Potential of Sulforaphane as a Natural Immune System Enhancer: A Review

Abstract

Brassicaceae are an outstanding source of bioactive compounds such as ascorbic acid, polyphenols, essential minerals, isothiocyanates and their precursors, glucosinolates (GSL). Recently, GSL gained great attention because of the health promoting properties of their hydrolysis products: isothiocyanates. Among them, sulforaphane (SFN) became the most attractive one owing to its remarkable health-promoting properties. SFN may prevent different types of cancer and has the ability to improve hypertensive states, to prevent type 2 diabetes-induced cardiomyopathy, and to protect against gastric ulcer. SFN may also help in schizophrenia treatment, and recently it was proposed that SFN has potential to help those who struggle with obesity. The mechanism underlying the health-promoting effect of SFN relates to its indirect action at cellular level by inducing antioxidant and Phase II detoxifying enzymes through the activation of transcription nuclear factor (erythroid-derived 2)-like (Nrf2). The effect of SFN on immune response is generating scientific interest, because of its bioavailability, which is much higher than other phytochemicals, and its capacity to induce Nrf2 target genes. Clinical trials suggest that sulforaphane produces favorable results in cases where pharmaceutical products fail. This article provides a revision about the relationship between sulforaphane and immune response in different diseases. Special attention is given to clinical trials related with immune system disorders.

Keywords: cellular mechanism; immunological response; sulforaphane.

Figure 1

Myrosinase—glucoraphanin system in Brassicaceae plants. Glucosinolates are located in specialized glucosinolate-containing cells, while myrosinase is stored in the vacuoles of the myrosin cells. After mechanical disruption of plant tissue, the substrate and enzyme come in contact and the hydrolysis occurs, resulting in different products, among which it is found sulforaphane [7].

Figure 2

Formation and metabolization of sulforaphane. Sulforaphane (SFN) is formed by the hydrolysis of glucoraphanin catalyzed by either plant or bacterial myrosinase. After intake, SFN is metabolized through the mercapturic acid pathway. Initially, isothiocyanates are conjugated with glutathione (GSH) in a glutathione transferase (GST)-catalyzed reaction. Then, successive cleavage reactions catalyzed by γ-glutamyltranspeptidase, cysteinylglycinase, and N-acetyltransferase occur to generate sulforaphane-N-acetylcysteine (SFR-NAC) [8].

Figure 3

Mechanism of inflammatory response suppression induced by sulforaphane in bacteria-infected monocytes.

Figure 4

Chemoprotective and chemotherapeutic mechanisms of SFN in cancer cells. SFN exerts chemoprevention by inducing HO-1 and Phase II enzymes, and increasing GSH concentration expression and activating NK cells, as well as downregulating pro-inflammatory cytokines. In both cases, the effect on immune system is mediated by transcription factors Nrf2 and Nfκβ.