NeuroI Cancer Research Results
NeuroI, NeuroInflammation: Click to Expand ⟱
| Source: |
| Type: |
| NeuroInflammation
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Scientific Papers found: Click to Expand⟱
*BBB↑, both caffeic and chlorogenic acid could cross the BBB
*cognitive↑, caffeic acid (10−50 mg/kg/d, p.o.) improved the cognitive and memory impairments in Aβ25−35injected (i.c.v.) mice by the inhibition of oxidative stress
*memory↑,
*ROS↓,
*p‑tau↓, Aβ25−35-induced tau hyperphosphorylation was also suppressed by caffeic acid through reducing the calcium-dependent GSK-3β activation.
*GSK‐3β↓,
*MAPK↓, inhibited p38 MAPK activation to reduce neuroinflammation, suppressed p53 expression to downregulate caspase-3-mediated apoptosis, and decreased AChE activity.
*NeuroI↓,
*P53↓,
*Casp3↓,
*AChE↓,
*APP↓, by suppressing APP expression, β-secretase (BACE) activity, and GSK-3β activation, implying its neuroprotective activity under cerebral insulin resistance.
*BACE/β-secretase↓,
*neuroP↑,
*Dose↝, lowest effective dose of caffeic acid was 10 mg/kg in rats (Table 3), while its content range in the mung bean was 0.03−38.72 mg/100 g
*neuroP↑, Gallic acid (3,4,5-trihydroxybenzoic acid) showed neuroprotective activity against AD in various roden
*Dose↝, gallic acid (20 or 30 mg/kg) improved the cognitive impairments no matter it was administrated from the early (4 months), middle (9 months) or late-stage (12 months) of AD pathology
*ADAM10↝, related mechanisms involved modulation of the activity of α-secretase (ADAM10) and βsecretase (BACE-1) to inhibit the amyloidogenic cleavage of APP, disruption of the salt bridge between Aβ to suppress its aggregatio
*BACE/β-secretase↓,
*cl‑APP↓,
*Aβ↓,
*Ca+2↓, improvement of synaptic plasticity, as well as inhibition of Ca2+ influx, oxidative stress, and neuroinflammation.
*ROS↓,
*NeuroI↓,
*iNOS↓, ISO inhibited the expression of iNOS and COX-2 induced by Aβ25–35.
*COX2/PTGS2↓,
*TNF-α↓, And, it inhibited the secretion of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6).
*IL6↓,
*ROS↓, ISO reduced the ROS production in Aβ25–35-induced BV2 cells and inhibited NF-κB activation.
*NF-kB↓,
*Apoptosis↓, ISO Blocks Aβ25–35-Induced Apoptosis in BV2 Microglial Cells
*Bcl-2↑, anti-apoptotic protein Bcl-2 was decreased, while the level of pro-apoptotic protein BAX was increased upon treatment of BV2 cells with 20 μM Aβ25–35. However, ISO reversed the expression of Bcl-2 and BAX
*BAX↓,
*cl‑Casp9↓, expression of cleaved caspases-9 and -3 as well as PARP, which are markers of apoptosis. Aβ promoted the cleavage of these proteins, whereas ISO treatment abrogated these effects
*cl‑Casp3↓,
*cl‑PARP↓,
*NeuroI↓, ISO ameliorated neuronal inflammation via inhibition of ROS generation and blockade of NF-kB activity
*Apoptosis↓, ISO significantly increased the BV-2 cells viability, blocked the protein expression of inducible nitric oxide synthase and cyclooxygenase-2, and decreased the production of nitric oxide, pro-inflammatory cytokines including tumor necrosis factor-α
*iNOS↓,
*COX2/PTGS2↓,
*NO↓,
*TNF-α↓,
*MAPK↓, The activation of mitogen-activated protein kinases (MAPKs) was blocked by ISO
*NF-kB↓, and NF-κB nuclear translocation was decreased by ISO both alone
*ROS↓, ISO strongly quenched intracellular reactive oxygen species (ROS) generation.
