Search Result
Results for "
stroke damage
" in MedChemExpress (MCE) Product Catalog:
| Cat. No. |
Product Name |
Target |
Research Areas |
Chemical Structure |
-
- HY-110281
-
|
|
Endogenous Metabolite
|
Cardiovascular Disease
Neurological Disease
|
|
Dehydroascorbic acid is an oxidized form of vitamin C that can cross the blood-brain barrier (BBB). Dehydroascorbic acid clears cytotoxic reactive oxygen species (ROS) produced after ischemic stroke by converting to ascorbic acid (AA), thereby reducing neuronal and glial cell damage and stabilizing cerebral microvascular NO signaling to maintain perfusion in the ischemic area. Dehydroascorbic acid can be used in research on ischemic stroke .
|
-
-
- HY-106950
-
|
Diphosphofructose; Esafosfan; FDP
|
Toll-like Receptor (TLR)
COX
|
Cardiovascular Disease
Neurological Disease
Metabolic Disease
|
|
Fosfructose is an orally active cyclooxygenase-2 inhibitor and Toll-like receptor 4 modulator. Fosfructose reduces the expression of cyclooxygenase-2, thereby decreasing prostaglandin production. By inhibiting the Toll-like receptor 4 signaling pathway, Fosfructose downregulates LPS-induced adhesion molecule expression. Fosfructose is applicable to research related to ischemic stroke, epilepsy, sepsis, myocardial injury, osteoporosis, and ultraviolet B-induced skin damage .
|
-
-
- HY-B1065
-
|
α-N-Acetyl-L-glutamine; N2-Acetylglutamine
|
Keap1-Nrf2
Akt
ASK1
Apoptosis
|
Neurological Disease
|
|
Aceglutamide (α-N-Acetyl-L-glutamine; N2-Acetylglutamine) is a neuroprotectant that can penetrate the blood-brain barrier. Aceglutamide can enhance the antioxidant systems of glutathione (GSH), thioredoxin (Trx) and Nrf2. Aceglutamide also inhibits ASK1 and TRAF1, activates the Akt/Bcl-2 anti-apoptotic pathway, enhances the activity of antioxidant enzymes and reduces oxidative damage. Aceglutamide can improve neurological deficits after cerebral ischemia, reduce infarct volume, and inhibit neuronal apoptosis, especially substantia nigra dopaminergic neurons. Aceglutamide can reduce cerebral ischemia/reperfusion injury, improve motor dysfunction, and is used in ischemic stroke-related research .
|
-
-
- HY-N12060
-
|
|
Bcl-2 Family
Caspase
Apoptosis
Autophagy
Reactive Oxygen Species (ROS)
Akt
JNK
ERK
|
Cardiovascular Disease
Neurological Disease
|
|
Ginkgo biloba extract is a natural product that can be isolated from Ginkgo biloba leaves . Ginkgo biloba extract alleviates oxidative stress-induced neuronal apoptosis (Apoptosis) by stabilizing mitochondrial function, regulating Bcl-2 family proteins and inhibiting caspase activation. Ginkgo biloba extract alleviates testicular injury by upregulating SKP2 and inhibiting Beclin1-independent autophagy (Autophagy) . Ginkgo biloba extract alleviates various types of neuronal damage in animal models. Ginkgo biloba extract reduces behavioral sensitization in rats. Ginkgo biloba extract counteracts Aβ-induced neurotoxicity by blocking a series of Aβ-triggered events, including glucose uptake, ROS accumulation, AKT activation, mitochondrial dysfunction, JNK and ERK 1/2 pathways, and apoptosis, and also interferes with the formation of Aβ oligomers. Ginkgo biloba extract is applicable to research related to cerebral hypoperfusion, testicular injury, Alzheimer's disease, Parkinson's disease, multi-infarct dementia, stroke, traumatic brain injury and amyotrophic lateral sclerosis .
