Ferulic Acid Improves Depressive-Like Behavior in Prenatally-Stressed Offspring Rats via Anti-Inflammatory Activity and HPA Axis

Abstract

Prenatal stress (PS) can increase the risk of nervous, endocrine and metabolic diseases, and immune dysfunction. Ferulic acid (FA) is a dietary phenolic acid that has pharmacological properties, including potent anti-inflammatory action. We used male, prenatally-stressed offspring rats to investigate the anti-depressive-like effects and possible anti-inflammatory mechanism of FA. We determined the animal behaviors, and the mRNA expression and concentration of inflammatory cytokines, and HPA axis. In addition, we assessed the modulation of hippocampal nuclear factor-κB (NF-κB) activation, neuronal nitric oxide synthase (nNOS) and glucocorticoid receptors (GR) expression via western blotting and immunohistochemistry. Administration of FA (12.5, 25, and 50 mg/kg/day, i.g.) for 28 days markedly increased sucrose intake, and decreased immobility time and total number of crossings, center crossings, rearing, and grooming in the male PS offspring. FA significantly reduced IL-6, IL-1β, and TNF-α concentration and increased IL-10 concentration in male, prenatally-stressed offspring, stimulated by the NF-κB pathway. In addition, FA inhibited interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α), and increased interleukin-10 (IL-10) mRNA and protein expression. Furthermore, FA markedly decreased the serum adrenocorticotropin (ACTH) and corticosterone concentration by the increase of GR protein expression. Taken together, this study revealed that FA has anti-depressive-like effects in male, prenatally-stressed offspring, partially due to its anti-inflammatory activity and hypothalamic-pituitary-adrenal (HPA) axis.

Ferulic Acid Alleviates Lipotoxicity-induced Hepatocellular Death Through SIRT1 Activating-regulated Autophagy Pathway, and Independently of AMPK and Akt in AML-12 Hepatocytes

“…Accumulated studies including ours have indicated that PA exposure transcriptionally stimulated expressions of pro-in ammatory factors, including IL-1beta and IL-6 [68][69][70]. In the present study, we observed that FA intervention markedly reversed PA-caused activation of proin ammatory factors in hepatocytes, which was in line with the facts that FA-inhibited pro-in ammatory reactions in other types of cells [71,72]. Therefore, we presumed that FA-blocked in ammation might be mechanistically participated in its lipotoxicity-alleviative role.…”

Ginsenoside-Rg1 Rescues Stress-Induced Depression-Like Behaviors via Suppression of Oxidative Stress and Neural Inflammation in Rats

“…Postmortem studies have revealed that major depression patients exhibit a reduced size in pyramidal neurons and a decreased number of GABAergic interneurons [9]. Within studies using animal models of depression, significant elevations in some critical proinflammatory cytokines including interleukin-1β (IL-1β), interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α) were present, whereas treatments with some putative antidepressant drugs or neuroprotective reagents reduced the levels of these proinflammatory cytokines to varying degrees while also producing antidepressant-like effects [10,11]. These results provide strong evidence indicating that inflammationinduced neuronal injury may represent a major risk factor for the development of depression.…”

Potential Advantages of Bioactive Compounds Extracted From Traditional Chinese Medicine to Inhibit Bone Destructions in Rheumatoid Arthritis

“…In fact, since RES has multiple intracellular targets, additional data are needed to determine the results of interactions or synergies between other polyphenols. FA has the functions of anti-inflammatory, anti-oxidation, inhibiting platelet aggregation, improving microcirculation, and so on (Zheng et al, 2019;Perez-Ternero et al, 2017). Zhu et al found FA significantly alleviated joint swelling and reversed the increase of C-reactive protein (CRP) and rheumatoid factor (RF) in CFA rats, its protective mechanism on joints is mainly to reduce the secretion of TNF-a and increase the secretion of TGF-b by inhibiting JAK/STAT pathway (Zhu et al, 2020b).…”