Honokiol abrogates lipopolysaccharide-induced depressive like behavior by impeding neuroinflammation and oxido-nitrosative stress in mice

Sulakhiya, Kunjbihari; Kumar, Parveen; Jangra, Ashok; Dwivedi, Shubham; Hazarika, Naba Kumar; Baruah, Chandana C.; Lahkar, Mangala

doi:10.1016/j.ejphar.2014.09.049

Cited by 101 publications

(52 citation statements)

References 64 publications

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“…In general, minocycline and cytokine antagonists are effective to block inflammation-induced depression when administered before immune stimulation. The same effect is obtained with a wide variety of anti-inflammatory or anti-oxidant natural compounds, such as curcumin, apigenine, honkiol, xiaobuxin-tang flavonoid extract, perillaldehyde, ginseng saponins, and alpha-tocopherol (Wang et al 2014; Li et al 2015a; Sulakhiya et al 2014; An et al 2015; Ji et al 2014; Kang et al 2011; Manosso et al 2013). However, it is not known whether the anti-inflammatory treatment can block behavioral signs of depression once they have developed.…”

Section: Targeting Inflammation-induced Depression: Translational Aspmentioning

confidence: 69%

Role of the Kynurenine Metabolism Pathway in Inflammation-Induced Depression: Preclinical Approaches

Dantzer

2016

Current Topics in Behavioral Neurosciences

196

151

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Physically ill patients with chronic inflammation often present with symptoms of depression. Our understanding of the pathophysiology of inflammation-associated depression has benefited from preclinical studies on the mechanisms of sickness and clinical studies on the symptoms of sickness and depression that develop in patients treated with immunotherapy. Sickness behavior develops when the immune system is activated by pathogen- or damage-associated molecular patterns. It is a normal biological response to infection and cell injury. It helps the organism to mobilize its immune and metabolic defenses to fight the danger. Depression emerges on the background of sickness when the inflammatory response is too intense and long lasting or the resolution process is deficient. The transition from sickness to depression is mediated by activation of the kynurenine metabolism pathway that leads to the formation of neurotoxic kynurenine metabolites including quinolinic acid, an agonist of N-methyl-D-aspartate receptors. The neuroimmune processes and molecular factors that have been identified in the studies of inflammation-associated depression represent potential new targets for the development of innovative therapies for the treatment of major depressive disorders.

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Section: Targeting Inflammation-induced Depression: Translational Aspmentioning

confidence: 69%

Role of the Kynurenine Metabolism Pathway in Inflammation-Induced Depression: Preclinical Approaches

Dantzer

2016

Current Topics in Behavioral Neurosciences

196

151

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“…Oxidative stress and inflammatory mediators generate a vicious cycle that further depletes the neurotrophic factor such as BDNF, nerve growth factor (NGF), and neurotrophin-3 (NT-3) levels in the cortex and hippocampus [36]. Exaggerated oxidative stress, neuroinflammation, and the resulted depletion of neurotrophic factors in the brain eventually manifest the development of anxiety and depressive-like behavior [3,22,37,38]. Our results are in line with the previous studies that suggested oxidative stress, neuroinflammation, and BDNF depletion play a key role in the pathogenesis of anxiety and depressive illness.…”

Section: Discussionmentioning

confidence: 99%

“…Sucrose preference test was performed during the 24-h interval following LPS administration. The time-point 3 and 24 h were considered for anxiety and depressive-like behavior assessment because previous studies suggested that the anxiety and depressive-like behavior peaks after 3 and 24 h, respectively, after the LPS administration [3,21,22]. Behavioral and biochemical tests were performed on different animals to avoid the possible influence of behavioral assessment on biochemical parameters.…”

Section: Animalsmentioning

confidence: 99%

Lipopolysaccharide-Induced Behavioral Alterations Are Alleviated by Sodium Phenylbutyrate via Attenuation of Oxidative Stress and Neuroinflammatory Cascade