|
-
-
- HY-N5048
-
|
6'-O-Galloyl paeoniflorin
|
NF-κB
ERK
JNK
Nuclear Factor of activated T Cells (NFAT)
Keap1-Nrf2
PI3K
Akt
Reactive Oxygen Species (ROS)
Apoptosis
DNA/RNA Synthesis
|
Infection
Neurological Disease
Metabolic Disease
Inflammation/Immunology
|
|
Galloylpaeoniflorin (6'-O-Galloyl paeoniflorin) is an orally active galloylated derivative of Paeoniflorin (HY-N0293) found in peony roots with various anti-inflammatory and antioxidant activities. Galloylpaeoniflorin suppresses RANKL-induced activation of ERK, JNK, c-Fos, c-Jun, and NFATc1, and reduces osteoclast-specific gene expression. Galloylpaeoniflorin activates Nrf2 and PI3K/Akt pathways, inhibits NF-κB activation, and scavenges ROS to reduce oxidative DNA, lipid, and protein damage. Galloylpaeoniflorin attenuates neuroinflammation, inhibits apoptosis, reduces Helicobacter pylori-induced gastric mucosa injury and UVB-induced cell damage. Galloylpaeoniflorin can be used for the research of osteoporosis, gastritis, ischemic stroke and skin diseases .
|
-
-
- HY-N2125
-
|
|
5-HT Receptor
iGluR
Caspase
Interleukin Related
TNF Receptor
SOD
NF-κB
|
Neurological Disease
Inflammation/Immunology
|
|
Parishin C is a brain-penetrant major bioactive component found in Gastrodia elata Blume. Parishin C is a 5-HT1A receptor agonist with an EC50 of 34 nM. Parishin C has antipsychotic and neuroprotective effects. Parishin C protects against Aβ-induced long-term potentiation damage and NMDA receptor current impairment. Parishin C reduces oxidative stress, pro-inflammatory cytokine levels, caspase activity, brain water content, and cerebral infarct volume; increases antioxidant enzyme activity and BDNF levels; improves nerve function and histopathological brain damage. Parishin C attenuates phencyclidine-induced immobility time increases, sociability deficits, and visual recognition memory impairment. Parishin C can be used for the research of ischemic stroke, Alzheimer's disease, and schizophrenia-like psychosis .
|
-
-
- HY-N4205
-
|
|
Cytochrome P450
|
Cancer
|
|
Tetrahydropiperine is an orally effective, selective inhibitor of NF-κB and MAPKs<、b>, and an activator of the PI3K/Akt/mTOR<、b> pathway. Tetrahydropiperine reduces the production of pro-inflammatory cytokines such as TNF-α, IL-6, and nitric oxide (NO) by inhibiting the nuclear translocation of NF-κB and the phosphorylation of MAPKs such as ERK, JNK, and p38. At the same time, Tetrahydropiperine inhibits excessive autophagy by activating the PI3K/Akt/mTOR pathway, protecting neurons from oxidative damage. Tetrahydropiperine has anti-inflammatory, anti-apoptotic, and neuroprotective effects, and is mainly used in the study of inflammatory diseases (such as endotoxemia, arthritis) and neurological diseases such as ischemic stroke .
|
-
-
- HY-125039
-
|
|
Glutathione Peroxidase
|
Cardiovascular Disease
Neurological Disease
|
|
N-Acetyl lysyltyrosylcysteine amide is a potent, reversible, specific, and non-toxic tripeptide inhibitor of myeloperoxidase (MPO). N-Acetyl lysyltyrosylcysteine amide effectively inhibits MPO generation of toxic oxidants in vivo. N-Acetyl lysyltyrosylcysteine amide reduces neuronal damage and preserves brain tissue and neurological function in the stroked brain. N-Acetyl lysyltyrosylcysteine amide inhibits MPO-dependent hypochlorous acid (HOCl) generation, protein nitration, and LDL oxidation .
|
-
-
- HY-101079
-
|
|
Opioid Receptor
|
Neurological Disease
|
|
BRL 52537 hydrochloride is a highly selective κ-Opioid receptor (KOR) agonist with Kis of 0.24 nM and 1560 nM for κ and μ subtypes, respectively. BRL 52537 hydrochloride decreases ischemia-evoked NO production as a potential mechanism of neuroprotection. BRL 52537 hydrochloride attenuates early stroke damage .
