Black Seed Oil (Nigella Sativa) has Thymoquinone and has many good properties. There are a lot of articles available that highlight the benefits of Black Seed Oil.
Here is a sample
acta.bibl.u-szeged.hu/62036...
Thymoquinone prevents neurodegeneration against MPTP in vivo
model of Parkinson’s disease and modulates α-synuclein aggregation
in vitro
Mustafa T. Ardah, Madiha Mohieldine Merghani and M. Emdadul Haque*
Department of Biochemistry, College of Medicine and Health Sciences, United Arab Emirates University, PO Box -
17666, Al Ain, UAE
*E-mail: ehaque@uaeu.ac.ae
Parkinson's disease (PD) is a common neurodegenerative disease, characterized by
progressive dopaminergic neurodegeneration with concomitant increase in oxidative
stress and subsequent neuroinflammation in the substantia nigra pars compacta (SNc)
of the midbrain. Studies are currently focusing on targeting neuroinflammation and
oxidative stress to effectively treat PD. This study evaluated the neuroprotective effect
of TQ, one of the active compounds in the black seed, against 1-methyl-4-phenyl
1,2,3,6 tetrahydropyridine (MPTP)-induced PD mouse model. Here, TQ treatment for 1
week (dose, 10 mg/kg b. wt.) prior to MPTP (25 mg/kg b. wt.) was performed. MPTP
administration caused decreased activities of superoxide dismutase, catalase and
depletion of reduced glutathione, with a concomitant rise in the lipid peroxidation
product. It significantly increased pro-inflammatory cytokines and elevated
inflammatory mediators such as COX-2 and iNOS in the striatum. Immunohistochemical
analysis revealed dopamine neuron loss in the SNc area and decreased dopamine
transporters in the striatum following MPTP administration. However, TQ treatment
significantly rescued dopaminergic neuronal loss and dopamine transporters. TQ
treatment further prevented glutathione depletion, inhibited lipid peroxidation, and
attenuated pro-inflammatory cytokines. TQ also reduced the increased levels of
inflammatory mediators, such as COX-2 and iNOS. In vitro analysis found that TQ
significantly inhibits α-synuclein aggregation and prevents cell death induced by pre-
formed fibrils. Thus, TQ not only scavenges the MPTP-induced toxicity but also
prevents α-synuclein-fibril formation and associated toxicity