Don't do anything with this until human testing is done.
Who amongst your stroke medical 'professionals' can look at this and see that human testing needs to be done while also accounting for rodent inflammation is not the same as human inflammation?
Or don't you have anymore smart enough to see this?
NIGELLA SATIVA SEED OIL MITIGATES LIPOPOLYSACCHARIDES-INDUCED NEURODEGENERATION AND COGNITIVE IMPAIRMENT IN MICE
Open AccessDOI:https://doi.org/10.1016/j.ibneur.2023.08.657
Background:
The hallmark of neurodegenerative diseases, such as Alzheimer’s disease, is chronic neuroinflammation. Nigella sativa
seed oil popularly called black seed oil (BSO) is known for its
anti-inflammatory and antioxidant properties. However, the mechanisms of
its neuroprotective effect against neuroinflammation-induced
neurodegeneration and memory dysfunction has not fully been explored. We
thus evaluated its neuroprotective effect on lipopolysaccharides
(LPS)-induced neurodegeneration and cognitive dysfunction in mice.
Outline of Material and Methods:
Twenty-eight Swiss mice were assigned into four groups (n=7): group1
(vehicle), group2 (BSO 0.5mL/kg), group3 (Donepezil/5mg/kg), group4
(vehicle). Animals in different groups were administered with vehicle,
BSO and donepezil for fourteen days. Starting from day 8, sixty-minutes
after administration of vehicle/BSO/donepezil, animals in groups 2, 3
and 4, received LPS (500µg/kg, i.p.) consecutively for seven days.
Twenty-four hour after treatment on day fourteen, Novel Object
Recognition, (NORT) Y-maze, were used to assess cognitive functions;
elevated plus maze, open field and light and dark box tests were used to
assess anxiety. Tumor necrosis factor-α (TNF-α), interlukin-1β,
acetylcholinesterase were assessed using ELISA technique, microglia,
beta-amyloid, choline acetyltransferase (ChaT), synaptophysin, were
quantified using immunohistochemistry, gene expressions of IL-10 and
β-secretase were measured with quantitative Polymerase Chain Reaction.
Cox Golgi staining technique was used to evaluate hippocampal damage.
Results:
LPS significantly impaired performance in the Y-maze and NORT and
induced behavioural abnormalities, compared to control. These were all
ameliorated by treatment with BSO. BSO also significantly (P<0.05)
reduced LPS-induced pro-inflammatory cytokines, acetylcholinesterase and
expressions of microglia and β-secretase/mRNA in hippocampus and
prefrontal cortex. In addition, BSO increased expressions of IL-10/mRNA
gene, ChaT, synaptophysin in hippocampus and PFC. BSO significantly
(P<0.05) decreased neurodegeneration of dendrite and neuronal cells
in the hippocampus of LPS-treated mice.
Conclusion:
Our results suggest that BSO may possess neuroprotective effect against
LPS-induced neurodegeneration and cognitive impairment via mechanisms
involving its anti-inflammatory properties.
Declaration of Interest Statement: None
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