|
-
-
- HY-W392413
-
|
|
Drug Derivative
Reactive Oxygen Species (ROS)
|
Cardiovascular Disease
Neurological Disease
Metabolic Disease
Inflammation/Immunology
|
|
Glutathione monoethyl ester is a glutathione derivative that can be transported into cells and hydrolyzed into glutathione. Glutathione monoethyl ester downregulates the gene expression of TEN1 and CTC1 while upregulating TERT expression. Glutathione monoethyl ester enhances telomerase activity, promotes proliferation and differentiation in aged bone marrow stromal cells, while elevating glutathione levels and reducing oxidative stress, protein aggregation and cell death in motor neuronal cells. Glutathione monoethyl ester confers broad multi-organ protection against cerebral ischemia, renal injury, liver damage, and pancreatitis. Glutathione monoethyl ester can be used for the research of amyotrophic lateral sclerosis, stroke, acute renal failure, liver injury, and acute pancreatitis .
|
-
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- HY-170790
-
|
|
TRP Channel
|
Neurological Disease
|
|
HZS60 is a NMDAR/TRPM4 inhibitor with brain permeability that can improve cerebral ischemia. HZS60 has significant neuroprotective effects on primary neuronal ischemic damage caused by NMDA and oxygen-glucose deprivation/reoxygenation. HZS60 exhibits good pharmacokinetic characteristics and can inhibit cerebral ischemia-reperfusion injury. HZS60 can be used as a potential inhibitor of ischemic stroke .
|
-
-
- HY-N8931
-
|
Lithospermic acid monomethyl ester
|
Akt
|
Neurological Disease
|
|
Monomethyl lithospermate activates the PI3K/AKT pathway, which plays a protective role in nerve injury. Monomethyl lithospermate can improve the survival ability of SHSY-5Y cells, inhibit the breakdown of mitochondrial membrane potential (MMOP) and inhibit cell apoptosis. Monomethyl lithospermate also reduced the level of oxidative stress in the brain tissue of rats with middle artery occlusion (MCAO) and improved nerve damage in rats with ischemic stroke (IS) .
|
-
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- HY-149094
-
|
|
Drug Derivative
|
Cardiovascular Disease
|
|
Neuroprotective agent 1 (2), a promising neuroprotective agent for the study of ischemic stroke, shows promising neuroprotective activity with the EC50 value of 16.07 μM in the model of glutamate-induced excitotoxicity and 19.30 μM in the model of H2O2-induced oxidative damage .
|
-
-
- HY-114659
-
-
-
- HY-159928
-
-
-
- HY-173307
-
|
|
Keap1-Nrf2
Apoptosis
Reactive Oxygen Species (ROS)
|
Cardiovascular Disease
|
|
Nrf2 activator 19 is a BBB-penetrable NRF2/HO-1 activator. Nrf2 activator 19 exerts potent antioxidant and neuroprotective effects. Nrf2 activator 19 can also effectively reduce brain damage, reduce Reactive Oxygen Species (ROS) accumulation. Nrf2 activator 19 inhibits neuronal apoptosis. Nrf2 activator 19 promotes the recovery of neurological function and motor ability. Nrf2 activator 19 shows significant potential in ischemic stroke research .
|
-
-
- HY-100458
-
|
|
NO Synthase
|
Neurological Disease
|
|
SCR-4026 is a neuroprotective agent with blood-brain barrier penetration ability. SCR-4026 exerts neuroprotective effects by disrupting the interaction between neuronal nNOS and PSD9, with an IC50 of 6.3 μM. SCR-4026 alleviates N-methyl-D-aspartate (NMDA)-induced excitotoxic damage in primary cortical neurons, and also protects neurons in the oxygen-glucose deprivation (OGD) model. SCR-4026 can reduce the cerebral infarct volume in the rat middle cerebral artery occlusion (MCAO) reperfusion model. SCR-4026 can be used for the study of stroke .
