{'fraction_non_alphanumeric': 0.04948075748320098, 'fraction_numerical': 0.020158827122785584, 'mean_word_length': 4.533783783783784, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Dexmedetomidine Attenuates Myocardial Injury Induced by Renal Ischemia/Reperfusion by Inhibiting the HMGB1-TLR4-MyD88-NF-κB Signaling Pathway.

OBJECTIVE
To investigate the effect of dexmedetomidine (DEX) on myocardial injury induced by renal ischemia/reperfusion (I/R) and to explore the role of the HMGB1-TLR4-MyD88-NF-κB signaling pathway.


METHODS
Adult male Wistar rats were randomly allocated into the control group, renal I/R group, renal I/R group pretreated with a low dose of DEX (L-Dex+I/R), renal I/R group pretreated with a medium dose of DEX (M-Dex+I/R), and renal I/R group pretreated with a high dose of DEX (H-Dex+I/R). Outcome measures included the plasma concentrations of HMGB1, IL-6, IL-10, IL-17, and TnI, the expression levels of HMGB1, TLR4, MyD88, NF-κBp65, and P-NF-κBp65, the pathological change, and the cell apoptosis.


RESULTS
Renal I/R led to severe myocardial histological injury and cell apoptosis. DEX reduced the plasma concentration of IL-17 and TnI in a dose-dependent manner in the renal I/R model rats and inhibited the protein expression of TLR4 and NF-κBp65 in a dose-dependent manner in the myocardial tissue. Additionally, mRNA expression of MyD88 was elevated in the I/R group compared with the control group, and DEX significantly reduced mRNA expression of MyD88 in the renal I/R model rats. DEX inhibited myocardial cell apoptosis in the renal I/R model rats.


CONCLUSION
DEX could attenuate myocardial injury induced by renal I/R in a dose-dependent manner. The potential mechanisms are associated with inhibition of the HMGB1-TLR4-NF-κB signaling pathway and myocardial cell apoptosis.