Five papers on beneficial effects from sulforaphane inhibiting histone deacetylases (HDACs), starting with a 2022 rodent cell study:
“Sulforaphane (SFN) has tissue specificity for subtypes of HDACs that are downregulated. For example:
- In breast cancer cells, HDAC1-3 are inhibited by SFN to induce cell apoptosis;
- In skin cells, HDAC1-4 are regulated by SFN [anti-skin cancer]; and
- In the cochlea, SFN inhibits HDAC2, 4, and 5 [attenuates hearing loss].
In the present study, SFN significantly inhibited HDAC2, 3, and 5 expression and HDACs activity in cardiomyocytes, thereby increasing H3 acetylation levels in the Nrf2 promoter and upregulating Nrf2 expression. Mechanism by which SFN prevents Ang II-induced cardiomyocyte apoptosis:
- Ang II activates oxidative stress by increasing ROS leading to inflammation, oxidative stress and fibrosis in cardiomyocytes.
- SFN prevents Ang II-induced cardiomyocyte apoptosis by inhibiting HDACs to activate Nrf2 and downstream antioxidant genes.
SFN activates Nrf2 by inhibiting HDACs expression and activation.”
https://www.aging-us.com/article/204247/text “Sulforaphane inhibits angiotensin II-induced cardiomyocyte apoptosis by acetylation modification of Nrf2”
A 2021 rodent study found:
“SFN significantly attenuated diabetes-induced renal fibrosis in vivo. SFN inhibited diabetes-induced increase in HDAC2 activity.
Bone morphologic protein 7 (BMP-7) has been shown to reduce renal fibrosis induced by transforming growth factor-beta1. SFN protects against diabetes-induced renal fibrosis through epigenetic up-regulation of BMP-7.”
https://e-dmj.org/journal/view.php?doi=10.4093/dmj.2020.0168 “Sulforaphane Ameliorates Diabetes-Induced Renal Fibrosis through Epigenetic Up-Regulation of BMP-7”
A 2019 human osteosarcoma cell study found:
“SFN inhibits mTOR in a concentration- and time-dependent manner. This inhibition occurs in the presence or in the absence of NRF2.
SFN inhibits HDAC6 and decreases catalytic activity of AKT, which partially explains the mechanism by which SFN inhibits mTOR.”
https://www.sciencedirect.com/science/article/pii/S0944711319302284 “The isothiocyanate sulforaphane inhibits mTOR in an NRF2-independent manner”
A 2022 review cited a 2018 cell study:
“HDAC expression and activity are dysregulated in various diseases including asthma, chronic obstructive pulmonary disease, cancer, cardiac hypertrophy, and neurodegenerative and psychological disorders. HDAC inhibitors could be a potential therapeutic target for many diseases.
In hypertension, aortic stiffness is usually increased and vascular smooth muscle cells (VSMCs) contribute to vascular stiffness. We used VSMCs to test the degree of acetylation of histones in this study.
Sulforaphane weakly inhibited HDAC2 and effectively inhibited HDAC9.”
https://www.sciencedirect.com/science/article/pii/S0006295222002052 “Zinc-dependent histone deacetylases: Potential therapeutic targets for arterial hypertension”
https://www.sciencedirect.com/science/article/abs/pii/S0753332217364636 “Inhibition of class IIa histone deacetylase activity by gallic acid, sulforaphane, TMP269, and panobinostat” (not freely available)