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Subchronic effects of HgCl2 on cognitive function and central inflammation in type 2 diabetic rats: involvement of
Douae Benloughmari1, Samir Bikri1,2, Meriam El Aboubi3
1Faculty of Sciences, Laboratory of Biology and Health, Ibn Tofail University, Kenitra, Morocco.
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 TNF-α, 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.
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