*NeuroI↓, indicating that ISO attenuated neuroinflammation by inhibiting the ROS-related MAPK/NF-κB signaling pathway
*GSK‐3β↓, Isoorientin, a 6-C-glycosylflavone, was previously shown to be a highly selective inhibitor of GSK-3β, while exerting neuroprotective effects in neuronal models of AD.
*neuroP↑,
*p‑tau↓, Chronic oral administration of isoorientin to APP/PS1 mice at 8 months of age attenuated multiple AD pathogenic hallmarks in the brains, including GSK-3β overactivation, tau hyperphosphorylation, Aβ deposition, and neuroinflammation.
*Aβ↓,
*NeuroI↓,
*cognitive↑, Strikingly, isoorientin reversed deficits in synaptic long-term potentiation and spatial memory relevant to cognitive functions.
*neuroP↑, Together, the findings suggest that isoorientin is a brain neuroprotector and may be a promising drug lead for treatment of AD and related neurodegenerative disorders.
*memory↑, IVX administration ameliorated spatial memory loss and blunted a cascade of neuro-noxious episodes – including increased amyloid-beta (Aβ)
*Aβ↓,
*NeuroI↓, neuroinflammation
*PI3K↓, via the inhibition of PI3K/Akt/mTOR signalling axis.
*Akt↓,
*mTOR↓,
*miR-107↑, ascinatingly, we observed that miR-107 expression was significantly (P < 0.05) reinstated by the treatment with IVX against the downregulation of miR-107 expression in AD mice
*BBB↑, indicating its BBB permeability
*neuroP↑, neuroprotective activity of protocatechuic acid was observed by several animal models
*Aβ↓, Mechanism studies showed that protocatechuic acid inhibited Aβ plaque deposits via multiple ways, such as reduction of Aβ peptides production by inhibiting βsecretase activity, suppression of Aβ aggregation, and destabilization of performed Aβ f
*p‑tau↓, indicated that protocatechuic acid inhibited tau hyperphosphorylation and autophagy induced by okadaic acid through decreasing the activation of GSK-3β
*autophagy↓,
*GSK‐3β↓,
*NeuroI↓, antineuroinflammatory activity as indicated by the reduced neuroinflammatory markers, iNOS, and COX2 in the brain of AD mice.
*iNOS↓,
*COX2/PTGS2↓,
*BDNF↑, protocatechuic acid upregulated the expression of several cytoprotective factors, such as BDNF and myocyte enhancer factor 2D (MEF2D),
*MEF2D↑,
*cognitive↑, upregulated the cytoprotective factors, thus improving the cognitive and memory function of AD rodents.
*memory↑,
*cognitive↑, Studies showed that sinapic acid attenuated cognitive and memory impairments in Aβ- or STZinduced AD models mainly by the mechanisms of antioxidation and antineuroinflammation.
*memory↑,
*antiOx↑,
*NeuroI↓,
*iNOS↓, downregulating the expressions of nitrotyrosine and iNOS
*3-NT↓,
*Ach↑, sinapic acid also promoted the synthesis of ACh as evidenced by the upregulated ChAT expression in the hippocampus of sinapic acid-treated rats.
*ChAT↑,
*Dose↝, sinapic acid might play a critical role in the neuroprotective activity of mung bean, considering its relatively low effective dose (2.5−20 mg/kg) and high content in mung bean (0.15−230.48 mg/100 g).
*neuroP↑,
*neuroP↑, Vanillic acid (4-hydroxy-3-methoxybenzoic acid) showed neuroprotective activities in various CNS disorders, such as AD, Parkinson’ disease, cerebral ischemia, and excessive iron-induced damage
*memory↑, vanillic acid improved the memory and learning deficits via multiple mechanisms
*Learn↑,
*Aβ↓, First, vanillic acid inhibited Aβ production, β-secretase (BACE-1) activity, and Aβ plaque deposits in Aβ or lipopolysaccharide (LPS)-induced AD models,
*BACE/β-secretase↓,
*NeuroI↓, vanillic acid exerted antineuroinflammatory effects by inhibition of the receptor for advanced glycation end products (RAGE)-mediated c-Jun n-terminal kinase (JNK) activation
*RAGE↓,
*antiOx↑, vanillic acid enhanced the antioxidant Nrf2/HO-1 pathway by inhibiting GSK-3β, thus reducing the oxidative stress of Aβ1−42 -injected (i.c.v.) mice.
