CHPG Sodium salt

CHPG sodium salt is a selective mGluR5 agonist, and attenuates SO2-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells[1]. CHPG sodium salt protects against traumatic brain injury (TBI) in vitro and in vivo by activation of the ERK and Akt signaling pathways.[2].

Signaling Pathways >> PI3K/Akt/mTOR >> Akt

Research Areas >> Inflammation/Immunology

Signaling Pathways >> GPCR/G Protein >> mGluR

Signaling Pathways >> MAPK/ERK Pathway >> ERK

Research Areas >> Neurological Disease

Signaling Pathways >> Stem Cell/Wnt >> ERK

mGluR5

NF-κB

ERK

Akt

CHPG sodium salt (10-500 µM; 24 hours) significantly increases the cell viability and decreases the LDH release after SO2 derivatives treatment[1]. CHPG sodium salt (0.5 mM; 30 mins ) protects BV2 cells against SO2-induced apoptosis[1]. CHPG sodium salt (0.5 mM; 30 mins) treatment alone increases the expression of TSG-6 in both mRNA and protein levels[1]. Cell Viability Assay[1] Cell Line: BV2 microglial cells Concentration: 10, 50, 100 and 500 µM Incubation Time: 24 hours Result: Increased the cell viability. Apoptosis Analysis[1] Cell Line: BV2 microglial cells Concentration: 0.5 mM Incubation Time: 30 mins Result: Protected BV2 cells against SO2-induced apoptosis. Western Blot Analysis[1] Cell Line: BV2 microglial cells Concentration: 0.5 mM Incubation Time: 30 mins Result: Increased the expression of TSG-6 in both mRNA and protein levels.

CHPG sodium salt (injection; 250 nM; for 7 days) reduces significantly cerebral lesion volume[2]. Animal Model: Adult Sprague-Dawley male rats weighing 280-320 g[2] Dosage: 250 nM Administration: Injection; for 7 days Result: Reduced significantly cerebral lesion volume.

[1]. Qiu JL, et al. The selective mGluR5 agonist CHPG attenuates SO₂-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells. Neurochem Int. 2015 Jun-Jul;85-86:46-52.

[2]. Chen T, et al. The selective mGluR5 agonist CHPG protects against traumatic brain injury in vitro and in vivo via ERK and Akt pathway. Int J Mol Med. 2012 Apr;29(4):630-6.