Gallic Acid: A Potential Therapeutic Agent for Managing Diabetes-Associated Neuroinflammation and Cognitive Decline
Year: 2025
Type: article
Abstract: Recent studies have implicated diabetes as a risk factor for neuroinflammation and cognitive decline, increasing the likelihood of dementia and other neurodegenerative disorders. Gallic acid, a polyphenolic compound extracted from gallnuts, is being studied for its possible therapeutic effects in glucose-related disorders. This study aimed to explore the potential of gallic acid as a therapeutic agent for managing diabetes-associated neuroinflammation and cognitive dysfunction. Thirty-two male Wistar rats used in this experiment were randomly divided into four groups: normal control, diabetic, and two groups receiving gallic acid at doses of 50 mg/kg and 100 mg/kg. The diabetic and gallic acid groups received 65mg/kg b.w. streptozotocin intraperitoneally and were subsequently treated with gallic acid. The open field test was used to assess long-term recognition memory, while brain tissue was collected for histology and biochemical analyses. Gallic acid treatment at a dose of 100mg/kg significantly improved habituation scores (p<0.05) and discrimination indices (p<0.05) in diabetic rats. Also, treatment with gallic acid prevented neuronal death and microglial depletion caused by diabetes, with mild microglial activation in the cerebral cortex. Furthermore, gallic acid treatment reduced neuroinflammation in a dose-dependent manner, characterised by decreased (p<0.05) interleukin-6 at 50 mg/kg and 100 mg/kg) and tumour necrosis factor-alpha levels (p<0.05) at 50 mg/kg and 100 mg/kg. The study found that gallic acid significantly protected cognitive function and reduced neuroinflammation in diabetic male Wistar rats. These findings suggest that gallic acid may serve as a therapeutic agent for managing diabetes-associated neuroinflammation and cognitive decline.
Source: NIgerian Journal of Neuroscience
Authors: Theresa E. Isamoh, Eru E. Mba, Michael E. Oku, Nsikak M. Umoh, Michael I. Odom, Emmanuel Peter, Prisca N. Umeh
Institution: University of Calabar
Language: English
Subfield: Neurology
Field: Neuroscience
Domain: Life Sciences
Open Access status: hybrid
OpenAlex ID: W4409862496