Tehran University of Medical Sciences

Science Communicator Platform

Stay connected! Follow us on X network (Twitter):
Share this content! On (X network) By
Effect of Cholestasis and Neuroaid Treatment on the Expression of Bax, Bcl-2, Pgc-1Α and Tfam Genes Involved in Apoptosis and Mitochondrial Biogenesis in the Striatum of Male Rats Publisher Pubmed



Nasehi M1 ; Torabinejad S2 ; Hashemi M2 ; Vaseghi S1 ; Zarrindast MR3, 4, 5
Authors
Show Affiliations
Authors Affiliations
  1. 1. Cognitive and Neuroscience Research Center (CNRC), Tehran Medical Sciences, Islamic Azad University, P.O. Box 13145-784, Tehran, Iran
  2. 2. Department of Genetics, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
  3. 3. Department of Pharmacology School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Institute for Cognitive Science Studies (ICSS), Tehran, Iran
  5. 5. Department of Neuroendocrinology, Endocrinology and Metabolism Research Institute, Tehran University of Medical Sciences, Tehran, Iran

Source: Metabolic Brain Disease Published:2020


Abstract

Cholestasis means impaired bile synthesis or secretion. In fact, it is a bile flow reduction following Bile Duct Ligation (BDL). Cholestasis has a main role in necrosis and apoptosis. Apoptosis is a form of programmed cell death that has intrinsic and extrinsic pathways. The intrinsic pathway is mediated by Bcl-2 (B cell lymphoma-2) proteins which integrate death and survival signals. Bcl-2 has anti-apoptotic and Bax has pro-apoptotic effects. Also, striatum is one of the brain regions that has high expressions of Bcl-2 proteins. Moreover, Tfam and Pgc-1α are involved in mitochondrial biogenesis. On the other hand, NeuroAid, is a drug that has neuroprotective and anti-apoptosis effects. In this study, using quantitative PCR, we measured the expression of all these genes in the striatum of male rats following BDL and NeuroAid administration. Results showed, BDL increased the expression of Bax and Tfam and decreased the expression of Bcl-2. NeuroAid restored the effect of BDL on the expression of Bax, while did not alter the effect of BDL on Bcl-2. In addition, it increased the expression of Tfam that was previously elevated by BDL and raised the expression of Tfam in normal rats. Both BDL and NeuroAid, had no effect on Pgc-1α. In conclusion, cholestasis increased the expression of Bax and decreased the expression of Bcl-2, and this effect may have related to enhanced susceptibility of mitochondrial pathways following oxidative stress. Tfam expression was increased following cholestasis and this effect may have related to cellular compensatory mechanisms against high accumulation of free radicals or mitochondrial biogenesis failure. Furthermore, NeuroAid may play a role against apoptosis and can be used to increase mitochondrial biogenesis. © 2019, Springer Science+Business Media, LLC, part of Springer Nature.
Other Related Docs
9. Cell Death Pathways and Viruses: Role of Micrornas, Molecular Therapy Nucleic Acids (2021)
13. Non-Coding Rnas and Brain Tumors: Insights Into Their Roles in Apoptosis, Frontiers in Cell and Developmental Biology (2022)
21. Mlc901 During Sleep Deprivation Rescues Fear Memory Disruption in Rats, Naunyn-Schmiedeberg's Archives of Pharmacology (2019)