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Icariin attenuates neuroinflammation and exerts dopamine neuroprotection via an Nrf2-dependent manner
Bei Zhang1, Guoqing Wang1, Jingyi He1
1Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, China.
Background:
Oxidative stress and neuroinflammation are considered the major central events in the process of Parkinson's disease (PD). Nrf2 is a key regulator of endogenous defense systems. New finds have contacted activation of Nrf2 signaling with anti-inflammatory activities. Therefore, the outstanding inhibition of neuroinflammation or potent Nrf2 signaling activation holds a promising strategy for PD treatment. Icariin (ICA), a natural compound derived from Herba Epimedii, presents a number of pharmacological properties, including anti-oxidation, anti-aging and anti-inflammatory actions. Recent studies have confirmed ICA exerted neuroprotection against neurodegenerative disorders. However, the underlying mechanisms were not fully elucidated.
Methods:
In the present study, mouse nigral stereotaxic injection of 6-hydroxydopamine (6-OHDA)-induced PD model was performed to investigate ICA-conferred dopamine (DA) neuroprotection. In addition, adult Nrf2 knockout mice and primary rat midbrain neuron-glia co-culture was applied to elucidate whether ICA-exerted neuroprotection was through an Nrf2-dependent mechanism.
Results:
Results indicated that ICA attenuated 6-OHDA-induced DA neurotoxicity and glial cells-mediated neuroinflammatory response. Furtherly, activation of Nrf2 signaling pathway in glial cells participated in ICA-produced neuroprotection, as revealed by the following observations. First, ICA enhanced Nrf2 signaling activation in 6-OHDA-induced mouse PD model. Second, ICA failed to generate DA neuroprotection and suppress glial cells-mediated pro-inflammatory factors production in Nrf2 knockout mice. Third, ICA exhibited neuroprotection in primary neuron-glia co-cultures but not in neuron-enriched cultures (without glial cells presence). Either, ICA-mediated neuroprotection was not discerned after Nrf2 siRNA treatment in neuron-glia co-cultures.
Conclusions:
Our findings identify that ICA attenuated glial cells-mediated neuroinflammation and evoked DA neuroprotection via an Nrf2-dependent manner.
Insights
Icariin (ICA) protects dopamine neurons in Parkinson's disease (PD) by reducing neuroinflammation. This neuroprotection relies on activating the Nrf2 pathway, particularly in glial cells.
Area of Science:
- Neuroscience
- Pharmacology
- Cell Biology
Background:
- Parkinson's disease (PD) involves oxidative stress and neuroinflammation.
- Nrf2 is a key regulator of cellular defense, and its activation shows anti-inflammatory effects.
- Icariin (ICA), a natural compound, has demonstrated neuroprotective properties, but its mechanism in PD is unclear.
Purpose of the Study:
- To investigate the neuroprotective effects of Icariin (ICA) in a Parkinson's disease (PD) model.
- To elucidate the role of the Nrf2 signaling pathway in ICA-mediated neuroprotection.
Main Methods:
- A 6-hydroxydopamine (6-OHDA) induced PD mouse model was used.
- Nrf2 knockout mice and primary rat neuron-glia co-cultures were employed.
- The study assessed dopamine (DA) neuroprotection and neuroinflammation markers.
Main Results:
- ICA reduced 6-OHDA-induced DA neurotoxicity and neuroinflammation.
- ICA enhanced Nrf2 signaling activation in the PD model.
- Neuroprotection by ICA was dependent on Nrf2 and the presence of glial cells.
Conclusions:
- Icariin (ICA) attenuates neuroinflammation mediated by glial cells.
- ICA confers dopamine (DA) neuroprotection through an Nrf2-dependent mechanism.
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