ORIGINAL RESEARCH article
Front. Toxicol.
Sec. Neurotoxicology
Volume 7 - 2025 | doi: 10.3389/ftox.2025.1610720
This article is part of the Research TopicImpact of environmental chemicals on the brain: Models, Mechanisms, and Therapeutic StrategiesView all articles
Subchronic Effects of HgCl₂ on Cognitive Function and Central Inflammation in Type 2 Diabetic Rats: Involvement of BDNF and Acetylcholinesterase
Provisionally accepted
- Faculty of Sciences, Ibn Tofail University, Kenitra, Morocco
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Introduction: Type 2 diabetes mellitus (T2DM) is a major global health concern frequently related with chronic low-grade inflammation and a spectrum of cognitive impairments, including deficits in learning and memory. Mercury chloride (HgCl₂), a widespread environmental pollutant, is recognized for its neurotoxic properties and its capacity to trigger inflammatory responses, particularly in patients with metabolic disorders such as T2DM. Aim; This study aimed to evaluate the subchronic effects of HgCl₂ on cognitive performance and neuroinflammation in a rat model of T2DM, with a particular focus on the roles of BDNF and acetylcholinesterase (AChE). Materials and methods: The experimental design included four groups: control, HgCl₂-treated, diabetic, and diabetic rats treated with HgCl₂. T2DM was induced by intraperitoneal injections of streptozotocin (STZ) and nicotinamide (NA). Rats in the HgCl₂-exposed groups received an oral dose of 0.375 mg/kg/day for 45 consecutive days. Cognitive performance was assessed using behavioral tests targeting spatial learning, recognition memory, and working memory. Additionally, hippocampal and prefrontal cortex (PFC) levels of TNFα, IL-6, BDNF, and AChE activity were measured to evaluate neuroinflammatory and neurotoxic responses. Results: The findings revealed a significant increase in fasting blood glucose levels in both diabetic and HgCl₂-treated diabetic groups compared to controls (P < 0.001). Moreover, HgCl₂ administration in diabetic rats led to a more pronounced impairment in cognitive functions compared to untreated diabetic rats (P < 0.05). These deficits were associated with enhanced neuroinflammatory markers (TNF-α and IL-6), decreased AChE activity, and reduced BDNF expression in the PFC and hippocampus (P < 0.05). Conclusion: Overall, these results highlight the synergistic impact of hyperglycemia and HgCl₂ exposure in exacerbating neuroinflammation and cognitive decline, suggesting a critical interaction between metabolic and environmental neurotoxic factors.
Keywords: type 2 diabetes, Mercury chloride, Neuroinflammation, learning and memory, BDNF, Acetylcholinesterase
Received: 12 Apr 2025; Accepted: 25 Jun 2025.
Copyright: © 2025 Douae, Samir, Meriam, Fatima-Zahra and Aboussaleh. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Bikri Samir, Faculty of Sciences, Ibn Tofail University, Kenitra, 14000, Morocco
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