Neuroprotection elicited by resveratrol in a rat model of hypothyroidism: Possible involvement of cholinergic signaling and redox status. (15th March 2021)

• Record Type: Journal Article
• Authors: de Souza Cardoso, Juliane; Baldissarelli, Jucimara; Reichert, Karine Paula; Teixeira, Fernanda Cardoso; Pereira Soares, Mayara Sandrielly; Chitolina Schetinger, Maria Rosa; Morsch, Vera Maria; Farias Martins Filho, Antônio Orlando; Duarte Junior, Humberto Ribeiro; Ribeiro Coriolano, Felipe Henrique; Spanevello, Roselia Maria; Stefanello, Francieli Moro; Tavares, Rejane Giacomelli
• Is Part Of: Molecular and cellular endocrinology. Volume 524(2021)
• Publication Date: 2021-03-15
• Subjects: Hypothyroidism -- Cholinergic signaling -- Oxidative stress -- Resveratrol -- Phenolic compound; Endocrinology -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Endocrinology -- Periodicals; Hormones -- Periodicals; Endocrinologie -- Périodiques; Cytology; Endocrinology; Molecular biology; Periodicals; 573.4
• DOI: 10.1016/j.mce.2021.111157
• Languages: English
• ISSNs: 0303-7207

Abstract

Abstract: Both the cholinergic pathway and oxidative stress are important mechanisms involved in the pathogenesis of hypothyroidism, a condition characterized by low levels of thyroid hormone that predispose the patient to brain dysfunction. Phenolic compounds have numerous health benefits, including antioxidant activity. This study evaluates the preventive effects of resveratrol in the cholinergic system and redox status in rats with methimazole-induced hypothyroidism. Hypothyroidism increases acetylcholinesterase (AChE) activity and density in the cerebral cortex and hippocampus and decreases the α7 and M1 receptor densities in the hippocampus. Hypothyroidism also increases cellular levels of reactive oxygen species (ROS) and thiobarbituric acid reactive substances (TBARS), but reduces total thiol content, and catalase and superoxide dismutase activities in the serum. In the cerebral cortex and hippocampus, hypothyroidism increases the levels of ROS and nitrites. In this study, resveratrol (50 mg/kg) treatment prevents the observed increase in AChE in the cerebral cortex, and increases the protein levels of NeuN, a marker of mature neurons. Resveratrol also prevents changes in serum ROS levels and brain structure, as well as the levels of TBARS, total thiol content, and serum catalase enzyme activity. These collective findings suggest that resveratrol has a high antioxidant capacity and can restore hypothyroidism-triggered alterations related to neurotransmission. Thus, it is a promising agent for the prevention of brain damage resulting from hypothyroidism. Graphical abstract: Image 1 Highlights: Neuroprotective effects of resveratrol in a rat model of hypothyroidism . Resveratrol restores cholinergic deficit in brain of rats with hypothyroidism. Resveratrol increases neuronal nuclei density in hippocampus of hypothyroid rats.