# Crinis Carbonisatus-Derived Carbon Dot Suspension Alleviates Temporal Lobe Epilepsy

## TL;DR

A new carbon dot suspension derived from Crinis Carbonisatus reduces seizures and related symptoms in a mouse model of temporal lobe epilepsy.

## Contribution

A novel eco-friendly method to synthesize carbon dots that show therapeutic potential for treating temporal lobe epilepsy.

## Key findings

- CC-CDs inhibited MAPK pathway phosphorylation and reduced pro-inflammatory cytokines in TLE mice.
- CC-CDs restored antioxidant enzyme activities and improved cognitive and anxiety-related behaviors in TLE mice.
- CC-CDs suppressed LPS-induced apoptosis in BV2 cells, indicating anti-inflammatory effects.

## Abstract

Background: Temporal lobe epilepsy (TLE), a prevalent refractory focal epilepsy frequently complicated by comorbid anxiety and depression, poses significant therapeutic challenges due to the inadequate efficacy of current antiepileptic drugs in seizure control. Carbon dots (CDs) demonstrate notable biological activities and represent a promising class of nanomedicines for TLE intervention. Methods: This study established an eco-friendly calcination protocol to synthesize a novel suspension of Crinis Carbonisatus-derived carbon dots (CC-CDs) as a candidate therapeutic for TLE. Results: In a TLE mouse model, the CC-CDs suspension significantly inhibited phosphorylation of the MAPK pathway (p-JNK, p-ERK, p-p38; p < 0.01, p < 0.05), leading to reduced levels of pro-inflammatory cytokines (IL-6, IL-1β, TNF-α; p < 0.01, p < 0.05), upregulation of TGF-β1 (p < 0.01, p < 0.05), and restoration of antioxidant enzyme activities (SOD, GSH, CAT; p < 0.01, p < 0.05). These modifications subsequently regulated the Glu/GABA balance, alleviating excitotoxicity (p < 0.05), attenuating neuronal damage and Nissl body loss in hippocampal CA1/CA3 regions, and improving cognitive function alongside reducing anxiety-like behaviors (p < 0.01, p < 0.05). In vitro, the CC-CDs suspension suppressed LPS-induced apoptosis in BV2 cells. Conclusions: The CC-CDs suspension ameliorates TLE by inhibiting MAPK signaling, thereby reducing neuroinflammation and oxidative stress, rectifying Glu/GABA imbalance, attenuating excitotoxicity, and ultimately improving behavioral deficits. These findings underscore the therapeutic potential of CC-CDs suspension for TLE treatment.