IMR Press / FBL / Volume 26 / Issue 8 / DOI: 10.52586/4942
Open Access Original Research
Effects of Telmisartan, an AT1 receptor antagonist, on mitochondria-specific genes expression in a mouse MPTP model of Parkinsonism
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1 Department of Pharmacology, JSS College of Pharmacy, JSS Academy of Higher Education & Research, 570015 Mysuru, India
2 Centre for Experimental Pharmacology and Toxicology, Central Animal Facility, JSS Academy of Higher Education & Research, 570015 Mysuru, India
3 Molecular Biophysics, Saarland University, 66123 Saarland, Germany
4 Department of Clinical Sciences, College of Dentistry, Ajman University, 346 Ajman, UAE
5 Center of Medical and Bio-allied Health Sciences Research, Ajman University, 346 Ajman, UAE
6 College of Pharmacy & Health Sciences, University of Science and Technology of Fujairah, 2202 Fujairah, UAE
7 Department of Food Science and Nutrition, CAMS, Sultan Qaboos University, 123 Muscat, Oman
8 Aging and Dementia Research Group, Sultan Qaboos University, 123 Muscat, Oman
*Correspondence: (Saravana Babu Chidambaram); (Musthafa Mohamed Essa)
Front. Biosci. (Landmark Ed) 2021, 26(8), 262–271;
Submitted: 21 February 2021 | Accepted: 14 April 2021 | Published: 30 August 2021
Copyright: © 2021 The Author(s). Published by BRI.
This is an open access article under the CC BY 4.0 license (

Background: Mitochondrial dysfunction plays a crucial role in Parkinson’s disease (PD) pathogenesis. The present study was undertaken to investigate the effects of Telmisartan (TEL), an angiotensin II type 1 receptor (AT1R) blocker, on the mitochondria-specific genes expression in a mouse model of Parkinsonism. Materials and methods: Mice were divided into 5 groups with 6 in each; Group I received 0.5% CMC (control) + saline, Group II received 0.5% CMC + 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (positive control), Group III & IV received MPTP + TEL 3 and 10 mg/kg, p.o. respectively, Group V received TEL 10 mg/kg, p.o. (drug control). MPTP was given 80 mg/kg intraperitoneal in two divided doses (40 mg/kg × 2 at 16 h time interval). Vehicle or TEL was administered 1 h before the MPTP injection. Motor function was assessed 48 h after the first dose of MPTP and animals were euthanized to collect brain. Results: Mice intoxicated with MPTP showed locomotor deficits and significant upregulation of α-synuclein (α-syn), downregulation of metastasis-associated protein 1 (MTA1), and Ubiquitin C-terminal hydrolase L1 (UCHL1) in the substantia nigra pars compacta (SNpc) and Striatum (STr) regions of brains. In addition, MPTP intoxication down-regulated mitochondria-specific genes such as DJ-1, PTEN-induced putative kinase 1 (PINK1), Parkin, enriched with leucine repeats kinase 2 (LRRK2) gene expfression. Pre-treatment with TEL restored locomotor functions and upregulated PINK1, Parkin, LRRK2, DJ-1, MTA1 and UCHL1. Conclusion: The present study evidences that TEL has the ability to improve mitochondrial functions in PD.

Parkinson’s disease
Fig. 1.
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