This 2021 rodent study investigated sulforaphane pretreatment’s role in reducing liver injuries:
“As a double blood supply organ of the portal vein and artery, the liver is highly sensitive to ischemia, and is one of the common organs to suffer from hepatic ischemia-reperfusion injury (HI/RI). HI/RI leads to overproduction of reactive oxygen species (ROS).
- Overdoses of ROS promote reaction of lipid peroxidation and generation of the extremely aggressive oxidants nitric oxide (NO) and malondialdehyde (MDA).
- HI/RI decreased antioxidant enzyme activity of glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD).
- Sulforaphane (SFN) intervention significantly decreased levels of MDA and NO by increasing activity of GSH, CAT, and SOD.
Inflammation is the most serious secondary injury experienced in HI/RI.
- Monocyte chemotactic protein 1 (MCP-1) is involved in an inflammatory reaction with regulation of monocytes, T lymphocytes, and NK cells. MCP-1 can also increase infiltration of inflammatory cells by activating NF-κB.
- Tumor necrosis factor-α (TNF-α) is a promoter of the inflammatory response. Interleukin-6 (IL-6) is an inflammatory mediator in the acute reaction period.
- SFN treatment significantly decreased HI/RI-induced expression of TNF-a, IL-6, and MCP-1.
In conclusion, SFN has a protective effect on HI/RI. The mechanism is associated with activating Nrf2/HO-1 signaling to suppress oxidative stress and inflammation.”
https://www.sciencedirect.com/science/article/abs/pii/S0966327421000794 “Sulforaphane alleviates hepatic ischemia–reperfusion injury through promoting the activation of Nrf-2/HO-1 signaling” (not freely available)
A human equivalent of this study’s 5 mg / kg sulforaphane dose was (.161 x 5 mg) x 70 kg ≈ 56 mg. For comparison, my estimated daily sulforaphane intake from microwaved sprouts is 52 mg.