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<p>This study investigated the 3,3′-Diindolylmethane (DIM) memory-enhancing and neuroprotective effects in Wistar rats against scopolamine (Scop)-induced neurotoxicity. Rats were divided into six groups: healthy control, Scop (1&#xa0;mg/kg), DIM (25, 50, and 100&#xa0;mg/kg), and donepezil (5&#xa0;mg/kg). All groups except the control received Scop for 14 days, with DIM or DPZ administered concurrently. NORT and Y-maze tests were employed to assess cognition and memory. Activity of acetylcholinesterase (AChE), acetylcholine (ACh) levels, oxidative stress parameters (MDA, ROS, SOD, CAT, NRF2, HO-1), inflammatory mediators (TNF-α, NF-κB, IL-6, IL-10), and apoptotic factors (cytochrome c, and caspases) were measured in brain samples, and H&amp;E staining was performed. DIM significantly improved cognition and memory as demonstrated by enhanced spontaneous alternations (%) and recognition index from behavioural analysis. DIM reduces AChE activity and increases ACh levels, indicating that improvement in cholinergic function is the reason for improved cognition and memory. Additionally, DIM treatment enhanced the antioxidant markers like CAT, SOD, NRF2, and HO-1, while reducing the total ROS and MDA levels in the brain, indicating its antioxidant potential. Similarly, DIM attenuated neuroinflammatory mediators IL-6, TNF-α, NF-κB, and elevated IL-10, an anti-inflammatory cytokine, suggesting DIM acts as an anti-inflammatory agent. Moreover, DIM reduced the neuronal apoptosis markers, cytochrome C, caspase 9 and 3, and improved the hippocampal CA1 neuronal architecture, indicating that it preserved the neuronal architecture. Correlation analysis between memory and other biochemical parameters provides a stronger negative correlation with AchE and neuroinflammation and a positive correlation with NRF2, indicating that DIM enhanced memory and neuroprotection involved multiple pathways. In conclusion, DIM enhances cognition and memory by improving cholinergic dysfunction and exhibits neuroprotective effects by reducing oxidative stress, inflammation, and apoptosis against scopolamine-induced neurotoxicity.</p>

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Diindolylmethane confers nootropic and neuroprotection effects against scopolamine-induced brain injury in Wistar rats

  • 期刊论文

  • 发表日期：

    2026年7月15日

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  • Vinjavarapu Lakshmi Anusha,
  • Hari Krishna Reddy Dontiboina,
  • Srikanth Yadava,
  • Naresh Dumala,
  • Narender Malothu,
  • Chakravarthi Guntupalli,
  • Hemlata Kaurav,
  • Kakarla Ramakrishna

摘要

This study investigated the 3,3′-Diindolylmethane (DIM) memory-enhancing and neuroprotective effects in Wistar rats against scopolamine (Scop)-induced neurotoxicity. Rats were divided into six groups: healthy control, Scop (1 mg/kg), DIM (25, 50, and 100 mg/kg), and donepezil (5 mg/kg). All groups except the control received Scop for 14 days, with DIM or DPZ administered concurrently. NORT and Y-maze tests were employed to assess cognition and memory. Activity of acetylcholinesterase (AChE), acetylcholine (ACh) levels, oxidative stress parameters (MDA, ROS, SOD, CAT, NRF2, HO-1), inflammatory mediators (TNF-α, NF-κB, IL-6, IL-10), and apoptotic factors (cytochrome c, and caspases) were measured in brain samples, and H&E staining was performed. DIM significantly improved cognition and memory as demonstrated by enhanced spontaneous alternations (%) and recognition index from behavioural analysis. DIM reduces AChE activity and increases ACh levels, indicating that improvement in cholinergic function is the reason for improved cognition and memory. Additionally, DIM treatment enhanced the antioxidant markers like CAT, SOD, NRF2, and HO-1, while reducing the total ROS and MDA levels in the brain, indicating its antioxidant potential. Similarly, DIM attenuated neuroinflammatory mediators IL-6, TNF-α, NF-κB, and elevated IL-10, an anti-inflammatory cytokine, suggesting DIM acts as an anti-inflammatory agent. Moreover, DIM reduced the neuronal apoptosis markers, cytochrome C, caspase 9 and 3, and improved the hippocampal CA1 neuronal architecture, indicating that it preserved the neuronal architecture. Correlation analysis between memory and other biochemical parameters provides a stronger negative correlation with AchE and neuroinflammation and a positive correlation with NRF2, indicating that DIM enhanced memory and neuroprotection involved multiple pathways. In conclusion, DIM enhances cognition and memory by improving cholinergic dysfunction and exhibits neuroprotective effects by reducing oxidative stress, inflammation, and apoptosis against scopolamine-induced neurotoxicity.