Bolt Note: This is about Nigella Sativa. I use the seeds (ground in a coffee grinder. 2 grams a day with some water).
The mechanistic role of thymoquinone in Parkinson's disease: focus on neuroprotection in pre-clinical studies pubmed.ncbi.nlm.nih.gov/334...
Abstract
Thymoquinone (TQ) is one of the leading phytochemicals, which is abundantly found in Nigella sativa L. seeds. TQ exhibited various biological effects such as antioxidant, anti-inflammatory, antimicrobial, and anti-tumoral in several pre-clinical studies. Parkinson's disease (PD) is a long-term neurodegenerative disease with movement difficulties, and the common feature of neurodegeneration in PD patients is caused by dopaminergic neural damage in the substantia nigra pars compacta. The neuroprotective activity of TQ has been studied in various neurological disorders. TQ-mediated neuroprotection against PD yet to be reported in a single frame; therefore, this review is intended to narrate the potentiality of TQ in the therapy of PD. TQ has been shown to protect against neurotoxins via amelioration of neuroinflammation, oxidative stress, apoptosis, thereby protects neurodegeneration in PD models. TQ could be an emerging therapeutic intervention in PD management, but mechanistic studies have been remained to be investigated to clarify its neuroprotective role.
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Traumatic brain injury and microglial activation are pathological markers that lead to several neural disorders, that is, Alzheimer's disease and Parkinson's disease. Higher concentrations of free radicals and pro-inflammatory cytokines are released during the chronic activation of microglia. Thymoquinone (12.5 μM for 24 hr) phytochemical work as preventive agent when treated with interferon-gamma (IFN-γ)-activated BV-2 microglial cells and lipopolysaccharide (LPS) by momentously enhancing the expression of 4 antioxidant, neuroprotective proteins: glutaredoxin-3, biliverdin reductase A, 3-mercaptopyruvate sulfurtransferase, and mitochondrial ion protease, as well as also lowering the expression of inflammatory cytokines, IL-6, IL-2, IL-4, IL-10, and IL-17a, respectively. Additionally, thymoquinone also downregulated the chemokine (CC) motif ligand 5, chemokine (CC motif) ligand 3, and complement factor B (CFB) (Cobourne-Duval et al., 2018).
Thymoquinone has protective role on arsenic (10 mg/kg/body weight; p.o.)-induced toxicity in hippocampi of Wistar rats. It momentously decreased the mitochondrial dysfunction, mitochondrial membrane potential (Δψm), intracellular ROS generation, and apoptotic events (Firdaus et al., 2018). Different researchers and investigators found that different doses of thymoquinone at the rate of 2.5 and 10 mg/kg in rats exhibited neuromodulatory effect via inducing apoptotic cell death and Aβ formation resulting from glutamate administration (Cascella et al., 2018; Farkhondeh et al., 2018; Fouad et al., 2018). Thymoquinone also prevents rats from the progression of Parkinson's disease induced by rotenone. The supplementation of thymoquinone at the rate of 7.5 and 15 mg kg day−1, po, in male Wistar rats prevented rotenone-induced motor defects and caused changes in the dynamin-related protein-1, parkin, dopamine, and TH levels in the striatum and substantia nigra of dopaminergic areas (Ebrahimi et al., 2017). Similarly, encapsulated thymoquinone in polylactic coglycolic acid chitosan nanoparticles considerably enhanced the locomotor activity and grip strength and lowered the ischemia infarct volume in the middle cerebral artery-occluded rats (Xiao et al., 2016). Ramachandran and Thangarajan (2016) investigated that effective role of solid lipid nanoparticles encapsulated thymoquinone (10 and 20 mg/kg) against 3-nitropropionic acid-induced huntington's disease animals via multiple mechanisms such as improving the muscle strength, movement, rigidity, and memory performances, attenuating the levels of NO, LPO, and protein carbonyls in 3-NP-induced animals, controlling the mitochondrial SDH inhibition, restoring the antioxidant defense system, and alleviating anticholinergic effect upon 3-NP induction. Moreover, thymoquinone also plays effective role against 3-NP toxicity by protecting the striatal structural microelements (Ramachandran & Thangarajan, 2016). In experimental rats, orally administrated thymoquinone (5 mg kg−1 day−1) enhanced the neuron density in contralateral hippocampal regions (CA1, CA2-3, and CA4) and lowered malondialdehyde level (Gülşen et al., 2016). With acrylamide-induced neurotoxicity in both in vitro and in vivo of male Wistar rats, thymoquinone dose-dependently (2.5, 5, and 10 mg/kg IP) significantly decreased abnormalities and lowered the level of MDA in cerebral cortex (Mehri et al., 2014). Thymoquinone also rescued dopaminergic neurons and decreased the release of lactate dehydrogenase, increased