NEUROPROTECTIVE EFFECT OF BOSWELLIA SERRATA AND ITS ACTIVE CONSTITUENT ACETYL 11-KETO-β-BOSWELLIC ACID AGAINST OXYGEN-GLUCOSE-SERUM DEPRIVATION-INDUCED CELL INJURY.

Oxidative stress plays a key role in pathophysiology of brain ischemia. This study aimed to test whether B. serrata hydroalcoholic extract (BSE) and its active constituent 3-acetyl-1 1-keto-β-boswellic acid (AKBA) could protect neurons against ischemic condition induced by oxygen, glucose and serum deprivation (OGSD). First, PC12 neural cells were incubated with BSE (0-400 pg/mL) or AKBA (0-40 pg/mL) for 24 h to find non-cytotoxic concentrations of BSE and AKBA. Then, the cells were pre- (for 2 h) and co-treated with 1.5-6 μg/mL BSE or 0.5-2.5 pg/mL AKBA, and then exposed to OGSD condition for 6 h. The IC50. values of BSE and AKBA were 95 and 12.2 μg/mL, respectively. BSE (3 and 6 pg/mL) and AKBA (1 and 2.5 pg/mL) significantly increased viability of ischemic cells, in a concertation-dependent manner. The levels of intracellular oxygen free radicals, lipid peroxidation and oxidative DNA damage were also significantly and concentration-dependently decreased following treatment of ischemic cells with BSE or AKBA. Using HPLC analysis, the mount of AKBA in a sample of BSE was found to be 9.2%. In conclusion, B. sernata and AKBA reduce neuronal cell death induced by OGSD and this neuroprotective effect is mediated via attenuation of oxidative stress.