high expression of tlr4 has been observed in the tissue around brain trauma in both animal models and clinical studies , while tlr4 knockout mice showed significantly alleviated secondary brain injury after brain trauma , and a specific tlr4 inhibitor also significantly alleviated brain damage , suggesting that therapies targeting tlr4 have great potential in improving the prognosis of tbi . in this study ,
tlr4 protein expression significantly increased after tbi , and hyperbaric oxygen therapy significantly inhibited tlr4 expression , reduced apoptosis of neurons after tbi and improved the neurological function of the rats , suggesting that down - regulation of tlr4 is an important part of the neuron - protective effect of hyperbaric oxygen therapy .
when bound by its receptor during tbi , tlr4 interacts with downstream myeloid differentiation factor 88 and activates ikk , which phosphorylates ib and leads to the degradation of ib
. then , nf-b p65 protein is released from ib and translocates from the cytoplasm to the nucleus to interact with the promoters of its target genes , regulating the expression of a series of inflammatory cytokines .
nf-b is the master regulator of a series of inflammatory cytokines and is significantly elevated in the tissue surrounding brain trauma , and specific nf-b inhibitors significantly reduced the expression of inflammatory cytokines after tbi and relieved secondary brain injury .
in addition , recent studies have shown that hyperbaric oxygen therapy significantly inhibited microglia activation and inflammatory cytokine production in the central nervous system . in this study
, we found that p65 expression was significantly increased in peri - trauma tissue after tbi , which is consistent with previous studies , and hyperbaric oxygen therapy significantly inhibited p65 expression in the nucleus .
taken together , it is speculated that the inhibition of nf-b signaling may be the basic mechanism in the neuroprotective effect of hyperbaric oxygen therapy .
hyperbaric oxygen therapy significantly reduces apoptosis in peri - trauma tissue after tbi , inhibits the expression of inflammatory cytokines , and significantly improves the neurological function of rats after tbi .
backgroundthe aim of this study was to investigate the efficacy of hyperbaric oxygen in secondary brain injury after trauma and its mechanism in a rat model.material/methodsa rat model of tbi was constructed using the modified feeney s free - fall method , and 60 sd rats were randomly divided into three groups  the sham group , the untreated traumatic brain injury ( tbi ) group , and the hyperbaric oxygen - treated tbi group . 
 the neurological function of the rats was evaluated 12 and 24 hours after tbi modeling ; the expression levels of tlr4 , ib , p65 , and cleaved caspase-3 in the peri - trauma cortex were determined by western blot ; levels of tnf- , il-6 , and il-1 were determined by elisa ; and apoptosis of the neurons was evaluated by tunel assay 24 hours after tbi modeling.resultshyperbaric oxygen therapy significantly inhibited the activation of the tlr4/nf-b signaling pathway , reduced the expression of cleaved caspase-3 , tnf- , il-6 and il-1 ( p<0.05 ) , reduced apoptosis of the neurons and improved the neurological function of the rats ( p<0.05).conclusionshyperbaric oxygen therapy protects the neurons after traumatic injury , possibly through inhibition of the tlr4/nf-b signaling pathway .