Advances in the study of the mechanism of the protective mechanism of small-carinatine-alkali on neurons.

Small pyridine is atyline alkaloid extracted from plants such as jaundice and jaundice, with poor absorption rate of the intestinal wall after oral administration and rapid liver metabolism.
in addition, it can penetrate the blood-brain barrier and accumulate in the hippocampus to interact with neurons.
is easy to bind to proteins, and its toxicity is mainly related to intravenous administration.
aulose has a therapeutic effect on cardiac hypertrophy, vascular remodeling and inflammation, insulin resistance, hyperlipidemia, and chlamydia pneumonia.
cannot be ignored for its potential to treat neurological diseases such as Alzheimer's disease, Parkinson's disease and cerebral ischemia, which have anti-neurotoxicity, anti-neuropsychoticanda and anti-neurodegenerative pharmacological properties.
literature reports that the small jaundice is involved in the process of anti-neuronal damage, but the study of potential mechanisms may be repeated or overlapping.
classical pathways include survival and apoptosis pathways, inflammation involved in cerebral ischemia and reperfusion of in vitro or in vivo models.
other pathways similar to the p53 pathways involved in periodic stagnation in the multiple sclerosis model and the ERK1/2 pathways that inhibit the expression of beta-secretion enzymes.
by summarizing the applications of osteogenic in the brain ischemia/reperfusion, oxidative stress, Alzheimer's disease, Parkinson's disease, neurotoxicity, experimental autoimmune encephalomyelitis, epilepsy, diabetic peripheral neuropathy and traumatic brain injury, the possible mechanism of neutrino-alkali neuroprotection is explored, and the clinical application of neutrinobase neuron protection is facilitated.
1 PI3K/AKT/Bcl-2 pathway and apoptosis Akt are a serine/suthine kinase, also known as protein kinase B (PKB/Akt), which can act as a key regulatory factor for cell survival, growth, apoptosis and proliferation when it comes to growth factors and extracellular stimulation. the activation of
Akt is usually mediated by PI3K, which is collected on the mass film and binds to P13K products involving exposed phosphorylation sites.
apoptosis is an important event in neurodegenerative diseases, and chlorpyrifos can be used as a therapeutic agent to reduce memory disorders and motor dysfunction in Parkinson's disease by preventing hippocampus apoptosis and the loss of black striatum dopamine neurons.
Akt/PKB as a key medium for PI3K-initiated signal conduction, performing various tasks by promoting the phosphorylation of many cell substrates inhibited by apoptosis.
in NSC34 motor neuron-like cells, the anti-apoptosis function induced by the osteyl base by increasing the survival of the anti-apoptotic protein Bcl-2 and motor neuron protein, as well as by reducing the apoptosis protein.
amalyne has been shown to prevent apoptosis in neuronal cells in the hippocampus of mice with Parkinson's disease, enhanceb-2 expression after treatment and reduce Bax expression, and further improve short-term memory disorders.
is also known as the expression of cytochrome C and the recovery of Bcl-2/Bax and Bcl-xL/Bax ratios to combat Alzheimer's-induced apoptosis.
2 Akt/Nrf-2/HO-1 pathway and the neuroprotective action of oxidizing stress in the jaundice are often combined with anti-neurotoxicity of anti-inflammatory and anti-cell apoptosis activity, and many studies have shown that the enhancement of antioxidant defense is also necessary for oxidative stress protection.
the antioxidant stress effect of the ostrichaline is beneficial to improve the seizure and memory disorders of the epileptic model of the mice induced by the hair-fruit-scented alkali.
oxidative stress by increasing the production of lipid peroxide and nitric oxide and reducing the presence of glutathione and various antioxidant enzymes, i.e. superoxide dismutase, hydrogen peroxide enzymes, glutathione peroxidase and glutathione reductase.
the small linen to relieve oxidative stress in diabetic rats induced by streptococcus, reduced dismutase activity and increased nitrite levels.
the overexpression of tau protein in HEK293 cells, the increase of calyculin A-induced propylene dialdehyde and the decrease in the activity of the superoxide dismutase.
in the peptide-induced temporal lobe epilepsy rat model, the chlorpyrifos improved lipid peroxide and nitrite levels, but did not affect the superoxide dismutase levels.