|
-
-
- HY-174126
-
|
|
P2Y Receptor
|
Cardiovascular Disease
|
|
P2Y1 antagonist 2 (Compound 19) is a P2Y1 receptor antagonist (IC50: 0.49 μM). P2Y1 antagonist 2 has significant antiplatelet aggregation activity and exerts its effects by inhibiting P2Y1 receptor. P2Y1 antagonist 2 can upregulate nuclear Nrf2 protein levels, exhibit neuroprotective effects, and resist oxidative stress damage. P2Y1 antagonist 2 can effectively reduce cerebral infarction area and improve neurobehavioral function, and can be used in the study of ischemic stroke .
|
-
-
- HY-N2125R
-
|
|
Reference Standards
5-HT Receptor
iGluR
Caspase
Interleukin Related
TNF Receptor
SOD
NF-κB
|
Neurological Disease
Inflammation/Immunology
|
|
Parishin C (Standard) is the analytical standard of Parishin C (HY-N2125). This product is intended for research and analytical applications. Parishin C is a brain-penetrant major bioactive component found in Gastrodia elata Blume. Parishin C is a 5-HT1A receptor agonist with an EC50 of 34 nM. Parishin C has antipsychotic and neuroprotective effects. Parishin C protects against Aβ-induced long-term potentiation damage and NMDA receptor current impairment. Parishin C reduces oxidative stress, pro-inflammatory cytokine levels, caspase activity, brain water content, and cerebral infarct volume; increases antioxidant enzyme activity and BDNF levels; improves nerve function and histopathological brain damage. Parishin C attenuates phencyclidine-induced immobility time increases, sociability deficits, and visual recognition memory impairment. Parishin C can be used for the research of ischemic stroke, Alzheimer's disease, and schizophrenia-like psychosis .
|
-
-
- HY-P10977
-
|
|
Sodium Channel
RIP kinase
|
Neurological Disease
|
|
Tat-ASIC1a (1-20) (mouse, rat) is a competitive ASIC1a membrane-penetrating peptide. Tat-ASIC1a (1-20) (mouse, rat) has significantly neuroprotection effects, and reduces neuronal damage against acidotoxicity by targeting the ASIC1a-RIPK1 pathway and auto-inhibitory mechanism. Tat-ASIC1a (1-20) (mouse, rat) effectively protects brains from ischemic injury in ischemic stroke mice model. Tat-ASIC1a (1-20) (mouse, rat) can be used for neurodegenerative diseases research, such as Huntington disease and Parkinson’s disease .
|
-
-
- HY-B1065R
-
|
α-N-Acetyl-L-glutamine (Standard); N2-Acetylglutamine (Standard)
|
Reference Standards
Keap1-Nrf2
Akt
ASK1
Apoptosis
|
Neurological Disease
|
|
Aceglutamide (α-N-Acetyl-L-glutamine; N2-Acetylglutamine) (Standard) is the analytical standard of Aceglutamide (HY-B1065). This product is intended for research and analytical applications. Aceglutamide (α-N-Acetyl-L-glutamine; N2-Acetylglutamine) is a neuroprotectant that can penetrate the blood-brain barrier. Aceglutamide can enhance the antioxidant systems of glutathione (GSH), thioredoxin (Trx) and Nrf2. Aceglutamide also inhibits ASK1 and TRAF1, activates the Akt/Bcl-2 anti-apoptotic pathway, enhances the activity of antioxidant enzymes and reduces oxidative damage. Aceglutamide can improve neurological deficits after cerebral ischemia, reduce infarct volume, and inhibit neuronal apoptosis, especially substantia nigra dopaminergic neurons. Aceglutamide can reduce cerebral ischemia/reperfusion injury, improve motor dysfunction, and is used in ischemic stroke-related research .
|
-
-
- HY-181069
-
-
-
- HY-183654
-
|
|
HIF/HIF Prolyl-Hydroxylase
|
Cardiovascular Disease
Neurological Disease
|
|
Vadadustat prodrug-1 is a near-infrared activated photocaged, blood-brain barrier-permeable neuroprotective prodrug of Vadadustat. Vadadustat prodrug-1 masks the acidic pharmacophore of Vadadustat, and releases active Vadadustat upon irradiation at 650 nm to inhibit PHD2. Vadadustat prodrug-1 reduces cell damage, infarct volume and cerebral edema, and promotes neurological function recovery. Vadadustat prodrug-1 can be used for the research of ischemic stroke .
