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Arundic Acid is an orally effective astrocyte function modulator and neuroprotective agent. Arundic Acid increases the expression and function of the astrocytic glutamate transporter EAAT1 by activating the ERK, Akt and NF-κB pathways. Arundic Acid attenuates retinal ganglion cell death in a normal-tension glaucoma model. Arundic Acid exerts neuroprotective effects in a mouse model of Parkinson's disease. Arundic Acid is a S100β protein synthesis inhibitor that prevents neurological deficits and brain tissue damage after intracerebral hemorrhage in rats. Arundic Acid downregulates neuroinflammation and astrocytic dysfunction after status epilepticus in immature rats. Arundic Acid is applicable to research related to Parkinson's disease, cerebral ischemia, glaucoma, intracerebral hemorrhage and epilepsy.
For research use only. We do not sell to patients.
Arundic Acid is an orally effective astrocyte function modulator and neuroprotective agent. Arundic Acid increases the expression and function of the astrocytic glutamate transporter EAAT1 by activating the ERK, Akt and NF-κB pathways. Arundic Acid attenuates retinal ganglion cell death in a normal-tension glaucoma model. Arundic Acid exerts neuroprotective effects in a mouse model of Parkinson's disease. Arundic Acid is a S100β protein synthesis inhibitor that prevents neurological deficits and brain tissue damage after intracerebral hemorrhage in rats. Arundic Acid downregulates neuroinflammation and astrocytic dysfunction after status epilepticus in immature rats. Arundic Acid is applicable to research related to Parkinson's disease, cerebral ischemia, glaucoma, intracerebral hemorrhage and epilepsy[1][2][3][4][5].
In Vitro
Arundic acid (0-100 μM; 3-24 h) enhances the promoter activity of EAAT1/EAAT2 in the human astrocytic H4 cell line[1]. Arundic acid (6.25-100 μM; 24 h) mediates the upregulation of EAAT1 promoter activity, mRNA and protein levels, and glutamate uptake function in human astrocytic H4 cells via the Akt, ERK and NF-κB pathways[1]. Arundic acid (50 μM; 3-24 h) activates the NF-κB pathway in human astrocyte H4 cells by reducing the cytoplasmic level of IκBα and inducing nuclear translocation of NF-κB p65[1]. Arundic acid (50 μM; 5 min-24 h) activates the Akt and ERK signaling pathways within 5 min of treatment[1]. Arundic acid (50 μM; 24 h) attenuates Mn-induced inhibition of EAAT1 expression by suppressing Mn-activated YY1 expression in human astrocyte H4 cells[1]. Arundic acid (100 μM; 14 days) enhances the glutamate uptake rate of primary cultured mouse Müller cells by increasing Vmax without altering glutamate affinity[2]. Arundic acid (0-100 μM; 14 days) upregulates the expression of GLAST mRNA in primary cultured mouse Müller cells[2]. Arundic acid modulates multiple astrocyte activation responses in cultured rat cerebral astrocytes, including inhibition of S-100β upregulation and pro-inflammatory gene expression, without altering GFAP levels[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Enhanced NF-κB reporter gene activity and reduced IκBα levels in cytoplasmic components
In Vivo
Arundic acid (10 mg/kg; p.o.; daily; 14 days) upregulates retinal GLAST expression, enhances glutamate uptake, and increases the retinal ganglion cell count by approximately 19.7% in GLAST heterozygous mice with normal-tension glaucoma-like degeneration[2]. Arundic acid (30 mg/kg; i.p.; 5 post-MPTP doses) protects dopaminergic neurons in mice from the neurotoxicity of MPTP (HY-W114750) in the MPTP-induced Parkinson's disease mouse model, maintains 52% of dopamine levels in the striatum and 44% of dopaminergic neurons in the substantia nigra, and ameliorates motor function deficits[3]. Arundic acid (0.02-20 μg/μL; i.c.v.; single dose) reduces the levels of S100B and GFAP in the striatum of healthy male Wistar rats[4]. A single intracerebroventricular (i.c.v.) dose of Arundic acid (2 μg/μL) reverses intracerebral hemorrhage (ICH)-induced neurological deficits, reduces striatal lesion volume, inhibits reactive astrogliosis, prevents neuronal apoptosis, normalizes central and peripheral S100B levels, and enhances early antioxidant defense capacity in male Wistar rats[4]. Arundic acid (10 mg/kg; i.p.; single injection; 6 h or 24 h post-SE induction) exerts neuroprotective effects on rats with lithium-pilocarpine-induced status epilepticus (SE) by alleviating hippocampal neuroinflammation, reversing astrocytic dysfunction, restoring glutamate homeostasis and improving glucose uptake, with administration at 24 h post-SE induction showing more stable efficacy across all endpoint indicators[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
C57BL/6J (backcrossed for ≥10 generations; GLAST heterozygous; postnatal day 22 to 35)[2]
Dosage:
10 mg/kg
Administration:
p.o.; daily; 14 days
Result:
Increased retinal GLAST mRNA levels relative to vehicle controls. Increased retinal GLAST protein expression relative to vehicle controls. Increased retinal glutamate uptake velocity by 1.23-fold relative to vehicle-treated GLAST+/- mice. Increased GCL neuron count to 438 cells per retina, compared with 366 cells in vehicle-treated GLAST+/- mice. Showed no effect on glutamate uptake in GLAST-/- mice.
i.p.; 5 doses at 1 minute, 6 h, 24 h, 48 h, 72 h after last MPTP injection
Result:
Preserved striatal dopamine levels at 52% of normal control values. Preserved striatal DOPAC and HVA levels at 47% and 60% of normal control values, respectively. Significantly reduced motor function deficits in the pole test (T-turn and T-LA) and catalepsy test. Preserved the number of tyrosine hydroxylase-positive dopaminergic neurons in the substantia nigra pars compacta at 42% of normal control values 3 days after MPTP injection and 44% of normal control values 7 days after MPTP injection. Induced earlier appearance of GFAP-positive reactive astrocytes (by 3 days post-MPTP) compared to MPTP-only mice, with GFAP immunoreactivity comparable to MPTP-only mice at 7 days. Reduced S-100 immunoreactivity in the substantia nigra at 3 days and in the striatum at 7 days post-MPTP compared to MPTP-only mice. Showed no significant effect on microglial activation relative to MPTP-only mice.
