Background:

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].

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].

CHPG sodium salt (injection; 250 nM; for 7 days) reduces significantly cerebral lesion volume[2].

参考文献:
[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.