Two 2022 papers, starting with a review of sulforaphane’s effects on intestinal inflammation:

“This review summarizes characteristics of intestinal inflammation, the anti-inflammatory mechanism of sulforaphane (SFN) and its various protective effects on intestinal inflammation, and possible future applications of SFN for promoting intestinal health.

SFN is an effective agonist of Nrf2, and it is also able to inhibit expression of inflammation-related genes by activating Nrf2. This kind of anti-inflammatory mechanism has already been confirmed in treatment of intestinal mucositis using SFN.

The main absorption site of SFN after oral administration is the small intestine, and its achievable dose for the hind intestine may be lower than the expected dose. Although absorbed SFN can reach the large intestine through intestinal blood and other transportation routes, its therapeutic effect on target tissues may not be as efficient as it would be when the expected dose is directly absorbed by hindgut cells.

Considering that there are several predisposing factors that lead to intestinal inflammation, more research on the effect of SFN on intestinal inflammation with different causes and characteristics should be carried out. Appropriate carriers should be selected according to the onset site and related physiological environment, and a scientific and effective intestinal targeted delivery system for SFN needs to be developed.”

https://pubs.rsc.org/en/content/articlelanding/2022/FO/D1FO03398K “The functional role of sulforaphane in intestinal inflammation: a review” (not freely available). Thanks to Professor Lei Zheng for providing a copy.

Reference 89 – Sulforaphane Normalizes Intestinal Flora and Enhances Gut Barrier in Mice with BBN-Induced Bladder Cancer (not freely available) – in the above graphic was cited for:

“The effect of SFN intervention on intestinal injury in mice with bladder cancer was investigated. It was found that SFN significantly reduced tissue damage in the colon and cecum of mice and normalized the imbalance in intestinal flora caused by BBN, which manifested as an increase in Bacteroides fragilis and Clostridium cluster 1, thus promoting SCFA production.

SFN administration upregulated expression of tight junction proteins including ZO-1, occludin, claudin-1 and glucagon-like peptide 2 (GLP2) to repair damage of mucosal epithelium of the colon and caecum, while reducing release of IL-6 and the secreted immunoglobulin A (SIgA). This study showed for the first time SFN’s alleviating effect on intestinal inflammation may be produced by regulating intestinal flora structure, suggesting that the protective effect of SFN on intestinal health could be multidirectional.”

That study’s 2022 follow-on rodent study also used oral sulforaphane doses:

“This study was undertaken to assess the potential efficacy of SFN in ameliorating dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice and to elucidate underlying mechanisms.

Male C57BL/6 mice were treated with various doses of SFN (2.5, 5, 10, and 20 mg/kg body weight). In DSS colitis mice, the hallmarks of disease observed as shortened colon lengths, increased disease activity index scores and pathological damage, higher proinflammatory cytokines and decreased expression of tight junction proteins, were alleviated by SFN treatment.

• 5, 10, and 20 mg/kg/day of SFN treatment significantly ameliorated inflammatory damage in mice colon tissue when compared to the colitis group.
• 5, 10, and 20 mg/kg/day of SFN remarkably mitigated morphological alterations and protected colonic tissue integrity.
• Nrf2 expression was increased significantly by 5, 10, and 20 mg/kg/day of SFN treatment.
• SFN partially restored perturbed gut microbiota composition, and increased production of volatile fatty acids (especially caproic acid) induced by DSS administration.
• The contents of butyric acid, iso-butyric acid, valeric acid, and iso-valeric acid were all decreased in DSS-induced colitis mice and in 2.5 mg/kg/day of the SFN treatment group, whereas this decreased tendency was reversed by 10 and 20 mg/kg/day of SFN.

A proposed mechanism by which SFN protects against colitis:

Nuclear factor (erythroid-derived 2)-like 2 (Nrf2), Signal Transducer and Activator of Transcription 3 (STAT3), and Phase II enzyme UDP-glucuronosyltransferase (UGT) were involved in the protective effect of SFN against DSS-induced colitis.

Nrf2 activation followed by STAT3 signaling pathway play a pivotal role in the protective effect of SFN on colitis. SFN can be considered a potential candidate in the treatment of IBD.”

https://www.frontiersin.org/articles/10.3389/fnut.2022.893344/full “The Protective Effect of Sulforaphane on Dextran Sulfate Sodium-Induced Colitis Depends on Gut Microbial and Nrf2-Related Mechanism”

A human equivalent dose of the second paper’s oral dose of 20 mg sulforaphane / kg body weight is (.081 x 20 mg) x 70 kg = 113 mg. Per Estimating daily consumption of broccoli sprout compounds, I ate about half that every day by microwaving 3-day-old broccoli sprouts through Week 56, when I cut back to about 35 mg a day. I dialed that back in Week 87 to about 17 mg a day (100 μmol), which is used in a plethora of studies.

I’ve never had ulcerative colitis or inflammatory bowel disease. If I would be diagnosed with either, it would take about five minutes to get back to this study’s equivalent of 10 mg / kg body weight with broccoli seeds and sprouts.

Doubling that to 20 mg may involve taking supplements, though. Haven’t checked for commercial availability lately, but I’ve read a dozen or so studies on encapsulating sulforaphane so that it could reach the colon.