*NRF2↑,
*HO-1↑,
*GSK‐3β↓,
*ROS↓,
*AChE↓, vanillic acid also ameliorated the cholinergic deficits as evidenced by the inhibited AChE activity in STZ-induced AD mice
*Dose↝, effective dose of vanillic acid in rodents was 30−100 mg/kg, while its content of vanillic acid in mung bean (0.97 mg/100 g) was quite low, which implied its limited contribution to the neuroprotective activity of mung bean
*Dose↝, Sco (2 mg/kg/day, i.p.), Sco + vitexin (30 mg/kg/day, oral), Sco + donepezil (1.5 mg/kg/day, i.p.), vitexin alone, and donepezil alone
*Learn↑, co significantly impaired spatial learning and memory while increasing anxiety-like behaviors. Vitexin treatment markedly improved these deficits, with efficacy comparable to donepezil
*memory↑,
*AChE↓, Sco elevated acetylcholinesterase activity, lipid peroxidation, and oxidative/nitrosative stress markers (TOS, OSI, MDA, Peroxynitrite, NO, and NOS) while decreasing total antioxidant status (TAS). Vitexin reversed these changes.
*lipid-P↓,
*TOS↓,
*MDA↓,
*ONOO↓,
*NO↓,
*NOS2↓,
*TAC↑,
*BDNF↑, Sco reduced hippocampal BDNF, GDNF, PSD95, and synaptophysin levels and increased GFAP, IL-6, TNF-α, NF-κB p65, and COX-2 expression. Vitexin restored neurotrophic and synaptic proteins, suppressed astrocyte activation and inflammatory signaling, a
*GDNF↑,
*PSD95↑,
*GFAP↓,
*NF-kB↓,
*COX2/PTGS2↓,
*NRF2↑, and activated the Nrf2/HO-1 pathway.
*HO-1↑,
*neuroP↑, vitexin exerts significant neuroprotective and synaptoprotective effects against Sco-induced cognitive impairment by simultaneously restoring redox balance
*NeuroI↓, suppressing neuroinflammation, and preserving synaptic integrity.
Showing Research Papers: 1 to 10 of 10
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10
Pathway results for Effect on Cancer / Diseased Cells:
Total Targets: 0
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
3-NT↓, 1, autophagy↓, 1, GDNF↑, 1, GFAP↓, 1, Learn↑, 2, MEF2D↑, 1, miR-107↑, 1, NeuroI↓, 10, ONOO↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 2, HO-1↑, 2, lipid-P↓, 1, MDA↓, 1, NRF2↑, 2, ROS↓, 5, TAC↑, 1, TOS↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Apoptosis↓, 2, BAX↓, 1, Bcl-2↑, 1, Casp3↓, 1, cl‑Casp3↓, 1, cl‑Casp9↓, 1, iNOS↓, 4, MAPK↓, 2,
Transcription & Epigenetics(tgid=7) ⓘ
Ach↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
P53↓, 1, cl‑PARP↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
GSK‐3β↓, 4, mTOR↓, 1, PI3K↓, 1,
Migration(tgid=13) ⓘ
APP↓, 1, cl‑APP↓, 1, Ca+2↓, 1, RAGE↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
NO↓, 2,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 4, IL6↓, 1, NF-kB↓, 3, TNF-α↓, 2,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 3, ADAM10↝, 1, BDNF↑, 2, ChAT↑, 1, PSD95↑, 1, p‑tau↓, 3,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 5, BACE/β-secretase↓, 3,
Drug Metabolism & Resistance(tgid=21) ⓘ
Dose↝, 5,
Clinical Biomarkers(tgid=22) ⓘ
IL6↓, 1, NOS2↓, 1, RAGE↓, 1,
Functional Outcomes(tgid=23) ⓘ
cognitive↑, 4, memory↑, 6, neuroP↑, 8,
Total Targets: 57
Scientific Paper Hit Count for: NeuroI, NeuroInflammation
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
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