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Sulforaphane Is Protective against Warm Ischemia/Reperfusion Injury and Partial Hepatectomy in Rats
Richi Nakatake1, Tetsuya Okuyama1, Yuki Hashimoto1
1Department of Surgery, Kansai Medical University, Hirakata 573-1010, Osaka, Japan.
International Journal of Molecular Sciences
|January 11, 2024
Summary
Sulforaphane (SFN) protects the liver from warm hepatic ischemia/reperfusion injury (HIRI) and partial hepatectomy (PH) by reducing inflammation and cell death. This natural compound also significantly lowers mortality rates in affected rats.
Area of Science:
- Hepatology
- Inflammation research
- Natural product pharmacology
Background:
- Warm hepatic ischemia/reperfusion injury (HIRI) is a significant clinical challenge, often exacerbated by partial hepatectomy (PH).
- The role of sulforaphane (SFN), a natural compound, in mitigating HIRI-induced inflammatory responses remains largely unexplored.
- Understanding SFN's impact on inflammatory mediators is crucial for developing novel therapeutic strategies.
Purpose of the Study:
- To investigate the potential hepatoprotective effects of SFN against HIRI combined with partial hepatectomy (HIRI + PH) in a rat model.
- To elucidate the molecular mechanisms underlying SFN's action, particularly its influence on inflammatory signaling pathways.
- To assess the impact of SFN on mortality associated with severe HIRI + PH.
Main Methods:
- An in vivo rat model of HIRI + PH was established, involving hepatic ischemia followed by hepatectomy and reperfusion.
- SFN was administered intraperitoneally at specific time points before the ischemic event.
- In vitro studies utilized interleukin-1β (IL-1β)-treated primary rat hepatocytes to analyze signaling pathways, including NF-κB activation and TNF-α expression.
Main Results:
- SFN administration significantly reduced serum liver enzyme levels and pathological liver injury markers, including apoptosis and neutrophil infiltration.
- SFN treatment suppressed tumor necrosis factor-alpha (TNF-α) mRNA expression and inhibited nuclear factor-kappa B (NF-κB) activation in the HIRI + PH model.
- Mortality rates were significantly decreased in rats treated with SFN.
- In vitro, SFN inhibited inflammatory cytokine expression and NF-κB activation in IL-1β-stimulated hepatocytes.
Conclusions:
- SFN demonstrates significant hepatoprotective effects in the context of HIRI + PH.
- SFN exerts its protective effects, at least in part, by inhibiting the induction of key inflammatory mediators like TNF-α.
- Suppression of the NF-κB signaling pathway in hepatocytes appears to be a critical mechanism underlying SFN's therapeutic benefits.
