Open AccessPOTENTIAL EFFECTS OF GLIBENCLAMIDE ON PROTEIN EXPRESSION IN ALCL3-INDUCED NEUROTOXICITY: IMPLICATIONS IN NEURODEGENERATIVE DISORDERS
Author(s) -
Maria Majeed,
Saadia Zahid
Publication year - 2020
Publication title -
nust journal of natural sciences
Language(s) - English
Resource type - Journals
eISSN - 2710-222X
pISSN - 2072-4659
DOI - 10.53992/njns.v4i2.8
Subject(s) - neurotoxicity , glibenclamide , hippocampal formation , pathological , disease , dementia , medicine , insulin resistance , atrophy , biology , pharmacology , diabetes mellitus , bioinformatics , neuroscience , endocrinology , toxicity
Alzheimer’s disease (AD), the most common form of dementia, affects 46.8 million people worldwide while Type 2 diabetes mellitus (T2DM), a metabolic disorder, affects 382 million people globally. Both these devastating diseases share some common pathological features including insulin resistance. Based on this common pathological similarity the present study aimed to investigate the effects of an antidiabetic drug on hippocampal protein expression in a mouse model of aluminum chloride (AlCl3) induced neurotoxicity that displays brain atrophy and neuronal damage as in neurodegenerative disorders (NDDs). Age matched male Balb/c mice were divided into 4 groups and administered with AlCl3, Glibenclamide (GLI) (10mg /body weight), AlCl3 followed by GLI and control. Significant expression alterations were observed for seven proteins while substantial restoration of protein expression was also detected, as an effect of GLI administration. However; it is worth mentioning that GLI exhibit negative regulation of expression for few of the expressed proteins. In conclusion, GLI may have the potential to restore altered protein expression during neurotoxicity with few exceptions, which is speculated to be dependent on the nature of the protein. Further characterization of the expressed proteins will be helpful to validate the observed significant effects of GLI that may provide a novel approach to combat cellular and metabolic alterations in neurotoxicity and neurodegenerative disorders.