Captopril suppresses hepatic mammalian target of rapamycin cell signaling and biomarkers of inflammation and oxidative stress in thioacetamide-induced hepatotoxicity in rats

Abstract

Background

The potential inhibitory effects of captopril, the angiotensin-converting enzyme inhibitor, on thioacetamide (TAA)-induced hepatic mammalian target of rapamycin (mTOR), liver injury enzymes, blood pressure, and biomarkers of inflammation and oxidative stress have not been investigated before.

Materials and methods

Rats were either injected with TAA (200 mg/kg; twice a week for 8 weeks) before being sacrificed after 10 weeks (model group) or were pretreated with captopril (150 mg/kg) daily for two weeks prior to TAA injections and continued receiving both agents until the end of the experiment (protective group).

Results

Captopril significantly (p < .05) inhibited TAA-induced hypertension, liver tissue levels of mTOR, TIMP-1, TNF-α, IL-6, MDA; and blood levels of lipids, ALT, and AST. We further demonstrated a significant (p < .01) positive correlation between mTOR scoring and the levels of inflammatory, oxidative and liver injury biomarkers.

Conclusions

Captopril protects against TAA-induced mTOR, liver injury enzymes, dyslipidemia, hypertension, inflammation, and oxidative stress.

Keywords:

• Captopril
• mTOR
• thioacetamide
• liver injury
• rat model

Acknowledgements

The author would like to thank Dr Mariam Al-Ani from Dental Care Partnership, Sutton Coldfield, Birmingham, UK, for proofreading the manuscript.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by the Research Deanship of King Khalid University, Abha, Saudi Arabia; Grant number KKU-Project No. R.G.P1./88/40.