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Drug Development.

Varinder Singh1, Pratham Gautam2

  • 1Department of Pharmaceutical Sciences and Technology, Maharaja Ranjit Singh Punjab Technical University, Bathinda, Punjab, India.

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|December 26, 2025
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Summary
This summary is machine-generated.

Hesperidin protects against lead-induced cognitive impairment by reducing oxidative stress and inflammation, potentially via transcription factor EB (TFEB) activation. This highlights hesperidin

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Area of Science:

  • Neuroscience
  • Environmental Health
  • Pharmacology

Background:

  • Lead exposure is a significant environmental neurotoxin causing cognitive impairment.
  • Mechanisms include oxidative stress, inflammation, and mitochondrial dysfunction.
  • Transcription factor EB (TFEB) role in neuroprotection is under investigation.

Purpose of the Study:

  • Investigate hesperidin's neuroprotective effects against lead-induced cognitive dysfunction.
  • Determine the role of TFEB in hesperidin's mechanism of action.

Main Methods:

  • Lead acetate administered to Wistar rats to induce memory deficits.
  • Hesperidin administered post-exposure, cognitive function assessed via behavioral tests.
  • Biochemical assays for oxidative stress, inflammation, and mitochondrial function.
  • Hippocampal histopathology evaluated neuronal damage.

Main Results:

  • Hesperidin improved memory, restored glutathione, enhanced mitochondrial activity, and reduced oxidative/inflammatory markers.
  • Histopathology showed reduced neuronal damage in hesperidin-treated rats.
  • TFEB inhibition abolished hesperidin's protective effects, confirming TFEB's essential role.

Conclusions:

  • Hesperidin alleviates lead neurotoxicity by mitigating oxidative stress, inflammation, and neuronal damage.
  • TFEB activation is a key mechanism in hesperidin's neuroprotective action.
  • Hesperidin shows therapeutic potential for heavy metal-induced neurotoxicity and cognitive disorders.