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Caffeic Acid Mitigates Behavioral and Biochemical Alterations in Lead-induced Neurotoxicity in Rats With Possible
Pratham Gautam1, Varinder Singh2,3, Navjot Kanwar1
1Department of Pharmaceutical Sciences and Technology, Maharaja Ranjit Singh Punjab Technical University, Bathinda, Punjab, India.
Neurotoxicity Research
|July 20, 2026
Summary
Caffeic acid (CFA) protects against lead (Pb) neurotoxicity by improving mitochondrial function and reducing inflammation. These neuroprotective effects are linked to the activation of Transcription Factor EB (TFEB) signaling pathways.
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Lead (Pb) neurotoxicity causes cognitive and motor deficits by disrupting mitochondrial function, oxidative balance, and neuroinflammation.
- Transcription Factor EB (TFEB) regulates cellular quality control, and its impairment exacerbates Pb-induced neurodegeneration.
Purpose of the Study:
- To evaluate the neuroprotective effects of caffeic acid (CFA) against Pb-induced neurotoxicity.
- To investigate the role of TFEB signaling in CFA's neuroprotective mechanisms.
Main Methods:
- Wistar rats were exposed to lead acetate and treated with CFA, with or without a TFEB inhibitor (eltrombopag).
- Behavioral tests (Morris Water Maze, rota rod) and biochemical analyses (mitochondrial activity, oxidative stress, inflammation markers) were performed.
Main Results:
- Pb exposure induced spatial memory deficits, motor impairment, reduced mitochondrial activity, oxidative stress, and inflammation.
- CFA treatment reversed these Pb-induced alterations.
- The beneficial effects of CFA were abolished by TFEB inhibition.
Conclusions:
- Caffeic acid (CFA) attenuates lead-induced neurotoxicity, improving cognitive and motor functions.
- CFA's neuroprotective effects are mediated, in part, through the TFEB signaling pathway, highlighting its role in mitigating Pb-induced cellular damage.
