Abstract
Carbon tetrachloride (CCL4) induces oxidative stress by free radical toxicities, inflammation, and neurotoxicity. Quercetin (Q), on the other hand, has a role as anti-inflammatory, antioxidant, antibacterial, and free radical-scavenging. This study explored protection given by quercetin against CCL4 induced neurotoxicity in rats at given concentrations. Male Wistar rats were divided into four groups Group C: control group; Group CCL4: given a single oral dose of 1 mL/kg bw CCL4; Group Q: given a single i.p injection of 100 mg/kg bw quercetin; and Group Q + CCL4: given a single i.p injection of 100 mg/kg bw quercetin before two hours of a single oral dose of 1 mL/kg bw CCL4. The results from brain-to-body weight ratio, morphology, lipid peroxidation, brain urea, ascorbic acid, reduced glutathione, sodium, and enzyme alterations (aspartate aminotransferase (AST), alanine aminotransferase (ALT), catalase, and superoxide dismutase) suggested alterations by CCL4 and a significant reversal of these parameters by quercetin. In silico analysis of quercetin with various proteins was conducted to understand the molecular mechanism of its protection. The results identified by BzScore4 D showed moderate binding between quercetin and the following receptors: glucocorticoids, estrogen beta, and androgens and weak binding between quercetin and the following proteins: estrogen alpha, Peroxisome proliferator-activated receptors (PPARγ), Herg k+ channel, Liver x, mineralocorticoid, progesterone, Thyroid α, and Thyroid β. Three-dimensional/four-dimensional visualization of binding modes of quercetin with glucocorticoids, estrogen beta, and androgen receptors was performed. Based on the results, a possible mechanism is hypothesized for quercetin protection against CCL4 toxicity in the rat brain.
Highlights
The present study evaluated the toxicity of CCL4 in rat brains and investigated whether quercetin can protect against the damage caused by it
All body tissues rapidly take up CCL4, but the toxicity on the blood–brain barrier
All body tissues rapidly take up CCL4, but the toxicity on the brain brain remains poorly understood
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Environmental changes, and drugs can cause harmful effects and injuries through the metabolic production of reactive oxygen species (ROS). The description of oxidative stress is an imbalance between ROS production and antioxidant defense, which causes cell damage at high levels. The ROS and their pathophysiological effects depend on the concentration, type, and specific production site. When ROS are at a high level, they react with DNA, proteins and cell membrane, and other molecules, causing cellular damage and producing other more reactive radicals [1]. The formation of ROS leads to DNA strand breaks and oxidative DNA damage that induce changes in mRNA expression of DNA damage responsive genes [2]
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