the mitochondrial membrane potential, enhanced lysosomal degradation, and inhibited mitochondria-mediated apoptotic cell death (Radad et al., 2015). Thymoquinone (10 mg/kg) supplemented to male Wistar albino rats with spinal cord injury (SCI) lowered the histological features of spinal cord damage (Üstün et al., 2014). In animals, pentylenetetrazole (50 mg/kg) has been used to induce generalized seizures and mortality, prolong the onset of seizures, and lower the polyspike and epileptiform discharges and high-grade seizures. It also caused reduction in calmodulin-dependent protein kinase II (CaMKII), suppression in phosphorylation of cAMP response element-binding protein (CREB) in cortex and hippocampus, and decline in gamma-aminobutyric acid B1 receptor (GABAB1R) levels. It also enhanced the Bax, decreased Bcl-2 expression, and activated caspase-3. Thymoquinone in combination with vitamin C reversed these changes (Ullah et al., 2015). In unilateral intrastriatal 6-hydroxydopamine (6-OHDA)-lesioned rats, diverse concentrations of thymoquinone (5 and 10 mg/kg BW) caused reduction in the number of neurons on the left side of the substantia nigra pars compacta, nitrite, and MDA level, and improved turning behavior (Sedaghat et al., 2014). In primary cultured cerebellar granule neurons, supplemented thymoquinone with different doses (0.1 and 1 μM) lessened the β-amyloid peptide 1–40 sequence by preventing neurotoxic effects and neural cell death (Ismail et al., 2013). Multiple evidences and findings are reported by different researchers and investigators and found preventive role against Alzheimer's amyloid-β peptide (Aβ)-induced neurotoxicity in in vitro study in rat primary neurons. There are multiple pathways such as attenuation of Aβ1-42-induced neurotoxicity, suppression of mitochondrial membrane potential depolarization, inhibition of reactive oxygen species production, suppression of Aβ1-42 aggregation, and restoration of synaptic vesicle recycling inhibition (Alhebshi et al., 2013; Kanter, 2011; Khan et al., 2012).
GC-MS Analysis of Nigella Sativa Seed Extract and Its Ameliorative Effects on Transgenic Drosophila Model of Parkinson Disease 2021 ijisrt.com/assets/upload/fi...
The ethanolic extract of Nigella sativa seed (200 and 400 mg/kg orally) was investigated in chlorpromazine induced experimental animal model of catalepsy. The cataleptic score was significantly reduced (P<0.001) by the extract. The extract also improved the depleted levels of reduced glutathione (P<0.001) and total protein (P<0.001) and decreased the elevated levels of lipid peroxidation in brain tissue (P<0.001) [35].
Thymoquinone improved behavioral and cellular abnormalities and markers of oxidative stress in an experimental model of early Parkinson’s disease in rats. The unilateral intrastriatal 6- hydroxydopamine (6-OHDA)-lesioned rats were daily pretreated orally with thymoquinone at doses of 5 and/or 10 mg/Kg three times at an interval of 24 h.
Thymoquinone pretreatment significantly improved turning behavior, prevented loss of neurons in substantia nigra and lowered level of MDA, which. suggested that thymoquinone could afford neuroprotection in neuro-degenerative disorders including Parkinson’s disease [36].
Black Seed Oil (Nigella sativa, Black Cumin) is an annual herb and spice belonging to the Ranunculaceae (Buttercup) family of flowering plants. nootropicsexpert.com/black-...
I updated the first post. I don't use the oil. I am cheap and not convinced it is any better than the seeds. The seeds are cheap. I just grind them in a coffee grinder and have 2 grams mixed with about 4 ounces of water.
Is black cumin the same as cumin seed sold as a culinary spice?~
I don't have time to look up your post in Hashimoto's/autoimmunity in PD (wish this site were easier to search), but you may be interested in this article on MSA and Sjogren's: pubmed.ncbi.nlm.nih.gov/326...
Black seed is the spice. I buy Terrasoul Superfoods Organic Black Cumin Seeds (Nigella Sativa), which is raw seeds. I grind them in a coffee grinder. amazon.com/gp/product/B072F...
Thanks for the link. It does seem to be use as a spice, but it is not the same as the cumin seed I already have in my cupboard. I have heard a lot about black seed oil and have been thinking about trying it.
Nigella sativa is an excellent antibiotic, and it is rich in antioxidants, antimicrobics, and antifungals. Moreover, it contains numerous minerals, such as calcium, potassium, iron, and phosphor. In addition to amino acids, such as lysine, tyrosine, leucine, proline, and methionine. Using Nigella sativa helps improve digestive system function, and relieve chronic constipation.
Thanks. I just wanted everybody to be able to see the ingredients. I take a lot of things not in there (but I could see using this to lower the number of supplements).
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