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<p>Bisphenol A (BPA), a main component of polycarbonate plastics and epoxy resins, has been reported to cause chronic neuroinflammation and cognitive impairment in animal models. However, the precise molecular mechanisms of BPA-induced chronic neuroinflammation remain unknown. In this study, male C57BL/6 mice were administered BPA at different doses for one month, followed by a one-month washout period. We then conducted behavioral tests, oxidative stress assays, and immunohistochemistry to quantify neuronal density and the activation of microglia and astrocytes in the central nervous system. We also carried out RT-qPCR gene expression analysis of the hippocampus for the cGAS-STING-NLRP3 pathway, cytokine assays, and microglial markers to decipher the immune responses in the hippocampus following BPA exposure. BPA induced dose-dependent behavioral deficits, which were most pronounced at 50&#xa0;mg/kg. These findings suggest that cGAS–STING signaling acts as a key upstream mediator of BPA-induced hippocampal neuroinflammation and cognitive dysfunction.</p>

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Chronic bisphenol A exposure activates the cGAS-STING-NLRP3 axis driving persistent hippocampal neuroinflammation and cognitive impairment

  • 期刊论文

  • 发表日期：

    2026年5月21日

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  • Veena V Tom,
  • Sumit Mallick,
  • Athira Sasidharan,
  • Tanika Biswas,
  • Bipasha Bose,
  • Yogish  Somayaji,
  • Ronald Fernandes

摘要

Bisphenol A (BPA), a main component of polycarbonate plastics and epoxy resins, has been reported to cause chronic neuroinflammation and cognitive impairment in animal models. However, the precise molecular mechanisms of BPA-induced chronic neuroinflammation remain unknown. In this study, male C57BL/6 mice were administered BPA at different doses for one month, followed by a one-month washout period. We then conducted behavioral tests, oxidative stress assays, and immunohistochemistry to quantify neuronal density and the activation of microglia and astrocytes in the central nervous system. We also carried out RT-qPCR gene expression analysis of the hippocampus for the cGAS-STING-NLRP3 pathway, cytokine assays, and microglial markers to decipher the immune responses in the hippocampus following BPA exposure. BPA induced dose-dependent behavioral deficits, which were most pronounced at 50 mg/kg. These findings suggest that cGAS–STING signaling acts as a key upstream mediator of BPA-induced hippocampal neuroinflammation and cognitive dysfunction.