What does this research mean for the field?

Emodin improves redox balance and reduces oxidative damage in synaptic terminals of aged rats. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

The study aims to evaluate the effects of emodin on redox parameters in synaptic terminals from young and old rats.

February 22, 2026Degenerative Neurological and Neuromuscular Disease0 citationsOpen Access

Emodin, a Phytotherapeutic Anthraquinone, Potently Attenuates Synaptic Redox Pathology in Aged Rats

PSPriyanka SahaAll India Institute of Medical Sciences FAFaraz AhmadVellore Institute of Technology University

Key Points

The study aims to evaluate the effects of emodin on redox parameters in synaptic terminals from young and old rats.
Isolated brain synaptosomes from young and aged male Wistar rats.
Assessed antioxidant capacities using ABTS and FRAP assays.
Quantified reactive oxygen species (ROS) and examined oxidative modifications to proteins and lipids.
Investigated the antioxidant effects of emodin on synaptic oxidative stress.
Observed significant decline in antioxidant capacity and increased ROS levels in aged rat synaptosomes.
Detected oxidative damage, including elevated protein carbonylation and lipid peroxidation.
Emodin treatment improved redox balance, reducing ROS levels and oxidative damage markers in older rats.

Abstract

Background: Aging is associated with increased oxidative stress, which leads to synaptic vulnerability and psychiatric and cognitive deficits. Maintaining redox homeostasis is crucial for synaptic health. However, age-related alterations in synapse-specific antioxidant capacity remain poorly understood. Moreover, effective therapeutic strategies to counteract these changes are lacking. This study aimed to assess redox parameters in ex vivo synaptic terminals from young and old rat brains and evaluate the modulatory effects of the phytotherapeutic compound emodin. Methods: Brain synaptosomes were isolated from young and old male Wistar rats. The antioxidant capacities were determined using 2,2′-azinobis-3-ethylbenzothiazoline-6-sulfonic acid (ABTS) and ferric-reducing antioxidant power (FRAP) assays. Oxidative stress and damage were assessed by quantifying reactive oxygen species (ROS) and nitrogen species (RNS) and examining oxidative modifications of proteins and lipids. The antioxidant effects of emodin were investigated in mitigating synaptic oxidative stress and damage. Results: A significant decline in antioxidant capacity and increase in ROS levels were observed in the synaptosomes of aged animals. Oxidative damage was also evident as increased protein carbonylation, thiol oxidation, and lipid peroxidation. Emodin treatment improved redox balance by reducing ROS levels, decreasing oxidative damage markers, and enhancing antioxidant defenses, particularly in older animals. Conclusion: Aging disrupts synaptic redox homeostasis and increases the susceptibility to oxidative damage. Emodin exerts protective antioxidant effects by mitigating oxidative stress and enhancing the redox capacity of the synaptosomes. These findings suggest that emodin may have therapeutic potential in preserving synaptic function under conditions of age-related oxidative stress, although further functional and molecular studies are warranted to validate its neuroprotective efficacy. Keywords: ageing, oxidative stress, antioxidants, synaptosomes, emodin

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