Volume 17, Issue 40, July - December, 2023

The protective effects of methylene blue on thioacetamide-induced acute liver and brain injury

Omar ME Abdel-Salam^1♦, Eman R Youness², Fatma A Morsy³, Amany Ameen Sleem⁴

¹Department of Toxicology and Narcotics, National Research Centre, Cairo, Egypt
²Department of Medical Biochemistry, National Research Centre, Cairo, Egypt
³Department of Pathology, National Research Centre, Cairo, Egypt
⁴Department of Pharmacology, National Research Centre, Cairo, Egypt

^♦Corresponding author
Department of Toxicology and Narcotics, National Research Centre, Cairo, Egypt

ABSTRACT

This study aimed to investigate the potential protective effects of methylene blue (MethyB) on thioacetamide (TAA)-induced acute liver and brain injury in rats. TAA (300 mg/kg) was administrated intraperitoneally (i.p.) with or without MethyB at 10, 20, or 40 mg/kg for two successive days, and rats were euthanized 24 hours after the last treatments. Markers of oxidative stress, including malondialdehyde (MDA), reduced glutathione (GSH), and nitric oxide, were determined in liver and brain tissues. Histological examination of liver tissue and different brain regions such as the cerebral cortex, hippocampus, and cerebellum were carried out. Results indicated that compared with the respective saline controls, MDA and nitric oxide levels were significantly raised in the TAA control group, but GSH levels were significantly decreased in the liver and brain tissues. Administration of MethyB to TAA-treated rats resulted in a significant and doserelated decrease in lipid peroxidation (MDA) and nitric oxide. At the same time, the levels of GSH increased in the liver and brain compared with the TAA control group. TAA evoked marked liver tissue damage with micro and macrovesicular steatosis, swelling and apoptosis of hepatocytes, and inflammatory cell aggregates. In addition, TAA caused neuronal cell loss, necrosis, apoptosis of neurons, vacuolar degeneration in cortex and focal gliosis. The hippocampus suffered structural deformity, and shrinkage of large pyramidal cells, with darkened nuclei. In the cerebellum, widely displaced or emptiness of most Purkinje cells, and vacuolation of white matter were observed. MethyB prevented the pathological changes caused by TAA in the brain and liver in a dosedependent manner, with the highest dose of 40 mg/kg providing a remarkable protective effect. The study indicated that MethyB prevented the harmful effects of acutely administered TAA in the liver and brain of rats. These effects of MethyB involved lowered levels of oxidative stress.

Keywords: Thioacetamide; methylene blue; liver damage; hepatic encephalopathy; oxidative stress

Drug Discovery, 2023, 17(40), e32dd1951

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DOI: https://doi.org/10.54905/disssi.v17i40.e32dd1951

Published: 18 September 2023