Nrf-2 and NF-B are two important transcription factors that maintain the cell's coordinated response to oxidative stress and inflammation.
under stress conditions, Nrf2 dissoced from Keap1 and transposed into the nucleus to activate the antioxidant reaction element (ARE) and to increase the transcription OF HO-1 of Nrf2 regulatory genes such as HO-1 (hemoglobin-oxygenase-1) which is the core of Nrf2-mediated NF-B inhibition.
3 GSK-3 (Akt or Wnt) Pathway Glycol synthase 3 (GSK-3) inhibited by mediating its phosphorylation, or mTOR signalconducting or through Wnt signalconduction, the visorol phosphate 3-kinase (P13K)-Akt pathway inhibition.
GSK-3 targets include Bcl-2 family protein, NF-B signaling pathway, Myc, CyclinD, CyclinE, beta-catenin and Jun.
reported that the incarnores the activation of GSK-3 beta to prevent Alzheimer's disease.
, the treatment of osteyl alkaloids weakened the effects of high-sugar-induced neurotoxicity reduction of Akt and GSK-3 beta phosphorylation.
through the PI3K/Akt/GSK3 beta signaling pathway, the chlorpyrifos also activates the adenosine-activated protein kinase (AMPK) pathway and inhibits the phosphorylation of amyloid precursor proteins (APP).
at the same time, the small argon in the cerebellum neurons in the form of receptor and time correlation to regulate the expression of neuronlioprotein receptors, indicating participation in the Wnt/GSK3 beta pathway.
4 MAPK (ERK, p38, and JNK) pathway fissic activated protein kinase (MAPK) pathway is important for the anti-inflammatory effect of the small carbapenem, which is related to the inhibition of NF-B in all studies.
MAPK/ERK pathways involve cell proliferation, differentiation, aging and apoptosis.
p38 are activated by a variety of inflammatory extracellular media, while JNK the same type is strongly activated in various cellular stress responses. The study of MAPK signaling pathways in neuronal disease models
small-carina-alkali treatment was inconsistent and even contradicted to some extent.
this indicates an increase in the phosphorylation activation status of MAPK (p38) and MAPK (ERK-1/2) when cortical neurons are hypoxia, while the phosphorylation status response to MAPK (p38) and MAPK (ERK-2) in the hippocampus slicing model in rats increases to an increase in hypoxia.
the small linen may mediate different MAPK pathways with neuronal defects in different regions of the brain.
5 AMPK is a cellular energy sensor that is overactive in neurodegenerative diseases such as Alzheimer's disease, but it is not clear whether it is the main cause or the cell's response to repair damage.
early reports of AMPK inhibition on the neuroprotective effects of stroke.
another study on the improvement of the bioactive of chlorpyrifos and sodium pyridine (HGSD) to protect the brain ischemia re-infusion due to its anti-apoptosis mediated by AMPK activation reduction.
neurocystic growth is essential for nervous system development and is highly energy-dependent processes regulated by AMPK-related pathways.
inhibits the growth of nerve denitus in the early stages of neuronal polarization and affects the stability of the cytoskeleton, which is mediated by energy state and AMPK activation reduction.
liver kinase B1 and PI3K-Akt-GSK3 beta signaling pathways are also involved.
in addition, mitochondrial dysfunction and endosomeary network stress lead to a decrease in the energy state induced by the small carbapenem.
6 Alzheimer's disease -beta-amyloid (Beta) Alzheimer's disease is associated with beta-amyloid protein entanglement of extracellular amyloid plaques and neurogentocell fibers.
