Abstract
Allyl isothiocyanate (AITC), present in Wasabia japonica (wasabi), is an aliphatic isothiocyanate derived from the precursor sinigrin, which is a glucosinolate present in vegetables of the Brassica family. Traditionally, it has been used to treat rheumatic arthralgia, blood circulation, and pain. This study focuses on its anti-apoptotic activity through the regulation of lipopolysaccharide (LPS)-induced neuroinflammation. Furthermore, we assessed its neuroprotective efficacy, which it achieves through the upregulation of nerve growth factor (NGF) production. Pretreatment with AITC significantly inhibited inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression, decreased tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), prostaglandin E2 (PGE2), and nitric oxide (NO) production in activated microglia, and increased the nerve growth factor (NGF) and neurite outgrowth in neuroblastoma cells. AITC inhibited the nuclear factor (NF-κB-mediated transcription by modulating mitogen activated protein kinase (MAPK) signaling, particularly downregulating c-Jun N-terminal kinase (JNK) phosphorylation, which was followed by a reduction in the TNF-α expression in activated microglia. This promising effect of AITC in controlling JNK/NF-κB/TNF-α cross-linking maintains the Bcl-2 gene family and protects neuroblastoma cells from activated microglia-induced toxicity. These findings provide novel insights into the anti-neuroinflammatory effects of AITC on microglial cells, which may have clinical significance in neurodegeneration.
Highlights
Neuroinflammation and neuronal cell death are the major causes of most neurological diseases [1]
allyl isothiocyanate (AITC) and sinapic acid (SA) were screened for their ability to inhibit nitric oxide (NO) production and their cell viability against LPS-activated BV2 cells; together with its extract wasabi, AITC was found to be more potent without cellular toxicity (Figure 1)
This showed that the presence of significant amounts of SA and AITC in the wasabi extract might have played an important role in the amelioration of irritable bowel syndrome-like symptoms in a zymosan-induced mouse model [28]
Summary
Neuroinflammation and neuronal cell death are the major causes of most neurological diseases [1]. The most common neurodegenerative and neuroinflammatory conditions are Alzheimer’s disease (AD) and Parkinson’s disease (PD) [3,4] Injury and toxins, such as lipopolysaccharide (LPS), trigger the defense systems of the brain, which leads to neurodegeneration [5]. LPS induces an inflammatory cascade in microglia through an increased production and accumulation of cytotoxic and inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (PGE-2), arachidonic acid, eicosanoids, and reactive oxygen species (ROS). It elevates the levels of proinflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), which are responsible for neuronal death [6,7]. Controlling microglial activation can be a therapeutic approach in the treatment of neuroinflammation as well as neurodegenerative conditions
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
