LncRNA-TUG1: Implications in the Myocardial and Endothelial Cell Oxidative Stress Injury Caused by Hemorrhagic Shock and Fluid Resuscitation.

BACKGROUND

LncRNA taurine-upregulated gene 1 () can regulate vascular endothelial cell injury, a critical mechanism in treating hemorrhagic shock and fluid resuscitation (HS/R). Therefore, this study explored the influence of in HS/R.

METHODS

An rat model of ischemia-reperfusion (I/R) injury post-HS/R and an model of oxidative stress injury in rat cardiomyocyte cell line (H9C2) were constructed. , we silenced and quantified its expression along with inflammatory factors through quantitative reverse transcription polymerase chain reaction (qRT-PCR), mean arterial pressure (MAP) detection and blood gas analysis. Myocardial functional impairment was assessed via Triphenyl-2H-Tetrazolium Chloride (TTC), Hematoxylin and eosin, and Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) stainings. Oxidative stress level in rat serum was measured. , we examined the changes of cell viability, apoptosis, oxidative stress levels, inflammatory factor secretion and nuclear factor-κB (NF-κB)/p65 expression by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, Enzyme-linked immunosorbent assay (ELISA) and Western blot.

RESULTS

level was elevated in rats of I/R model caused by HS/R. silencing ameliorated the decline in MAP, acid-base imbalance and myocardial tissue damage, and suppressed oxidative stress and inflammatory factor levels in model rat. silencing enhanced viability, impeded apoptosis, and reduced oxidative stress, inflammatory factor contents and NF-κB/p65 expression in HO treated H9C2 cells.

CONCLUSION

participates in regulating oxidative stress damage and inflammation induced by HS/R.