Table 1.
Summary of the effects and mechanisms of action of sulforaphane (SFN), moringin (MG), phenethyl isothiocyanate (PEITC), 6-(methylsulfinyl) hexyl ITC (6-MSITC) and erucin (ER) on severe inflammatory and neurodegenerative diseases (NDDs).
| ITCs or Extract | NDD or Models | Effect on NDDs | Mechanism of Action | Reference |
|---|---|---|---|---|
| SFN | AD (in vitro) SH-SY5Y Human neuroblastoma cell line | Abolished apoptosis | Modulation of Bax/Bcl2 and Nrf2 pathways | [27] |
| AD (in vitro) Neuro-2A & N1E-115 murine neuroblastoma cell line | Increased proteasome activity | Enhancement of Nrf2 pathway | [29] | |
| AD (in vitro) cell line | Increased proteasome activity | Enhancement of Nrf2 pathway | [30] | |
| AD (in vitro) HeLa & COS-1 Cell line | Increased proteasome activity & proper folding | Triggering Aβ-fragment’s clearance | [28] | |
| AD (in vivo) mice induced by AlCl3 & D-Galactose | Ameliorated cognitive impairment | Modulation of Nrf2/ARE pathway | [32] | |
| AD (in vivo) rat model | Improved cognitive function | Modulation of Ach transferase activity | [34] | |
| AD (in vivo) rat model | Ameliorated cognitive impairment | Modulation of pro-inflammatory production via Nrf2/ARE pathway | [35] | |
| PD (in vitro) N1E-115 murine neuroblastoma cell line | Abolished apoptotic pathway & improve cognitive function | Modulation of phase II antioxidant enzymes | [38] | |
| PD (in vitro) PC-12 cell line | Stopped apoptosis | Modulation of pro-inflammatory markers production pathway via Nrf2/ARE pathway | [39] | |
| PD (in vitro) SH-SY5Y Human neuroblastoma cell line | Abolished apoptosis | Modulation of Nrf2/ARE pathway | [40] | |
| PD (in vivo) rat model | Decreased the disease progression | Modulation of pro-inflammatory & apoptotic pathway via activation of ERK1/2 | [36] | |
| M. oleifera crude extract | AD (in vivo) rats colchicine induction | Ameliorated memory impairment | Up-regulation of phase II antioxidant enzymes | [46] |
| AD (in vivo) rats Ethyl choline induction | Improved spatial memory and reduce neuronal cell death | Up-regulation of SOD & CAT | [47] | |
| MG | CIR (in vivo) rats model | Improved cognitive function | Modulation of pro-inflammatory biomarkers production & Nfr2/ARE pathway | [44] |
| ALS (in vivo) rats model | Delayed the disease onset | Modulation of expression of vital proteins involved in the disease pathology such as Nrf2, iNOS & PARP, and modulation of apoptotic pathway | [45] | |
| MS (in vivo) mouse model | Abolished series of inflammation | Down regulation of pro-inflammatory & production of oxidative species as well as modulation of apoptotic pathway | [49] | |
| SCI (in vivo) rats model | Protected neuronal death | Modulation of up-regulated inflammatory markers | [52] | |
| PEITC | NDD (in vitro) cell lines | Abolished inflammation | Initiation of Nrf2 translocation and modulation of Nrf2/ARE signaling pathway | [53] |
| NDD (in vivo) transgenic mice model | Alleviated severe pathological condition | Restoration of Nrf2 expression | [60] | |
| 6-MSITC | NDD (in vitro) cell lines | Slow down inflammation | Enhancement of Nrf2 activity and slow down expression of pro-inflammatory biomarkers | [65] |
| NDD (in vivo) rat model | Stopped inflammation | Enhancement of Nrf2/ARE complex formation and their signaling pathway | [66] | |
| PD (in vivo) animal model | Decreased apoptosis, increased cognitive function, improved behavior | Modulation of Nrf2/ARE pathway | [54] | |
| ER | NDD (in vitro) cell lines | Stopped inflammation | Counteraction of pro-inflammatory markers’ expression | [71] |
| NDD (in vitro) cell lines | Decreased inflammation | Inhibition of NF-κB signaling pathway | [53] | |
| NDD (in vitro) SH-SY5Y cell lines | Slow down apoptosis | Increase expression of GSH and its activities | [70] | |
| NDD (in vitro & in vivo) cell lines and animal models | Reduced inflammation | Counteraction of JNK, Erk1/2 and P38 signaling pathway by Nrf2 | [72] |
NDD represents neurodegenerative diseases; AD, Alzheimer’s disease; PD, Parkinson’s disease; ALS, Amyotrophic lateral sclerosis; MS, Multiple sclerosis; SCI, Spinal cord injury; CIR, Cerebral ischemia/reperfusion; ITCs, Isothiocyanates; SOD, Superoxide dismutase; CAT, catalase; iNOS, inducible nitric oxide synthase; PARP, poly ADP ribose polymerase. NB: severe inflammation lead to up-regulation of cytokines and other pro-inflammatory markers which result in neurodegenerative diseases if not arrested at early stage.