Arundic Acid

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 V_max 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]. 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].