Hericium erinaceus (HE) is a common edible mushroom consumed in several Asian countries and considered to be a medicinal mushroom with neuroprotective effects.
Erinacine A (EA) is a bioactive compound in Hericium erinaceus mycelium (HEM) that has been shown to have a neuroprotective effect against neurodegenerative diseases, e.g., Parkinsonβs disease (PD). Although the etiology of PD is still unclear, neuroinflammation may play an important role in causing dopaminergic neuron loss, which is a pathological hallmark of PD. However, glial cell activation has a close relationship with neuroinflammation.
Thus, this study aimed to investigate the anti-neuroinflammatory and neuroprotective effects of EA on lipopolysaccharide (LPS)-induced glial cell activation and neural damage in vitro and in vivo. For the in vitro experiments, glial cells, BV-2 microglial cells and CTX TNA2 astrocytes were pretreated with EA and then stimulated with LPS and/or IFN-Ξ³.
The expression of proinflammatory factors in the cells and culture medium was analyzed. In addition, differentiated neuro-2a (N2a) cells were pretreated with EA or HEM and then stimulated with LPS-treated BV-2 conditioned medium (CM).
The cell viability and the amount of tyrosine hydroxylase (TH) and mitogen-activated protein kinases (MAPKs) were analyzed. In vivo, rats were given EA or HEM by oral gavage prior to injection of LPS into the substantia nigra (SN). Motor coordination of the rats and the expression of proinflammatory mediators in the midbrain were analyzed. EA pretreatment prevented LPS-induced iNOS expression and NO production in BV-2 cells and TNF-Ξ± expression in CTX TNA2 cells.
In addition, both EA and HEM pretreatment significantly increased cell viability and TH expression and suppressed the phosphorylation of JNK and NF- ΞΊB in differentiated N2a cells treated with CM. In vivo, both EA and HEM significantly improved motor dysfunction in the rotarod test and the amphetamine-induced rotation test and reduced the expression of TNF-Ξ±, IL-1Ξ² and iNOS in the midbrain of rats intranigrally injected with LPS.
The results demonstrate that EA ameliorates LPS-induced neuroinflammation and has neuroprotective properties.
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Nearly a year of experimentation since Iberia's first prototype model of an invasive BMI inhibitor chip has accumulated a sizeable log of bugs and patches that require fixing. The more concerning attributes that have been discovered include:
- Incoherent, slurred speech (~45%)
- Disproportionate appetite; patients cannot be sated (<15%)
- Absence of conventional fatigue following strenuous activity (~33%)
- Congenital analgesia (>95%)
- Phlegmatic disposition (~85)
- Lapses of situational cognitiveness awareness followed by heightened stress (<0.8%)
- Disregard for Workplace Command instructions (~0.75%)
Coronal examination of the basolateral amygdaloid complex identified improperly generated dopaminergic neurons across the ventromedial sector of the lateral nucleus and piriform cortex in 82.025% of patients that tested positive for five or more listed symptoms (N=740).
Artificial replacements for these areas that have been grown in vitro were transplanted in replacement for the persistent vegetative cohort (N=67) to moderate success. Though the surviving patients experienced no relapses in the following four to six months, the middling survival rate for the neurosurgery (40%) implicates that this attempted stratagem is a band-aid solution at best that must be remedied at the earliest convenience.
###CNS scan depicting structural resolution to in vivo neurotrophic factor abberations
Whilst the inhibitor chip will remain a vital servicing tool instilled throughout the Workforce, a physical structure to ensure maximum control over amygdala functionality will be set in place to prevent deviations from idealised performance. The unit listed above will not serve as the singular point of control, in case of breakage or failure, but it will add a 65km range for control whilst preventing further complications.
I have never heard about this development in the science of chronic pain. Read and share with every chronic pain warrior you know. Fascinating and affirming. No paywall.
Not sure if this is allowed here, so remove if not.
First post, new to this community and my lab.
Does anyone have any protocols or links to articles on freezing rodent glial cells?
I need to long term store glial cells for later neuronal cultures and am struggling finding information. Iβm kind of at a loss here.
Any help would be appreciated.
Thanks.
I need to write an essay about glial cells, has to be original and stuck on what topic to write it on. Topics linked with pathology like epilepsy or psychiatric diseases interest me but not sure what about those topics I would write, but also want to hear some ideas from other people.
Edit : I also just thought about maybe substance use disorder and addiction and the role of glia in that.
