Abstract
Parkinson’s disease (PD), the second primary neurodegenerative disease affecting human health, is mainly characterized by dopaminergic neuron damage in the midbrain and the clinical manifestation of movement disorders. Studies have shown that neuroinflammation plays an important role in the progression of PD. Excessively activated microglia produce several pro-inflammatory mediators, leading to damage to the surrounding neurons and finally inducing neurodegeneration. Echinocystic acid (EA) exhibits an anti-inflammatory effect in peripheral tissues. However, whether it inhibited neuroinflammation remains unclear. Therefore, the current study investigates the effect of EA on neuroinflammation and whether it can improve PD symptoms through inhibiting neuroinflammation. In our experiments, we discovered that EA inhibited the production of pro-inflammatory mediators in LPS-exposed BV2 cells. Further mechanism-related studies revealed that EA inhibited inflammation by activating PI3K/Akt and inhibiting NF-κB and MAPK signal pathways in LPS-induced BV2 cells. Research revealed that EA eases microglia-mediated neuron death in SN4741 and SHSY5Y cells. In in vivo studies, the results demonstrated that EA improves weight loss and behavioral impairment in MPTP-induced mice. Further studies have revealed that EA inhibited dopaminergic neuron damage and inflammation in the mice midbrain. In conclusion, our study demonstrated that EA inhibits neuroinflammation and exerts neuroprotective effects by activating PI3K/Akt and inhibiting NF-κB and MAPK signal pathways in vivo and in vitro.
Highlights
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder, and its clinical manifestations are mainly motor symptoms such as resting tremor and muscle rigidity
PD, the second most prevalent neurodegenerative disorder affecting human health, is characterized by dopaminergic neuron damage in the substantia nigra of the midbrain, resulting in reduced dopamine content in the striatum, which leads to movement disorders in patients (Dauer and Przedborski, 2003; Hawkes et al, 2010)
The treatment of PD mainly focuses on increasing the number of dopaminergic neurons in the midbrain substantia nigra of the patient or enhancing the capacity of the remaining dopaminergic neurons to produce dopamine
Summary
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder, and its clinical manifestations are mainly motor symptoms such as resting tremor and muscle rigidity. Studies have shown that the combined effects of aging, genetics, and environmental factors lead to the onset of PD (Pollak, 2004; Nakano-Kobayashi et al, 2020; Ramli et al, 2020). The commonly used clinical treatment methods mainly focus on Echinostic Acid Inhibits Neuroinflammation rehabilitation training to assist drug therapy, but the rehabilitation training has little effect on severely ill patients. The commonly used clinical drugs have limited effects, and their long-term use has strong side effects (Bomalaski et al, 2017; Houman, 2018; Elkouzi et al, 2019). Exploring the pathogenesis of PD and discovering effective and alleviating drugs for PD treatment are required
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