# Neuroprotective effects of cobalt oxide nanoparticles through mitigating oxidative stress and reactive glial responses in traumatic brain injury

## TL;DR

Cobalt oxide nanoparticles may help protect the brain after injury by reducing harmful stress and inflammation.

## Contribution

Dimercaptosuccinic acid-coated cobalt oxide nanoparticles show novel therapeutic potential for traumatic brain injury.

## Key findings

- Co3O4 NPs reduced oxidative stress and neuronal death in a TBI mouse model.
- The nanoparticles mitigated reactive glial activation and improved motor recovery.
- They decreased astrocytic NOX2 expression and neuronal ROS levels.

## Abstract

Traumatic brain injury (TBI) is a leading global cause of mortality and long-term neurological deficits. TBI involves primary mechanical damage and secondary injury processes, including oxidative stress and reactive glial responses. Oxidative stress, driven by excessive reactive oxygen species (ROS), exacerbates neuronal damage, causing cellular apoptosis and prolonged inflammation. Traditional antioxidants have limited efficacy due to poor bioavailability and targeting. Nanotechnology-based antioxidants offer a promising alternative due to their intrinsic antioxidative activities. In the present study, we explored the neuroprotective effects of dimercaptosuccinic acid-coated cobalt oxide nanoparticles (Co3O4 NPs) in a mouse TBI model. Co3O4 NPs significantly reduced oxidative stress, neuronal death, brain tissue loss, and reactive glial activation, thereby enhancing long-term motor function recovery. Mechanistically, Co3O4 NPs lowered neuronal ROS levels. Co3O4 NPs also decreased astrocytic NOX2 expression, mitigating reactive glial responses. These findings suggest that Co3O4 NPs might offer therapeutic potential for TBI.

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