|
-
-
- HY-180828
-
|
|
NO Synthase
|
Cardiovascular Disease
Neurological Disease
|
|
iNOs-IN-8 (Compound 13h) is an efficient and highly selective inducible nitric oxide synthase (iNOS) inhibitor, with an IC50 of 238 nM. iNOs-IN-8 exhibits significant neuroprotective effects in oxygen-glucose deprivation/reoxygenation (OGD/R) and hydrogen peroxide-induced neuronal and endothelial cell damage. iNOs-IN-8 significantly reduces the volume of cerebral infarction and improves neurological function in rat models. iNOs-IN-8 can be used for the study of ischemic stroke .
|
-
-
- HY-N13729
-
|
|
NO Synthase
|
Cardiovascular Disease
Neurological Disease
|
|
Stephalonine P is a hasubanan-type alkaloid anti-inflammatory agent with neuroprotective effects against neuroinflammation. Stephalonine P regulates post-ischemic inflammatory responses by inhibiting NO production in LPS-activated BV2 microglia (IC50=34.01 μM), thereby reducing microglial activation and neuronal damage. Stephalonine P can be isolated from the whole plant of Stephania japonica. Stephalonine P can be used in research on stroke and other neuroinflammation-related diseases .
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-
-
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HY-L003
-
|
|
3,407 compounds
|
|
Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions, which is also called programmed cell death (PCD). Apoptosis plays a crucial role in developing and maintaining the health of the body by eliminating old cells, unhealthy cells and unnecessary cells. Too little or too much apoptosis contribute to many diseases. When apoptosis does not work correctly, cells that should be eliminated may persist and become immortal, for example, in cancer and leukemia. When apoptosis works overly well, it kills too many cells and inflicts grave tissue damage. This is the case in strokes and neurodegenerative disorders such as Alzheimer's, Huntington's, and Parkinson's disease.
MCE designs a unique collection of 3,407 apoptosis-related compounds mainly focusing on the key targets in the apoptosis signaling pathway and can be used in the research of apoptosis signal pathway and related diseases.
|
| Cat. No. |
Product Name |
Target |
Research Area |
-
- HY-P10977
-
|
|
Sodium Channel
RIP kinase
|
Neurological Disease
|
|
Tat-ASIC1a (1-20) (mouse, rat) is a competitive ASIC1a membrane-penetrating peptide. Tat-ASIC1a (1-20) (mouse, rat) has significantly neuroprotection effects, and reduces neuronal damage against acidotoxicity by targeting the ASIC1a-RIPK1 pathway and auto-inhibitory mechanism. Tat-ASIC1a (1-20) (mouse, rat) effectively protects brains from ischemic injury in ischemic stroke mice model. Tat-ASIC1a (1-20) (mouse, rat) can be used for neurodegenerative diseases research, such as Huntington disease and Parkinson’s disease .
|
| Cat. No. |
Product Name |
Category |
Target |
Chemical Structure |
-
- HY-110281
-
-
-
- HY-106950
-
-
-
- HY-B1065
-
|
α-N-Acetyl-L-glutamine; N2-Acetylglutamine
|
Microorganisms
Ketones, Aldehydes, Acids
Endogenous metabolite
Source Classification
|
Keap1-Nrf2
Akt
ASK1
Apoptosis
|
|
Aceglutamide (α-N-Acetyl-L-glutamine; N2-Acetylglutamine) is a neuroprotectant that can penetrate the blood-brain barrier. Aceglutamide can enhance the antioxidant systems of glutathione (GSH), thioredoxin (Trx) and Nrf2. Aceglutamide also inhibits ASK1 and TRAF1, activates the Akt/Bcl-2 anti-apoptotic pathway, enhances the activity of antioxidant enzymes and reduces oxidative damage. Aceglutamide can improve neurological deficits after cerebral ischemia, reduce infarct volume, and inhibit neuronal apoptosis, especially substantia nigra dopaminergic neurons. Aceglutamide can reduce cerebral ischemia/reperfusion injury, improve motor dysfunction, and is used in ischemic stroke-related research .
