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RETRACTED: 3‐Acetyl‐11‐keto‐β‐boswellic acid attenuated oxidative glutamate toxicity in neuron‐like cell lines by apoptosis inhibition
Author(s) -
Rajabian Arezoo,
Sadeghnia Hamid Reza,
Hosseini Azar,
Mousavi Seyed Hadi,
Boroushaki Mohammad Taher
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29413
Subject(s) - neuroprotection , propidium iodide , viability assay , lipid peroxidation , glutamate receptor , superoxide dismutase , pharmacology , chemistry , biochemistry , programmed cell death , western blot , apoptosis , oxidative stress , biology , receptor , gene
3‐Acetyl‐11‐keto‐β‐boswellic acid (AKBA), a pentacyclic triterpenic acid present in gum resin of Boswellia serrata , has been found to possess antioxidant and neuroprotective properties. In this study, we aimed to examine protective properties of AKBA against glutamate‐induced neuronal injury. To investigate the effects of AKBA (2.5‐10 µM) on glutamate injury in neuron‐like cells PC12 and N2a, two treatment regimens (incubation for 2 or 0 hours before glutamate exposure) were used. Then, the 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide method was used to determine viability of the cells. Cellular redox status was evaluated using fluorimetry and comet assays. Annexin V/propidium iodide double staining and Western blot analysis of relative apoptotic proteins were conducted. Based on the results, 24 hours incubation with glutamate (8 mM) increased the cell mortality of PC12 and N2a ( P < .001). However, AKBA (2.5‐10 µM) enhanced the cell viability in both treatment regimens ( P < .001). Also co‐ and pretreatment with AKBA significantly attenuated lipid peroxidation, reactive oxygen species production, and DNA injury ( P < .05 and P < .001). AKBA also restored the activity of cellular superoxide dismutase under glutamate toxicity; this effect was seen to be more significant during the pretreatment regimen ( P < .001). Moreover, Western blot analysis indicated that AKBA inhibited glutamate‐induced programmed cell death through depressing the elevation of the expression ratio of Bax/Bcl‐2 and cleaved‐caspase‐3 proteins, concentration‐dependently. Overall, the present findings suggest the neuroprotective activities of AKBA against glutamate‐induced cell injury probably by inhibiting oxidative damage and reducing apoptotic cell death.