Tag Archives: isoniazid
Embelin mitigates hepatotoxicity induced by isoniazid and rifampicin in rats
O. F. Mosa
Public Health Department, College of Al-Lieth Health Science,
Umm Al Qura University, Makkah, Saudi Arabia;
e-mail: drosama2030@gmail.com
Received: 09 March 2024; Revised: 29 April 2024;
Accepted: 31 May 2024; Available on-line: 17 June 2024
Isoniazid and rifampicin are reliable drugs against tuberculosis, but while effective, their use is associated with the risk of drug-induced liver damage. Embelin, a natural parabenzoquinone derived from the Embelia ribes plant, has gained attention for its potential therapeutic properties, antioxidant and organ-protective effects. The study aimed to assess the hepatoprotective properties of embelin against liver damage induced by isoniazid and rifampicin in rats. Wistar rats were used, and liver damage was induced by administration of isoniazid (100 mg/kg) and rifampicin (100 mg/kg). Embelin was given at doses of 50, 75, and 100 mg/kg for 21 days. All the drugs were given orally. Serum levels of the oxidative stress markers, aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP) activity measured by enzymatic assay kits (Elabscience, China), and the levels of tumour necrosis factor-α (TNF-α), interleukins IL-1β and IL-6 measured by ELISA kits (Randox, UK) were estimated. Embelin administration at varying doses effectively restored AST, ALT, ALP, SOD and catalase activity and notably decreased MDA and nitric oxide concentration as well as expression of inflammatory cytokines TNF-α, IL-1β and IL-6 in the serum of animals with drug-induced liver damage. These findings underscore embelin’s hepatoprotective effects, likely attributed to its radical scavenging properties and ability to suppress cytokine production.
Ferric oxide nanoparticles administration suppresses isoniazid induced oxidative stress in the rat brain tissue
H. Faramarzi1, J. Saffari-Chaleshtori2, S. Zolghadri3,
M. Beheshtroo4, A. Faramarzi5, S. M. Shafiee4,6*
1Department of Community Medicine, Faculty of Medicine, Shiraz University of Medical Sciences, Iran;
2Clinical Biochemistry Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran;
3Department of Biology, Jahrom Branch, Islamic Azad University, Jahrom, Iran;
4Department of Biochemistry, Shiraz Branch, Islamic Azad University, Shiraz, Iran;
5Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran;
6Autophagy Research Center, Shiraz University of Medical Sciences, Shiraz Iran;
*e-mail: shafieem@sums.ac.ir
Received: 08 November 2021; Revised: 27 June 2021;
Accepted: 29 September 2022; Available on-line: 06 October 2022
Isoniazid is one of the anti-tuberculosis therapeutic agents capable of causing side effects such as oxidative stress, brain tissue damage and mental disorders. This study aimed to investigate the effect of ferric oxide (Fe2O3) nanoparticles administration on isoniazid-induced oxidative stress parameters in rat brain tissue. Forty adult male Wistar rats (200–250 g) were randomly divided into a group with no treatment as control and four experimental groups. Animals of experimental groups received intraperitoneally for 12 days daily saline, 50 mg/kg of isoniazid, 50 mg/kg of isoniazid and 0.2 or 0.4 mg/kg Fe2O3 nanoparticles accordingly. The activity of catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST), the level of glutathione (GSH), malondialdehyde (MDA) and total protein were determined in brain tissue homogenates by spectrophotometric methods. It was shown that CAT and GST activities, as well as GSH and MDA levels in the brain tissue of animals in the isoniazid-treated group were increased compared with the control untreated group, while following the treatment with 0.2 or 0.4 mg/kg Fe2O3 nanoparticles the studied oxidative stress parameters returned to the control level (P < 0.05). No changes in SOD activity in any of the treated groups were observed compared to the control. This study showed that the administration of ferric oxide nanoparticles can suppress isoniazid-induced oxidative stress in the brain tissue of rats mentally damaged by isoniazid.