|
-
-
- HY-N12060
-
|
|
Structural Classification
Natural Products
Ginkgoaceae
Plants
Ginkgo biloba
Source Classification
|
Bcl-2 Family
Caspase
Apoptosis
Autophagy
Reactive Oxygen Species (ROS)
Akt
JNK
ERK
|
|
Ginkgo biloba extract is a natural product that can be isolated from Ginkgo biloba leaves . Ginkgo biloba extract alleviates oxidative stress-induced neuronal apoptosis (Apoptosis) by stabilizing mitochondrial function, regulating Bcl-2 family proteins and inhibiting caspase activation. Ginkgo biloba extract alleviates testicular injury by upregulating SKP2 and inhibiting Beclin1-independent autophagy (Autophagy) . Ginkgo biloba extract alleviates various types of neuronal damage in animal models. Ginkgo biloba extract reduces behavioral sensitization in rats. Ginkgo biloba extract counteracts Aβ-induced neurotoxicity by blocking a series of Aβ-triggered events, including glucose uptake, ROS accumulation, AKT activation, mitochondrial dysfunction, JNK and ERK 1/2 pathways, and apoptosis, and also interferes with the formation of Aβ oligomers. Ginkgo biloba extract is applicable to research related to cerebral hypoperfusion, testicular injury, Alzheimer's disease, Parkinson's disease, multi-infarct dementia, stroke, traumatic brain injury and amyotrophic lateral sclerosis .
|
-
-
- HY-N5048
-
|
6'-O-Galloyl paeoniflorin
|
Structural Classification
Paeonia lactiflora Pall.
Classification of Application Fields
Other Diseases
Phenols
Polyphenols
Plants
Paeoniaceae
Disease Research Fields
Source Classification
|
NF-κB
ERK
JNK
Nuclear Factor of activated T Cells (NFAT)
Keap1-Nrf2
PI3K
Akt
Reactive Oxygen Species (ROS)
Apoptosis
DNA/RNA Synthesis
|
|
Galloylpaeoniflorin (6'-O-Galloyl paeoniflorin) is an orally active galloylated derivative of Paeoniflorin (HY-N0293) found in peony roots with various anti-inflammatory and antioxidant activities. Galloylpaeoniflorin suppresses RANKL-induced activation of ERK, JNK, c-Fos, c-Jun, and NFATc1, and reduces osteoclast-specific gene expression. Galloylpaeoniflorin activates Nrf2 and PI3K/Akt pathways, inhibits NF-κB activation, and scavenges ROS to reduce oxidative DNA, lipid, and protein damage. Galloylpaeoniflorin attenuates neuroinflammation, inhibits apoptosis, reduces Helicobacter pylori-induced gastric mucosa injury and UVB-induced cell damage. Galloylpaeoniflorin can be used for the research of osteoporosis, gastritis, ischemic stroke and skin diseases .
|
-
-
- HY-N2125
-
|
|
Structural Classification
Gastrodia elata Bl.
Orchidaceae
Phenols
Plants
Source Classification
|
5-HT Receptor
iGluR
Caspase
Interleukin Related
TNF Receptor
SOD
NF-κB
|
|
Parishin C is a brain-penetrant major bioactive component found in Gastrodia elata Blume. Parishin C is a 5-HT1A receptor agonist with an EC50 of 34 nM. Parishin C has antipsychotic and neuroprotective effects. Parishin C protects against Aβ-induced long-term potentiation damage and NMDA receptor current impairment. Parishin C reduces oxidative stress, pro-inflammatory cytokine levels, caspase activity, brain water content, and cerebral infarct volume; increases antioxidant enzyme activity and BDNF levels; improves nerve function and histopathological brain damage. Parishin C attenuates phencyclidine-induced immobility time increases, sociability deficits, and visual recognition memory impairment. Parishin C can be used for the research of ischemic stroke, Alzheimer's disease, and schizophrenia-like psychosis .
|
-
-
- HY-N4205
-
|
|
Alkaloids
Piperidine Alkaloids
Classification of Application Fields
Piperaceae
Plants
Disease Research Fields
Piper nigrum Linn.
