3‐Acetyl‐11‐keto‐β‐boswellic acid attenuated oxidative glutamate toxicity in neuron‐like cell lines by apoptosis inhibition

• Published in: Journal of cellular biochemistry 2020-02, Vol.121 (2), p.1778-1789
• Main Authors: Rajabian, Arezoo, Sadeghnia, Hamid Reza, Hosseini, Azar, Mousavi, Seyed Hadi, Boroushaki, Mohammad Taher
• Format: Article
• Language: English
• Subjects: 3‐acetyl‐11‐keto‐β‐boswellic acid (AKBA); Adrenal Gland Neoplasms - chemically induced; Adrenal Gland Neoplasms - drug therapy; Adrenal Gland Neoplasms - pathology; Animals; Apoptosis - drug effects; cytotoxicity; DNA injury; glutamate; Glutamic Acid - toxicity; Lipid Peroxidation - drug effects; Mice; Neuroblastoma - chemically induced; Neuroblastoma - drug therapy; Neuroblastoma - pathology; neuroprotection; Oxidative Stress - drug effects; PC12 Cells; Pheochromocytoma - chemically induced; Pheochromocytoma - drug therapy; Pheochromocytoma - pathology; programmed cell death; Rats; Triterpenes - pharmacology
• ISSN: 0730-2312; 1097-4644; 1097-4644
• DOI: 10.1002/jcb.29413

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