Abstract
Safflower (Carthamus tinctorius. L.), a Chinese materia medica, is widely used for the treatment of cardiovascular and cerebrovascular diseases, with flavonoids being the major active components. Multiple flavonoids in safflower bind to Parkinson’s disease (PD)-related protein DJ-1. Safflower flavonoid extract (SAFE) improved behavioral indicators in a 6-hydroxydopamine (6-OHDA)-induced rat model of PD; however, the underlying mechanisms remain unclear. We used a 6-OHDA-induced mouse model of PD and a primary neuron-astrocyte coculture system to determine the neuroprotective effects and mechanisms of SAFE. After three weeks of SAFE administration, behavioral indicators of PD mice were improved. SAFE regulated the levels of tyrosine hydroxylase (TH) and dopamine metabolism. It significantly inhibited the activation of astrocytes surrounding the substantia nigra and reduced Iba-1 protein level in the striatum of PD mice. SAFE reduced the plasma content of inflammatory factors and suppressed the activation of nod-like receptor protein 3 (NLRP3) inflammasome. In the coculture system, kaempferol 3-O-rutinoside and anhydrosafflor yellow B significantly improved neuronal survival, suppressed neuronal apoptosis, and reduced IL-1β and IL-10 levels in the medium. Thus, SAFE showed a significant anti-PD effect, which is mainly associated with flavonoid anti-inflammatory activities.
Highlights
Parkinson’s disease (PD), known as tremor paralysis, is one of the most common neurodegenerative diseases [1]
We found that the main components of safflower flavonoid extract (SAFE), kaempferol 3-O-rutinoside (K3R) and anhydrosafflor yellow B (AYB), could bind with the PD-related protein DJ-1 [14]
Compared with the model group, the crossing number of autonomous activities of SAFE groups was significantly increased (50 mg/kg, p < 0.01 and 100 mg/kg, p < 0.05, Figure 1C), the latent period to fall in the rotarod test was prolonged (50 mg/kg and 100 mg/kg, p < 0.05, Figure 1D), and the time of dropping was significantly reduced (100 mg/kg, p < 0.05, Figure 1E)
Summary
Parkinson’s disease (PD), known as tremor paralysis, is one of the most common neurodegenerative diseases [1]. The main pathological features of PD are gradual loss of nigrostriatal dopaminergic neurons, appearance of characteristic Lewy bodies in the dense part of the substantia nigra (SN), decrease in dopamine (DA) release in the nigrostriatal striatum pathway, and significant reduction in striatum DA [2]. Neuroinflammation has been reported to play a crucial role in the pathogenesis of PD and other neurodegenerative diseases [3]. Knott et al found that astrocytes and microglia were activated in the brain of patients with PD [4]. In-depth study of the mechanism of interaction between astrocytes, microglia, and neurons is of great significance for the treatment of PD [5].
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