Neuroprotective Effect of <i>trans</i>-Cinnamaldehyde on the 6-Hydroxydopamine-Induced Dopaminergic Injury

Abstract

The anti-inflammatory and neuroprotective effects of trans-cinnamaldehyde (TCA) were investigated on the inflammatory cells and the dopaminergic degeneration in mice. TCA inhibited the up-regulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the lipopolysaccharide (LPS)-induced inflammatory BV2 microglial cells. To investigate the TCA efficacy on the 6-hydroxydopamine (6-OHDA)-induced dopaminergic degeneration in mice, an intracerebroventricular injection of 6-OHDA was given to the mice, and TCA (30 mg/kg) was intraperitoneally administered. At 7 d after the 6-OHDA injection, 6-OHDA led to a severe loss of tyrosine hydroxylase (TH)-positive dopaminergic neurons in the striatum and substantia nigra (SN). On the other hand, TCA dramatically maintained the number of TH-positive dopaminergic neurons in the striatum and SN regions of the 6-OHDA-treated mice, which indicates that TCA is able to inhibit the 6-OHDA-induced reduction of TH expression in the dopaminergic neurons in the striatum and SN regions. TCA also inhibited the induction of iNOS and COX-2 in the 6-OHDA model, similarly as shown in the LPS-induced inflammatory BV2 microglial cells. These results indicate that TCA has a neuroprotective effect on dopaminergic neurons and that this effect may be associated with the inhibition of inflammatory responses. These findings suggest that TCA may be a therapeutic candidate for the prevention of inflammationmediated neurodegenerative diseases.

Cinnamaldehyde Inhibits Staphylococcus aureus Virulence Factors and Protects against Infection in a Galleria mellonella Model

“…Our data show that cinnamaldehyde diminishes S. aureus -induced hemolysis, but is only able to inhibit this parameter in one of the tested E. faecalis strains. The effects of cinnamaldehyde on cell survival have been widely studied in different cells lines, including immune cells (Roth-Walter et al, 2014), neurones (Pyo et al, 2013), erythrocytes (Theurer et al, 2013), amongst others. Of importance, this compound was shown to cause hemolysis per se when incubated for 48 h with human erythrocytes (Theurer et al, 2013).…”

Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

“…As 6-OHDA shares certain structural similarities with DA, it can enter dopaminergic neurons via DA transporters, and consequently cause toxicity (Shi et al, 2011). It produces diverse toxic effects, such as mitochondrial dysfunction and oxidative stress, apoptosis, neuroinflammation, and dopaminergic cell death (Chan et al, 2009; Liang et al, 2011; Shi et al, 2011; Thornton and Vink, 2012; Guo et al, 2013; Pyo et al, 2013; Wang J. Y. et al, 2013; Elyasi et al, 2014; Magalingam et al, 2014; Mu et al, 2014; De Jesús-Cortés et al, 2015; Liu et al, 2015; Yan et al, 2015; Zhang et al, 2015; Mirzaie et al, 2016). Disturbance of the dopaminergic system may also cause glutamatergic NMDARs imbalances in the brain (Hallett et al, 2006).…”

trans‐Cinnamaldehyde Reverses Depressive‐Like Behaviors in Chronic Unpredictable Mild Stress Rats by Inhibiting NF‐κB/NLRP3 Inflammasome Pathway

“…TCA is a main active component in Cinnamomum cassia (C. cassia), which exhibits a variety of pharmacological effects, such as anti-inflammatory, antitumor, hypoglycemia, and enhanced obesity [15][16][17][18]. TCA has a certain antineuroinflammatory effect, and its protective effect on dopaminergic neurons may be related to the inhibition of inflammation [19]. TCA inhibits microglia activation and inflammatory response induced by lipopolysaccharide (LPS) [20].…”