Beta is a protein hydrolysis fragment that cross-membranes app and, together with its downstream tau protein, causes neurons to become pathological.
may be a promising multi-target drug for the prevention of Alzheimer's disease.
In addition to normal inflammation and oxidative stress defenses, the increase in insulin degradation enzymes (IDE) and A-beta 40 and a decrease in A beta 42 were also observed in the rat model of the ostrichaline treatment.
improved spatial learning capacity and memory retention in mice with Alzheimer's disease by promoting autophagy removal of A beta 40 and inhibiting A-beta production.
in Calyculin (CA)-induced neuroblastoma-2a cell-2a cell-carbapenems reduce metabolism and vitality of cytotoxicity, and it can significantly reverse axon transport disorders by regulating pp-2A activity, which is the cause of rate memory defects. Another way to treat Alzheimer's disease
is to process amyloid precursor proteins to reduce Beta A.
in a genetically modified mouse model of Alzheimer's disease, it was found that the argon was regulated by reducing the level of C-end fragments of the APP and the excessive phosphorylation of APP and tau.
fact, the argon is an effective drug for the treatment of Alzheimer's disease, including not only Alzheimer's disease, but also other types of dementia.
7 NMDA receptor pathway saccharide has also been shown to regulate the activity of several neurotransmitter systems, such as dopamine, nitric oxide, serotonin, and N-methyl-D-tininin.
N-methyl-D-Tinnine receptor (NMDA) involves neuroplasticity and excitatory toxicity.
to improve damage in the model of a rat iexclusiveidized tremor rat by blocking the release of NMDA receptors or glutamatease with dose-related behavior.
can improve the production of excess glutamine, cause cytotoxicity and be involved in many neurodegenerative diseases associated with neuronal loss, but no regulatory mechanism has been found.
8 MMP-9 pathway matrix metalloproteinase-9 (MMP-9) is a unique brain physiology and pathology participant that is significantly activated after stimulation and can be released from neurons, gliopaths and white blood cells to the brain, participate in synaptic plasticity, and participate in brain dysfunction through immune/inflammatory responses.
authal acid has been shown to inhibit the metastasis potential of cancer cells by reducing the enzyme activity and expression levels of MMP2 and MMP9.
the discovery of experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis, the ostein prevents neuronal damage in EAE by inhibiting the degradation of MMP-9 and layer sydgins.
concluding the conclusion over the past decade or so, new evidence has accumulated that there are many ways to participate in the process of neuroprotective behavior of the small carbapenem. in addition to the normal protection of apoptosis, inflammation, and oxidative stress, the
, in addition to the normal protection of apoptosis, inflammation, and oxidative stress, the ostebalyn base also regulates activities related to a number of other diseases, such as participating in insulin signaling pathways and improving insulin resistance to reduce cognitive dysfunction.
improve the behavior of hyperlipidemia, hyperglycemia and hyperinsulinemia will undoubtedly help the treatment of neurological disorders.
in short, it's hard to list all possible ways, and the oline has a protective effect on the central nervous system, but it can be turned to those classic pathways.
Akt/PKB-related signaling pathways and their downstream pathways such as Bcl-2, NF-B and GSK3 account for the majority of the apoptosis, anti-inflammatory and antioxidant processes.
pathways such as the MAPK pathway and the AMPK signaling pathway still help protect neurons from neurological diseases such as ischemia, epilepsy, and dementia.
in addition, the small linen has a unique effect on Alzheimer's disease and other neurodegenerative diseases by regulating amyloid-beta and NMDA receptors. however, the detailed mechanism of
needs to be further studied to perfect the theory.
References Source: Cai Yue, Yuan Jie, Liu Xiaolong, Chen Xiaojie. Advances in the study of the mechanism of the protective effect of the osteum on the protection of neurons. .J. Modern Drugs and Clinical, 2018, 33 (8): 2154-2158.