Significantly reduced striatal S100B immunocontent at 0.2 μg/μL and 2 μg/μL doses compared to control groups. Significantly reduced striatal GFAP immunocontent at 2 μg/μL dose compared to control groups. Showed no inhibitory effect on either S100B or GFAP levels at 20 μg/μL dose.
Animal Model:
Wistar rats (adult male, 90 days-old, 300-350 g, intracerebral hemorrhage induced by intrastriatal injection of type-IV collagenase)[4]
Dosage:
2 μg/μL
Administration:
i.c.v.; single dose; administered immediately before ICH induction
Result:
Reversed motor dysfunction completely at 7 days post-injury, with neurological scores and significantly. Reduced striatal lesion volume significantly at 7 days post-injury. Lowered striatal GFAP and S100B fluorescence intensity and immunostained surface area significantly at 7 days post-injury. Increased NeuN fluorescence intensity and number of NeuN-positive cells significantly at 7 days post-injury. Decreased cleaved caspase-3 fluorescence intensity and number of cleaved caspase-3-positive cells significantly at 7 days post-injury. Lowered striatal GFAP levels significantly at 7 days post-injury. Lowered striatal S100B levels significantly at 7 days post-injury; lowered cerebrospinal fluid S100B levels significantly at 72 hours post-injury; lowered serum S100B levels significantly at 24 hours and 7 days post-injury. Increased striatal GSH levels significantly at 24 hours post-injury. Decreased striatal GS activity significantly at 24 hours post-injury.
10 mg/kg (6 h post-SE induction); 10 mg/kg (24 h post-SE induction)
Administration:
i.p.; single injection
Result:
Partially reversed elevated hippocampal IL-1β levels, abolished elevated hippocampal TLR4 protein expression, partially reversed elevated hippocampal COX2 protein expression, increased hippocampal TGF-β levels, and did not alter TNF-α, RAGE, or Iba1 levels at 6 h post-SE. Prevented elevated hippocampal IL-1β levels, decreased hippocampal TNF-α levels, prevented elevated hippocampal RAGE and TLR4 protein expression, completely abolished elevated hippocampal COX2 protein expression, partially reversed elevated hippocampal Iba1 levels, and increased hippocampal TGF-β levels at 24 h post-SE. Prevented elevated hippocampal GFAP levels at 6 h and 24 h post-SE. Partially reversed elevated hippocampal S100B levels, reversed reduced hippocampal connexin-43 (Cx-43) protein expression, partially reversed elevated CSF S100B levels, and partially reversed reduced serum S100B levels at 6 h post-SE. Abolished elevated hippocampal S100B levels, and did not alter reduced hippocampal Cx-43 levels or CSF/serum S100B levels at 24 h post-SE. Reversed reduced hippocampal GLAST protein expression, partially reversed reduced hippocampal GLT1 protein expression, reversed increased hippocampal glutamate uptake, did not alter reduced hippocampal GSH levels, partially reversed reduced hippocampal glutamine synthetase (GS) activity, and reversed reduced hippocampal GS protein expression at 6 h post-SE. Partially reversed reduced hippocampal GLAST protein expression, partially reversed reduced hippocampal GLT1 protein expression, reversed increased hippocampal glutamate uptake, prevented reduced hippocampal GSH levels, did not alter reduced hippocampal GS activity, and reversed reduced hippocampal GS protein expression at 24 h post-SE. Abolished reduced hippocampal glucose uptake, and did not alter hippocampal GLUT1 protein expression at 6 h and 24 h post-SE.
Room temperature in continental US; may vary elsewhere.
Storage
Pure form
-20°C
3 years
4°C
2 years
In solvent
-80°C
6 months
-20°C
1 month
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (536.80 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Preparing Stock Solutions
ConcentrationSolventMass
1 mg
5 mg
10 mg
1 mM
5.3680 mL
26.8399 mL
53.6797 mL
5 mM
1.0736 mL
5.3680 mL
10.7359 mL
10 mM
0.5368 mL
2.6840 mL
5.3680 mL
View the Complete Stock Solution Preparation Table
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day. The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Solubility: 3.75 mg/mL (20.13 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 3.75 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (37.5 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Protocol 2
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
This protocol yields a clear solution of ≥ 3.75 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Taking 1 mL working solution as an example, add 100 μLDMSO stock solution (37.5 mg/mL) to 900 μLCorn oil, and mix evenly.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
Dosage
mg/kg
Animal weight (per animal)
g
Dosing volume (per animal)
μL
Number of animals
Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
DMSO+
%
+
%
Tween-80
+
%
Saline
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO,
. All of co-solvents are available by MedChemExpress (MCE).
, Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration:
mg/mL
Method for preparing stock solution:
mg
drug dissolved in
μL
DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take
μL DMSO stock solution, add
μL .
μL , mix evenly, next add
μL Tween 80, mix evenly, then add
μL Saline.
Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution
If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
*Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles. Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.
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