Protective effect of mangiferin against lipopolysaccharide-induced depressive and anxiety-like behaviour in mice

Jangra, Ashok; Lukhi, Manish M.; Sulakhiya, Kunjbihari; Baruah, Chandana C.; Lahkar, Mangala

doi:10.1016/j.ejphar.2014.07.031

Cited by 107 publications

(77 citation statements)

References 58 publications

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“…In addition to this anhedonia effect, LPS exposure has been shown to influence other behaviors of interest including sensitivity to painful stimuli [41], alcohol intake [42], and anxiety [43,44]. Future studies will examine the role of the NK1R in additional LPS-induced behaviors.…”

Section: Discussionmentioning

confidence: 99%

Cellular and behavioral effects of lipopolysaccharide treatment are dependent upon neurokinin-1 receptor activation

Fulenwider

Smith

Nichenko

et al. 2018

J Neuroinflammation

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Background: Several psychiatric conditions are affected by neuroinflammation and neuroimmune activation. The transcription factor nuclear factor kappa light-chain-enhancer of activated B cells (NFkB) plays a major role in inflammation and innate immunity. The neurokinin-1 receptor (NK1R) is the primary endogenous target of the neuroactive peptide substance P, and some data suggests that NK1R stimulation may influence NFkB activity. Both NK1R and NFkB have been shown to play a functional role in complex behaviors including stress responsivity, depression, and addiction. In this study, we test whether NFkB activity in the brain (stimulated by lipopolysaccharide administration) is dependent upon the NK1R. Methods: Adult male Wistar rats were treated systemically with the NK1R antagonist L822429 followed by administration of systemic lipopolysaccharide (LPS, a strong activator of NFkB). Hippocampal extracts were used to assess expression of proinflammatory cytokines and NFkB-DNA-binding potential. For behavioral studies, rats were trained to consume 1% (w/v) sucrose solution in a continuous access two-bottle choice model. After establishment of baseline, animals were treated with L822429 and LPS and sucrose preference was measured 12 h post-treatment. Results: Systemic LPS treatment causes a significant increase in proinflammatory cytokine expression and NFkB-DNA-binding activity within the hippocampus. These increases are attenuated by systemic pretreatment with the NK1R antagonist L822429. Systemic LPS treatment also led to the development of anhedonic-like behavior, evidenced by decreased sucrose intake in the sucrose preference test. This behavior was significantly attenuated by systemic pretreatment with the NK1R antagonist L822429. Conclusions: Systemic LPS treatment induced significant increases in NFkB activity, evidenced by increased NFkB-DNA binding and by increased proinflammatory cytokine expression in the hippocampus. LPS also induced anhedonic-like behavior. Both the molecular and behavioral effects of LPS treatment were significantly attenuated by systemic NK1R antagonism, suggesting that NK1R stimulation lies upstream of NFkB activation following systemic LPS administration and is at least in part responsible for NFkB activation.

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Section: Discussionmentioning

confidence: 99%

Cellular and behavioral effects of lipopolysaccharide treatment are dependent upon neurokinin-1 receptor activation

Fulenwider

Smith

Nichenko

et al. 2018

J Neuroinflammation

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“…1. SPB was prepared freshly in saline everyday, and the selected doses of SPB and LPS were chosen based on the previous study performed in our laboratory [3,18]. On the seventh day, LPS (0.83 mg/kg) was administrated into mice 30 min after drug administration.…”

Section: Animalsmentioning

confidence: 99%

“…Despite the high prevalence, no single medication is approved by Food and Drug Administration (FDA) agency for the treatment of anxiety and depression comorbidity. Experimental studies have shown the involvement of oxido-nitrosative stress and neuroinflammatory cascade in anxiety and depression pathogenesis [2,3]. Depression is closely coupled with high levels of malondialdehyde and 8-iso-prostaglandin F2 (markers of lipid and arachidonic acid peroxidation, respectively), 8-hydroxy-2-deoxyguanosine (product of DNA oxidation), RNA oxidation, and telomere shortening [4][5][6][7].…”

Section: Introductionmentioning

confidence: 98%

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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“…This compound exerts central nervous system-stimulating, anti-oxidant, analgesic, anti-inﬂammatory, and anti-diabetic activities [16]. In animal models, mangiferin (MA) treatment ameliorates oxidation in fatty liver [17], protects against lipopolysaccharide (LPS)-induced depressive and anxiety-like behavior in mice [18], and prevents the progression of inﬂammatory diseases such as colitis [19]. In kidney disease, MA has potential ameliorative effects in addition to its anti-diabetic effect in experimentally induced diabetic nephropathy rats [20,21].…”

Section: Introductionmentioning

confidence: 99%

Mangiferin Attenuate Sepsis-Induced Acute Kidney Injury via Antioxidant and Anti-Inflammatory Effects

Peng

Zhu

et al. 2014

Am J Nephrol

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Background: Acute kidney injury (AKI) is a frequent and serious complication of sepsis. A growing body of evidence now suggests that inflammatory reactions and tubular dysfunction induced by oxidative stressinvolved in the mechanisms of the disease. This study aimed to determine the role of anti-inflammatory and anti-oxidant activities of mangiferin (MA) in sepsis-induced AKI. Methods: We investigated the effects of MA on apoptosis of rat kidney proximal tubular cell (RPTC), together with renal function and morphological alterations of mice undergoing cecal-ligation and puncture (CLP). The levels of oxidative stress in kidney tissues were also determined. Moreover, we mainly focus on the effects of MA in regulating the production of NLRP3 and Nrf2 in the present study. Results: The exposure to LPS (5 Vg/ml) yielded a signiﬁcant increase of apoptosis in RPTC cells, which was largely inhibited by MA pretreatment. MA attenuates renal dysfunction and ameliorates the morphological changes in the septic mice induced by CLP. MA inhibits oxidative stress, decreases serum levels of IL-1F and IL-18, and prevents tubular epithelial cells apoptosis in kidneys of CLP mice model. Data in this study also suggest that MA promotes Nrf2 expression and suppresses renal NLRP3 inflammasome activation. Conclusion: In summary, MA protects against sepsis-induced AKI through NLRP3 inflammasome inhibition and Nrf2 up-regulation. Thus, the mangiferin could thus be a promising candidate for development of a multi-potent drug. i 2014 S. Karger AG, Basel

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Protective effect of mangiferin against lipopolysaccharide-induced depressive and anxiety-like behaviour in mice

Cited by 107 publications

References 58 publications

Cellular and behavioral effects of lipopolysaccharide treatment are dependent upon neurokinin-1 receptor activation

Cellular and behavioral effects of lipopolysaccharide treatment are dependent upon neurokinin-1 receptor activation

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

Mangiferin Attenuate Sepsis-Induced Acute Kidney Injury via Antioxidant and Anti-Inflammatory Effects

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