Abstract
Background:
The protective effects of sulforaphane on liver injury induced by high-fat diet and sodium valproate were previously reported. The present study preliminarily investigated the effect of sulforaphane on liver injury induced by traumatic hemorrhagic shock.
Materials and methods:
After a traumatic hemorrhagic shock model was established in rats, the survival of rats during the first 24 hours was analyzed by Kaplan-Meier analysis. The serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TB), tumor necrosis factor α (TNF-α), and interleukin 1β (IL-1β) were measured using a biochemical analyzer or enzyme-linked immunosorbent assay (ELISA). The cell apoptosis and histopathology of liver tissues were examined by TUNEL and hematoxylin-eosin (HE) staining. The mRNA and protein expressions of B-cell lymphoma-2 (Bcl-2), Bcl2 associated X (Bax), Caspase-3, TNF-α, IL-1β, Cyclooxygenase-2 (COX-2), nitric oxide synthase (iNOS), nuclear factor E2-related factor 2 (Nrf2), and heme oxygenase 1 (HO-1) in the liver tissues were determined by immunohistochemical staining, quantitative reverse transcription PCR (qRT-PCR) or western blot.
Results:
Sulforaphane promoted the health of the animal, reduced liver cell apoptosis and ameliorated the histopathological damage in the liver of rats with traumatic hemorrhagic shock. Sulforaphane downregulated the expressions of liver function-related factors (ALT, AST, TB), inflammation-related factors (TNF-α, IL-1β, COX-2, iNOS), and apoptosis-related factors (Bax, Caspase-3) and upregulated the expressions of factors related to apoptosis (Bcl-2) and Nrf2/HO-1 pathway (Nrf2, HO-1).
Conclusion:
Sulforaphane protected the liver against traumatic hemorrhagic shock through ameliorating the apoptosis and inflammation of the liver via activating the Nrf2/HO-1 pathway.
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