Abstract:Aim To investigate the effect and mechanism of hydrogen molecule on myocardial injury in severe traumatic brain injury (TBI) rats. Methods Using the fluid percussion injury (FPI)-induced TBI model. 72 SD rats were randomly divided into sham group, TBI group and hydrogen molecule-treated group, with 24 rats in each group, and the rats were executed at 48 h after the operation. HE staining was used to observe the myocardial injury and the infiltration of granulocytes, ELISA was used to detect the level of superoxide dismutase (SOD), Western blot was used to detect the expression of inflammation-related factors myeloperoxidase (MPO) and heme oxygenase-1 (HO-1) protein, RT-qPCR was used to detect the levels of cardiac troponin T (cTnT), inhibitory factor-1 (IF-1), NADH/ubiquinone oxidoreductase core subunit S7 (NDUFS7), nicotinamide adenine dinucleotide phosphate (NADP) and reduced nicotinamide adenine dinucleotide phosphate (NADPH). The changes of post-traumatic echocardiography and the 7-day survival rate and body weight in the rats were observed and recorded. Results Compared with the sham group, rats in the TBI group had significantly higher troponin levels, and the echocardiographic results showed higher left ventricular end-diastolic diameter (LVEDD) and significantly lower left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), and the above pathologic changes were significantly improved after treatment with the hydrogen molecule. Myocardial tissue was disorganized with erythrocyte infiltration, and myocardial fibers were infiltrated with granulocytes in the section, which were improved in the hydrogen molecule-treated group. The body weight of the rats decreased dramatically after the operation, and about 5 days later dropped to the lowest level, and then showed a trend of slow recovery. mNSS scores showed that the neurological function of the rats was severely impaired after TBI, and the postoperative myocardial tissues showed an increase in the expression levels of MPO and HO-1 proteins and a decrease in the expression levels of SOD, and the above pathological changes were significantly improved by hydrogen molecule treatment. In the TBI group, the expression levels of NADPH, IF-1 and NDUFS7 were reduced, and the expression levels of the above indicators were significantly increased after hydrogen molecule treatment. Conclusion Hydrogen molecule may be able to increase mitochondrial energy metabolism in cardiomyocytes and reduce myocardial oxidative stress by synergistically enhancing the protein expression of IF-1 and NDUFS7 on the mitochondrial oxidative respiratory chain to increase cardiac function and survival rate in the acute phase of TBI.
