Ferulic acid reverses depression-like behavior and oxidative stress induced by chronic corticosterone treatment in mice

Zeni, Ana Lúcia Bertarello; Camargo, Anderson; Dalmagro, Ana Paula

doi:10.1016/j.steroids.2017.07.006

Cited by 70 publications

(42 citation statements)

References 45 publications

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“…Oxido-nitrosative stress is another factor that determines the progression of depression. In rodents, different types of chronic stress have been shown to induce increased oxidative stress and decreased anti-oxidant defenses [44,45]. The changes in parameters reflecting the oxidative status can be observed in depressed patients [18].…”

Section: Effect Of Sb On Lps-induced Enhancement Of Oxido-nitrosativementioning

confidence: 99%

Lipopolysaccharide-Induced Depression-Like Behaviors Is Ameliorated by Sodium Butyrate via Inhibiting Neuroinflammation and Oxido-Nitrosative Stress

Qiu

Liu

et al. 2020

Pharmacology

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Depression is a common disease that afflicts one in 6 people. Numerous hypotheses have been raised in the past decades, but the exact mechanism for depression onset remains obscure. Recently, the neuroinflammatory response and oxidative stress are being attracted more and more attention due to their roles in depression pathogenesis. The inhibition of neuroinflammatory response and oxidative stress is now considered a potential strategy for depression prevention and/or therapy. Sodium butyrate (SB) is a sodium form of the endogenous butyrate. It can inhibit proinflammatory responses and oxidative stress in different models of disease. In the present study, we investigated the effect of SB on lipopolysaccharide (LPS)-induced depression-like behaviors, neuroinflammatory response, and oxido-nitrosative stress in the hippocampus and prefrontal cortex in C57BL6/J mice. Our results showed that 10 days of SB pretreatment at the dose of 300 but not 100 mg/kg markedly ameliorated LPS (0.83 mg/kg)-induced depression-like behaviors in the tail suspension test, forced swimming test, and sucrose preference test. Further analysis showed that 10 days of SB pretreatment not only prevented LPS-induced increases in proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor-α, in the hippocampus and prefrontal cortex but also prevented LPS-induced enhancement of oxido-nitrosative stress. Taken together, these results demonstrate that SB is such an agent that could be used to prevent depression onset and/or progression, and inhibition of neuroinflammatory response and oxido-nitrosative stress may be a potential mechanism for its antidepressant actions.

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Section: Effect Of Sb On Lps-induced Enhancement Of Oxido-nitrosativementioning

confidence: 99%

Lipopolysaccharide-Induced Depression-Like Behaviors Is Ameliorated by Sodium Butyrate via Inhibiting Neuroinflammation and Oxido-Nitrosative Stress

Qiu

Liu

et al. 2020

Pharmacology

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“… 6 Therefore, FA has been proven to be effective in many disease models such as depression, diabetes, ulcerative colitis, Alzheimer’s disease, epilepsy, and hepatotoxicity. 7 – 12 FA was previously reported to be able to enhance nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and up-regulate super oxide dismutase (SOD) expression. 13 , 14 Meanwhile, FA could inactivate nicotinamide adenine dinucleotide phosphate, reduced (NADPH) oxidase, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and cyclooxygenase-2 (COX-2) and inhibit expression of several pro-inflammatory cytokines including interleukin (IL)-1β and IL-6.…”

Section: Introductionmentioning

confidence: 99%

Pretreatment of ferulic acid attenuates inflammation and oxidative stress in a rat model of lipopolysaccharide-induced acute respiratory distress syndrome

Zhang

Wang

Zhao

et al. 2018

Int J Immunopathol Pharmacol

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Acute respiratory distress syndrome (ARDS) is a fatal clinical condition that can be caused by pulmonary and non-pulmonary diseases. Oxidative stress and inflammation play key roles in the development of ARDS. In this study, we investigated whether ferulic acid (FA), an anti-oxidant, was beneficial for prophylaxis of ARDS. We established an ARDS rat model using lipopolysaccharide (LPS) administration. Lung injury was assessed by lung wet/dry ratio and broncho-alveolar lavage fluid (BALF) analysis. Hematoxylin and eosin staining was performed to evaluate the histological changes of the lungs. Enzyme-linked immunosorbent assay (ELISA) and immunoblotting were performed to detect proteins in BALF and lung tissue, respectively. Pulmonary function was determined by testing the oxygen level in BALF. FA pretreatment significantly alleviated LPS-induced pulmonary histological changes. FA reversed LPS-induced changes of lung wet/dry ratio, total protein in BALF, P(A-a)O2, and PaO2/FiO2. In addition, LPS dramatically up-regulated the secretion of interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and IL-10 in BALF (P < 0.01). However, pretreatment of FA significantly improved LPS-induced inflammation. We found that FA indeed reduced oxidative stress in the lungs by testing malondialdehyde level, myeloperoxidase level, and total anti-oxidant capacity. We also proved that FA inactivated multiple mitogen-activated protein kinase signaling pathways in the lungs. In conclusion, FA alleviated LPS-induced ARDS through its anti-inflammatory and anti-oxidant activities.

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“…Moreover, several studies show that ferulic acid has no effect on locomotor activity in the OFT, indicating its specificity, while others show a reversal of decreased locomotor activity, suggesting ferulic acid's ability to reduce anxiety-like behaviors associated with depression. The antidepressant effect of ferulic acid has been attributed to diverse mechanisms, including modulation of serotonergic system by signaling pathway of protein kinase A (PKA), Ca 2+ /calmodulin-dependent protein kinase II (CaMKII), protein kinase C (PKC), mitogen-activated protein kinases/extracellular signal-regulated kinases (MAPK/ERK), and phosphoinositide 3-kinases (PI3K) [44,45].…”

Section: Antidepressant Activity Of Cinnamic Acidsmentioning

confidence: 99%

Antidepressant Potential of Cinnamic Acids: Mechanisms of Action and Perspectives in Drug Development

et al. 2019

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Depression is a health problem that compromises the quality of life of the world′s population. It has different levels of severity and a symptomatic profile that affects social life and performance in work activities, as well as a high number of deaths in certain age groups. In the search for new therapeutic options for the treatment of this behavioral disorder, the present review describes studies on antidepressant activity of cinnamic acids, which are natural products found in medicinal plants and foods. The description of the animal models used and the mechanisms of action of these compounds are discussed.

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Ferulic acid reverses depression-like behavior and oxidative stress induced by chronic corticosterone treatment in mice

Cited by 70 publications

References 45 publications

Lipopolysaccharide-Induced Depression-Like Behaviors Is Ameliorated by Sodium Butyrate via Inhibiting Neuroinflammation and Oxido-Nitrosative Stress

Lipopolysaccharide-Induced Depression-Like Behaviors Is Ameliorated by Sodium Butyrate via Inhibiting Neuroinflammation and Oxido-Nitrosative Stress

Pretreatment of ferulic acid attenuates inflammation and oxidative stress in a rat model of lipopolysaccharide-induced acute respiratory distress syndrome

Antidepressant Potential of Cinnamic Acids: Mechanisms of Action and Perspectives in Drug Development

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