Protective Effects of 6-(Methylsulfinyl)hexyl Isothiocyanate on Aβ1-42-Induced Cognitive Deficit, Oxidative Stress, Inflammation, and Apoptosis in Mice.
Fabiana MorroniGiulia SitaAgnese GraziosiEleonora TurriniCarmela FimognariAndrea TarozziRaffaella ArfèPublished in: International journal of molecular sciences (2018)
Alzheimer's disease (AD) is the most common form of dementia among older people. Although soluble amyloid species are recognized triggers of the disease, no therapeutic approach is able to stop it. 6-(Methylsulfinyl)hexyl isothiocyanate (6-MSITC) is a major bioactive compound in Wasabia japonica, which is a typical Japanese pungent spice. Recently, in vivo and in vitro studies demonstrated that 6-MSITC has several biological properties. The aim of the present study was to investigate the neuroprotective activity of 6-MSITC in a murine AD model, induced by intracerebroventricular injection of β-amyloid oligomers (Aβ1-42O). The treatment with 6-MSITC started 1 h after the surgery for the next 10 days. Behavioral analysis showed that 6-MSITC ameliorated Aβ1-42O-induced memory impairments. The decrease of glutathione levels and increase of reactive oxygen species in hippocampal tissues following Aβ1-42O injection were reduced by 6-MSITC. Moreover, activation of caspases, increase of inflammatory factors, and phosphorylation of ERK and GSK3 were inhibited by 6-MSITC. These results highlighted an interesting neuroprotective activity of 6-MSITC, which was able to restore a physiological oxidative status, interfere positively with Nrf2-pathway, decrease apoptosis and neuroinflammation and contribute to behavioral recovery. Taken together, these findings demonstrated that 6-MSITC could be a promising complement for AD therapy.
Keyphrases
- oxidative stress
- diabetic rats
- cerebral ischemia
- dna damage
- reactive oxygen species
- ischemia reperfusion injury
- induced apoptosis
- signaling pathway
- high glucose
- traumatic brain injury
- type diabetes
- minimally invasive
- cell proliferation
- mild cognitive impairment
- endoplasmic reticulum stress
- drug induced
- ultrasound guided
- working memory
- cell cycle arrest
- mesenchymal stem cells
- lipopolysaccharide induced
- adipose tissue
- bone marrow
- blood brain barrier
- metabolic syndrome
- insulin resistance
- smoking cessation
- heat shock protein
- percutaneous coronary intervention
- replacement therapy
- heat shock