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, 27 (3), 189-199

Antidepressant-like Effects of p-Coumaric Acid on LPS-induced Depressive and Inflammatory Changes in Rats

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Antidepressant-like Effects of p-Coumaric Acid on LPS-induced Depressive and Inflammatory Changes in Rats

Seok Lee et al. Exp Neurobiol.

Abstract

Depression causes mental and physical changes which affect quality of life. It is estimated to become the second most prevalent disease, but despite its commonness, the pathophysiology of depression remains unclear and medicine is not sufficiently protective. p-Coumaric acid (p-CA) is a dietary phenolic acid which has been proven to have antifungal, anti-HIV, anti-melanogenic, antioxidant and anti-inflammatory effects. Considering these effects, we investigated whether p-CA can prevent depressive symptoms by reducing inflammatory cytokines in animals injected with lipopolysaccharide (LPS). Changes in despair-related behaviors, inflammatory cytokines, neurotrophic factors and synaptic activity were measured. In these animals, p-CA improved despair-related behavioral symptoms induced by LPS in the forced swim test (FST), tail suspension test (TST) and sucrose splash test (SST). p-CA also prevented the increase of inflammatory cytokines in the hippocampus such as cycloxigenase-2 and tumor necrosis factor-α due to LPS. Similarly, it prevented the reduction of brain-derived neurotrophic factor (BDNF) by LPS. Electrophysiologically, p-CA blocked the reduction of long-term depression in LPS-treated organotypic tissue slices. In conclusion, p-CA prevented LPS-induced depressive symptoms in animals, as determined by behavioral, biochemical and electrophysiological measures. These findings suggest the potential use of p-CA as a preventive and therapeutic medicine for depression.

Keywords: Cytokines; Depression; Lipopolysaccharide (LPS); Long-term synaptic depression (LTD); p-coumaric acid (p-CA).

Figures

Fig. 1
Fig. 1. Chemical structure of p-coumaric acid.
Fig. 2
Fig. 2. Diagram of experimental schedule for p-CA and LPS administration and behavioral tests.
Fig. 3
Fig. 3. Effects of LPS and p-CA on depression-like behaviors (n=6/group). (A) Schematic diagram of the FST. (B) Immobility time in the forced swim test. (C) Accumulated climbing time in the FST. (D) Schematic diagram of the TST. (E) Immobility time in the TST. (F) Accumulated climbing time in the SST. Data are shown as mean±standard error of the mean (SEM). Control, saline; LPS, saline+LPS 200 µg/kg; p-CA 50, p-CA 50 mg/kg+LPS 200 µg/kg; p-CA 75, p-CA 75 mg/kg+LPS 200 µg/kg; p-CA 100, p-CA 100 mg/kg+LPS 200 µg/kg. *p<0.05, **p<0.01, ***p<0.001 versus LPS group and #p<0.05, ##p<0.01, ###p<0.01 versus LPS-treated group by ANOVA Scheffe post-hoc test.
Fig. 4
Fig. 4. Effects of LPS and p-CA on the hippocampal expression of inflammatory cytokines and BDNF (n=5/group). (A) Immunoblotting and band quantification of cycloxigenase-2. (B) Immunoblotting and band quantification of tumor necrosis factor-α. (C) Immunoblotting and band quantification of BDNF. Data are shown as mean±SEM. Control, saline+saline; LPS, saline+LPS 200 µg/kg; p-CA 50, p-CA 50 mg/kg+LPS 200 µg/kg; p-CA 75, p-CA 75 mg/kg+LPS 200 µg/kg; p-CA 100, p-CA 100 mg/kg+LPS 200 µg/kg. *p<0.05 versus control group and #p<0.05, ##p<0.01, ###p<0.001 versus LPS-treated group by ANOVA Scheffe post-hoc test.
Fig. 5
Fig. 5. Effects of p-CA on LTD in rat hippocampal tissue (n=5/group). (A) Grouped data showing the time course of LTD from all recordings in hippocampal tissue treated with LPS, with and without p-CA. (B) Average LTD amplitude measured at 30~40 minutes after LFS. Data are shown as mean±SEM. Control, vehicle only; LPS, LPS 1 µg/ml; p-CA, p-CA 50 µM; LPS+p-CA, LPS 1 µg/ml and p-CA 50 µM. **p<0.01 versus the control group. ##p<0.01 versus LPS treated group. Repeated measure ANOVA Dunnett T3 post-hoc test for (A) and ANOVA Dunnett T3 post-hoc test for (B).

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