Related Experiment Video
Updated: Mar 7, 2026

05:44
Author Spotlight: Creating a Versatile Experimental Autoimmune Encephalomyelitis Model Relevant for Both Male and Female Mice
Published on: October 13, 2023
2.6K
Celastrol Attenuates Multiple Sclerosis and Optic Neuritis in an Experimental Autoimmune Encephalomyelitis Model
Hongbin Yang1, Chang Liu2, Jie Jiang1
1Department of Ophthalmology, The First Affiliated Hospital of Harbin Medical University Harbin, China.
Frontiers in Pharmacology
|February 28, 2017
Summary
Celastrol, a natural compound, effectively treats multiple sclerosis and optic neuritis in rats by reducing inflammation and apoptosis. This study provides preclinical evidence for celastrol
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Multiple sclerosis (MS) and optic neuritis (ON) are debilitating neurological conditions characterized by inflammation and demyelination.
- Experimental autoimmune encephalomyelitis (EAE) is a widely used animal model for studying MS and ON.
- Celastrol is a natural compound derived from Tripterygium wilfordii, known for its diverse bioactivities, including anti-inflammatory properties.
Purpose of the Study:
- To investigate the therapeutic potential of celastrol in a rat model of EAE, mimicking MS and ON.
- To evaluate the effects of celastrol on neuroinflammation, demyelination, and cell apoptosis in the spinal cord and optic nerve.
- To assess the impact of celastrol on key inflammatory and apoptotic pathways.
Main Methods:
- EAE was induced in Sprague Dawley rats using myelin basic protein.
- Rats received daily intraperitoneal injections of celastrol (low and high doses) or vehicle.
- Neurobehavioral assessments, histological analyses of spinal cord and optic nerve, and molecular analyses (mRNA expression, protein activation) were performed.
Main Results:
- Celastrol treatment significantly ameliorated neurobehavioral deficits and reduced inflammatory infiltration and demyelination in EAE rats.
- Celastrol downregulated pro-inflammatory cytokines (interferon-γ, interleukin-17) and upregulated anti-inflammatory cytokines (interleukin-4).
- Celastrol inhibited nuclear factor kappa-B activation, reduced inducible nitric oxide synthase expression, and attenuated apoptosis of retinal ganglion cells in the optic nerve.
Conclusions:
- Celastrol demonstrates potent anti-inflammatory and anti-apoptotic effects in the EAE model.
- Celastrol administration effectively attenuates the pathological hallmarks of multiple sclerosis and optic neuritis.
- These findings support celastrol as a promising therapeutic candidate for treating multiple sclerosis and related optic neuropathies.

