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. CHPG sodium salt protects against traumatic brain injury (TBI) in vitro and in vivo by activation of the ERK and Akt signaling pathways..
IC50&Target
mGlu5
NF-κB
ERK
Akt
体外研究
CHPG sodium salt (10-500 µM; 24 hours) significantly increases the cell viability and decreases the LDH release after SO2 derivatives treatment.
CHPG sodium salt (0.5 mM; 30 mins ) protects BV2 cells against SO2-induced apoptosis.
CHPG sodium salt (0.5 mM; 30 mins) treatment alone increases the expression of TSG-6 in both mRNA and protein levels.
Cell Viability Assay
Cell Line:
BV2 microglial cells
Concentration:
10, 50, 100 and 500 µM
Incubation Time:
24 hours
Result:
Increased the cell viability.
Apoptosis Analysis
Cell Line:
BV2 microglial cells
Concentration:
0.5 mM
Incubation Time:
30 mins
Result:
Protected BV2 cells against SO2-induced apoptosis.
Western Blot Analysis
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.
体内研究
CHPG sodium salt (injection; 250 nM; for 7 days) reduces significantly cerebral lesion volume.
Animal Model:
Adult Sprague-Dawley male rats weighing 280-320 g
Dosage:
250 nM
Administration:
Injection; for 7 days
Result:
Reduced significantly cerebral lesion volume.
分子式
C8H7ClNNaO3
分子量
223.59
CAS号
1303993-73-8
运输条件
Room temperature in continental US; may vary elsewhere.