Protective effects of curcumin against thyroid hormone imbalance after gas explosion-induced traumatic brain injury via activation of the hypothalamic-pituitary-thyroid axis in male rats.

Gas explosion (GE)-induced traumatic brain injury (TBI) can affect thyroid hormone (TH) homeostasis in miners. This study evaluated the effects of hepatic transthyretin and hypothalamic-pituitary-thyroid (HPT) axis on thyroids and explored the protective effect and mechanism of curcumin on GE-induced TBI. Thirty rats were randomly divided into three groups (10 per group): first group (control group)-rats received GE treatment once; second group (GE group)-rats received GE treatment (200 m from the source of the explosion once); third group (GE + Cur group)-rats received curcumin (Cur) by lavage at a dose of 100 mg/kg/day once every other day for 7 days after receiving GE. After GE, the pathological changes were analyzed by hemotoxylin and eosin staining, and the levels of serum reactive oxygen species (ROS), urine iodine (UI), THs, nuclear factor-kappa B (NF-κB), superoxide dismutase (SOD), glutathione peroxidase (Gpx), and malondialdehyde (MDA) were analyzed using ELISA. Expression of proteins in the HPT axis of rats was examined by immunohistochemistry and Western blotting. We found that GE could induce pathologic changes in rat thyroid and liver. Serum levels of THs, NF-κB and serum redox state became unbalanced in rats after GE. GE could inhibit the biosynthesis and biotransformation of THs by affecting key HPT axis proteins. Additionally, GE reduced the level of hepatic transthyretin. Serum THs levels and thyroid sections were almost recovered to normal after curcumin treatment. The aforementioned key HPT axis proteins in the curcumin group showed opposite expression trends. In summary, GE affected THs balance while curcumin can protect against these injury effects by affecting TH biosynthesis, biotransformation, and transport, and inducing oxidative stress and inflammatory responses.

Evaluation of Gas Explosion Injury Based on Analysis of Rat Serum Profile by Ultra-Performance Liquid Chromatography/Mass Spectrometry-Based Metabonomics Techniques.

Gas explosion can lead to serious global public health issues. Early period gas explosion injury (GEI) can induce a series of histopathologic and specific metabolic changes. Unfortunately, it is difficult to treat GEI thoroughly. To date, the specific molecular mechanism of GEI is still unclear. To accurately diagnose and provide comprehensive clinical intervention, we performed a global analysis of metabolic alterations involved in GEI. The physiological and behavioral indicators' changes of rats after gas explosion were observed. These metabolic alterations were first investigated in a rat model using serum metabonomics techniques and multivariate statistical analysis. Significant heart rate (HR), mean blood pressure (mBP), and neurobehavioral index changes were observed in the GEI group after gas explosion. UPLC-MS revealed evident separated clustering between the control and GEI groups using supervised partial least squares discriminant analysis (PLS-DA). We designed an integrated metabonomics study for identifying reliable biomarkers of GEI using a time-course analysis of discriminating metabolites in this experiment. The metabonomics analysis showed alterations in a number of biomarkers (21 from serum). The meaningful biomarkers of GEI provide new insights into the pathophysiological changes and molecular mechanisms of GEI, including the disturbances in oxidative stress and neuroinflammatory reaction, as well as in metabolism of lipids, glucose, and amino acids in rats, suggesting that the process of GEI in humans is likely to be comprehensive and dynamic. Correlations between the GEI group and the biomarkers identified from the rat model will be further explored to elucidate the metabolic pathways responsible for GEI in the human body.