2016

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Oxido-nitrosative stress, neuroinflammation, and reduced level of neurotrophins are implicated in the pathophysiology of anxiety and depressive illness. A few recent studies have revealed the role of endoplasmic reticulum (ER) stress in the pathophysiology of stress and depression. The aim of the present study is to investigate the neuroprotective potential of sodium phenylbutyrate (SPB), an ER stress inhibitor against lipopolysaccharide (LPS)-induced anxiety and depressive-like behavior in Swiss albino mice. Anxiety and depressive-like behavior was induced by LPS (0.83 mg/kg; i.p.) administration. Various behavioral tests were conducted to evaluate the anxiety and depressive-like behavior in mice. Real-time PCR was employed for the detection and expression of ER stress markers (78-kDa glucose-regulated protein (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)). Pretreatment with SPB significantly ameliorated the LPS-induced anxiety and depressive-like behavior as revealed by behavioral paradigm results. LPS-induced oxidative stress was ameliorated by SPB pretreatment in hippocampus (HC) and prefrontal cortex (PFC) region. Neuroinflammation was significantly reduced by SPB pretreatment in LPS-treated mice as evident from reduction in proinflammatory cytokines (IL-1β and TNF-α). Importantly, LPS administration significantly up-regulated the GRP78 mRNA expression level in the HC which suggests the involvement of unfolded protein response (UPR) in LPS-evoked behavioral anomalies. These results highlight the neuroprotective potential of SPB in LPS-induced anxiety and depressive illness model which may be partially due to inhibition of oxidative stress-neuroinflammatory cascade.

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“…Oxido-nitrosative stress further diminishes the brain-derived neurotrophic factor (BDNF) in the brain [51]. Furthermore, aluminum can cause disruption of the proinflammatory cytokine/neurotrophin balance in the brain [52].…”

Section: Discussionmentioning

confidence: 99%

Hesperidin and Silibinin Ameliorate Aluminum-Induced Neurotoxicity: Modulation of Antioxidants and Inflammatory Cytokines Level in Mice Hippocampus

Jangra

Kasbe

Pandey

et al. 2015

Biol Trace Elem Res

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Mounting evidence suggests that long-term aluminum exposure results in severe toxic effects, including neurobehavioral and neurochemical anomalies. The present study was performed to examine the neuroprotective potential of hesperidin and silibinin against aluminum chloride (AlCl3)-induced neurotoxicity in mice. AlCl3 (100 mg/kg/day) was injected daily through oral gavage for 42 days. Concomitantly, hesperidin (50 and 100 mg/kg/day, p.o.) and silibinin (100 and 200 mg/kg/day, p.o.) was administered for 42 days in different groups. The extent of cognitive impairment was assessed by Morris water maze and novel object recognition test on the 43rd day. Neurotoxicity was assessed by measuring oxido-nitrosative stress and proinflammatory cytokines in the hippocampus of mice. Six weeks treatment with AlCl3 caused cognitive impairment as indicated by an increase in the retention latency time and reduction in the percentage of recognition index. AlCl3-treated group showed oxido-nitrosative stress as indicated by increase in the level of lipid peroxidation, nitrite and depleted reduced glutathione, catalase activity in the hippocampus. Moreover, the chronic AlCl3 administration raised the proinflammatory cytokines (interleukin-1β and tumor necrosis factor-α) level and increased acetylcholinesterase activity and reduced the BDNF content in the hippocampus of AlCl3-treated animals. However, chronic treatment with hesperidin and silibinin at higher doses significantly ameliorated the AlCl3-induced cognitive impairment and hippocampal biochemical anomalies. The present study clearly indicated that hesperidin and silibinin exert neuroprotective effects against AlCl3-induced cognitive impairment and neurochemical changes. Amelioration of cognitive impairment may be attributed to the impediment of oxido-nitrosative stress and inflammation in the hippocampus.

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Honokiol abrogates lipopolysaccharide-induced depressive like behavior by impeding neuroinflammation and oxido-nitrosative stress in mice

Cited by 101 publications

References 64 publications

Role of the Kynurenine Metabolism Pathway in Inflammation-Induced Depression: Preclinical Approaches

Role of the Kynurenine Metabolism Pathway in Inflammation-Induced Depression: Preclinical Approaches

Lipopolysaccharide-Induced Behavioral Alterations Are Alleviated by Sodium Phenylbutyrate via Attenuation of Oxidative Stress and Neuroinflammatory Cascade

Hesperidin and Silibinin Ameliorate Aluminum-Induced Neurotoxicity: Modulation of Antioxidants and Inflammatory Cytokines Level in Mice Hippocampus

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