Source Classification
Cancer
|
Cytochrome P450
|
|
Tetrahydropiperine is an orally effective, selective inhibitor of NF-κB and MAPKs<、b>, and an activator of the PI3K/Akt/mTOR<、b> pathway. Tetrahydropiperine reduces the production of pro-inflammatory cytokines such as TNF-α, IL-6, and nitric oxide (NO) by inhibiting the nuclear translocation of NF-κB and the phosphorylation of MAPKs such as ERK, JNK, and p38. At the same time, Tetrahydropiperine inhibits excessive autophagy by activating the PI3K/Akt/mTOR pathway, protecting neurons from oxidative damage. Tetrahydropiperine has anti-inflammatory, anti-apoptotic, and neuroprotective effects, and is mainly used in the study of inflammatory diseases (such as endotoxemia, arthritis) and neurological diseases such as ischemic stroke .
|
-
-
- HY-N8931
-
|
Lithospermic acid monomethyl ester
|
Labiatae
Samanea saman (Jacq.) Merr.
Phenols
Polyphenols
Plants
Source Classification
|
Akt
|
|
Monomethyl lithospermate activates the PI3K/AKT pathway, which plays a protective role in nerve injury. Monomethyl lithospermate can improve the survival ability of SHSY-5Y cells, inhibit the breakdown of mitochondrial membrane potential (MMOP) and inhibit cell apoptosis. Monomethyl lithospermate also reduced the level of oxidative stress in the brain tissue of rats with middle artery occlusion (MCAO) and improved nerve damage in rats with ischemic stroke (IS) .
|
-
-
- HY-N2125R
-
|
|
Structural Classification
Gastrodia elata Bl.
Orchidaceae
Phenols
Plants
Source Classification
|
Reference Standards
5-HT Receptor
iGluR
Caspase
Interleukin Related
TNF Receptor
SOD
NF-κB
|
|
Parishin C (Standard) is the analytical standard of Parishin C (HY-N2125). This product is intended for research and analytical applications. Parishin C is a brain-penetrant major bioactive component found in Gastrodia elata Blume. Parishin C is a 5-HT1A receptor agonist with an EC50 of 34 nM. Parishin C has antipsychotic and neuroprotective effects. Parishin C protects against Aβ-induced long-term potentiation damage and NMDA receptor current impairment. Parishin C reduces oxidative stress, pro-inflammatory cytokine levels, caspase activity, brain water content, and cerebral infarct volume; increases antioxidant enzyme activity and BDNF levels; improves nerve function and histopathological brain damage. Parishin C attenuates phencyclidine-induced immobility time increases, sociability deficits, and visual recognition memory impairment. Parishin C can be used for the research of ischemic stroke, Alzheimer's disease, and schizophrenia-like psychosis .
|
-
-
- HY-B1065R
-
|
α-N-Acetyl-L-glutamine (Standard); N2-Acetylglutamine (Standard)
|
Structural Classification
Microorganisms
Ketones, Aldehydes, Acids
Endogenous metabolite
Source Classification
|
Reference Standards
Keap1-Nrf2
Akt
ASK1
Apoptosis
|
|
Aceglutamide (α-N-Acetyl-L-glutamine; N2-Acetylglutamine) (Standard) is the analytical standard of Aceglutamide (HY-B1065). This product is intended for research and analytical applications. Aceglutamide (α-N-Acetyl-L-glutamine; N2-Acetylglutamine) is a neuroprotectant that can penetrate the blood-brain barrier. Aceglutamide can enhance the antioxidant systems of glutathione (GSH), thioredoxin (Trx) and Nrf2. Aceglutamide also inhibits ASK1 and TRAF1, activates the Akt/Bcl-2 anti-apoptotic pathway, enhances the activity of antioxidant enzymes and reduces oxidative damage. Aceglutamide can improve neurological deficits after cerebral ischemia, reduce infarct volume, and inhibit neuronal apoptosis, especially substantia nigra dopaminergic neurons. Aceglutamide can reduce cerebral ischemia/reperfusion injury, improve motor dysfunction, and is used in ischemic stroke-related research .
|
-
-
- HY-N13729
-
-
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