CHPG is a selective metabotropic glutamate receptor 5 (mGlu5) agonist[1]. Activation of mGlu5 suppresses oxidative stress and inflammation induced by lipopolysaccharide (LPS) or SO2 derivatives in microglia, thereby inhibiting neuronal apoptosis[1].
In vitro, CHPG (0.5mM; 30min) pretreatment showed no obvious cytotoxicity in BV2 cells, and significantly increased cell viability while reducing LDH release and apoptosis following SO2 derivatives treatment[1]. CHPG (0.5mM; 30min) attenuated SO2-induced oxidative stress, the expression of inflammatory cytokines, like IL-1β, IL-6 and TNF-α, in BV2 microglial cells[1]. CHPG (1mM; 30min) protected cultured cortical neurons against traumatic brain injury (TBI) and reduced the neuronal apoptotic rate[2].
In vivo, CHPG (250nM, 50µl; injected into the right lateral ventricle; 30min pretreatment) enhanced the activation of ERK and Akt, attenuated neuronal apoptosis, and reduced cerebral lesion volume in TBI rats[2].
References:
[1] Qiu, Jun-Ling et al. “The selective mGluR5 agonist CHPG attenuates SO2-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells.” Neurochemistry international vol. 85-86 (2015): 46-52.
[2] Chen, Tao et al. “The selective mGluR5 agonist CHPG protects against traumatic brain injury in vitro and in vivo via ERK and Akt pathway.” International journal of molecular medicine vol. 29,4 (2012): 630-6.