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Morroniside maintains mitochondrial homeostasis in microglia and mitigates neuroinflammation in experimental
Shaopeng Zhai1, Taotao Jiang1, Xiaorong Cheng2
1Department of Neurology, Lanzhou University Second Hospital, Lanzhou, China.
Abstract:
Microglia-mediated neuroinflammation in the central nervous system is a hallmark of both multiple sclerosis (MS) and the animal model experimental autoimmune encephalomyelitis (EAE). Current immunosuppressive therapies for MS have limited efficacy and notable side effects. This study aimed to investigate mechanisms underlying anti-neuroinflammatory effects of morroniside, an iridoid glycoside derived from Cornus officinalis, which is used in Chinese herbal medicine. Morroniside treatment significantly attenuated lipopolysaccharide-induced alterations and mitochondrial dysfunction in BV2 microglia cells. In vivo, morroniside treatment improved clinical scores and ameliorated pathological findings and neurological deficits in a mouse EAE model. Mechanistic investigations revealed that morroniside activated the Nrf2/HO-1 signaling axis, promoted Nrf2 nuclear translocation and elevated HO-1 expression. This activation also upregulated p62, thereby enhancing LC3-II/PINK1/Parkin-mediated mitophagosome formation. The resultant mitophagy suppressed p65 phosphorylation leading to anti-inflammatory effects. Collectively, our findings suggest that morroniside ameliorates EAE by increasing anti-inflammatory microglial activation through upregulating the Nrf2/HO-1/p62 axis to mitigate mitochondrial oxidative stress and enhance mitophagy. These results identify morroniside as a promising therapeutic candidate for MS and emphasize the importance of the Nrf2-p62-mitophagy axis in resolving neuroinflammation and maintaining mitochondrial homeostasis.
Insights
Morroniside, a compound from traditional Chinese medicine, reduces neuroinflammation in multiple sclerosis models by enhancing microglial anti-inflammatory activity and mitophagy. This study highlights its potential therapeutic benefits for multiple sclerosis (MS).
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Neuroinflammation, driven by microglia, is central to multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE).
- Existing MS therapies have limitations in efficacy and side effect profiles.
Purpose of the Study:
- To investigate the anti-neuroinflammatory mechanisms of morroniside, an iridoid glycoside from Cornus officinalis.
- To evaluate morroniside's therapeutic potential for MS by examining its effects on neuroinflammation and mitochondrial function.
Main Methods:
- Assessed morroniside's effects on lipopolysaccharide-induced inflammatory responses and mitochondrial dysfunction in BV2 microglia cells.
- Evaluated morroniside's efficacy in a mouse model of experimental autoimmune encephalomyelitis (EAE), monitoring clinical scores and neuropathology.
- Investigated the underlying molecular mechanisms, focusing on the Nrf2/HO-1 signaling pathway, p62, and mitophagy.
Main Results:
- Morroniside treatment attenuated inflammatory markers and mitochondrial dysfunction in microglia.
- In vivo, morroniside improved clinical outcomes, reduced pathological damage, and alleviated neurological deficits in EAE mice.
- Mechanistically, morroniside activated the Nrf2/HO-1 pathway, upregulated p62, enhanced mitophagy, and suppressed p65 phosphorylation, leading to anti-inflammatory effects.
Conclusions:
- Morroniside ameliorates EAE by promoting anti-inflammatory microglial activation via the Nrf2/HO-1/p62-mitophagy axis.
- This process mitigates mitochondrial oxidative stress and enhances mitophagy, resolving neuroinflammation.
- Morroniside shows promise as a therapeutic agent for MS, underscoring the role of the Nrf2-p62-mitophagy axis in neuroinflammation.
