Effect of melatonin on neuroinflammation and acetylcholinesterase activity induced by LPS in rat brain

Tyagi, Ethika; Agrawal, Rahul; Nath, Chandishwar; Shukla, Rakesh

doi:10.1016/j.ejphar.2010.04.041

Cited by 87 publications

(60 citation statements)

References 36 publications

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“…LPS injections in experimental animals led to increased levels of malondialdehyde, nitrite, and nitrate and reduced levels of glutathione within the brain -the latter finding evident across many psychiatric disorders [64,65] . Furthermore, the administration of antioxidants such as quercetin reduce LPS-induced O&NS [66] , indicating the reversible nature of these processes.…”

Section: Microbiota and Gut-derived Inflammation In Mddmentioning

confidence: 93%

Gut Microbiota, Bacterial Translocation, and Interactions with Diet: Pathophysiological Links between Major Depressive Disorder and Non-Communicable Medical Comorbidities

Slyepchenko

Maes

Jacka

et al. 2016

Psychother Psychosom

219

136

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Background: Persistent low-grade immune-inflammatory processes, oxidative and nitrosative stress (O&NS), and hypothalamic-pituitary-adrenal axis activation are integral to the pathophysiology of major depressive disorder (MDD). The microbiome, intestinal compositional changes, and resultant bacterial translocation add a new element to the bidirectional interactions of the gut-brain axis; new evidence implicates these pathways in the patho-aetiology of MDD. In addition, abnormalities in the gut-brain axis are associated with several chronic non-communicable disorders, which frequently co-occur in individuals with MDD, including but not limited to irritable bowel syndrome (IBS), chronic fatigue syndrome (CFS), obesity, and type 2 diabetes mellitus (T2DM). Methods: We searched the PubMed/MEDLINE database up until May 1, 2016 for studies which investigated intestinal dysbiosis and bacterial translocation (the ‘leaky gut') in the pathophysiology of MDD and co-occurring somatic comorbidities with an emphasis on IBS, CFS, obesity, and T2DM. Results: The composition of the gut microbiota is influenced by several genetic and environmental factors (e.g. diet). Several lines of evidence indicate that gut-microbiota-diet interactions play a significant pathophysiological role in MDD and related medical comorbidities. Gut dysbiosis and the leaky gut may influence several pathways implicated in the biology of MDD, including but not limited to immune activation, O&NS, and neuroplasticity cascades. However, methodological inconsistencies and limitations limit comparisons across studies. Conclusions: Intestinal dysbiosis and the leaky gut may constitute a key pathophysiological link between MDD and its medical comorbidities. This emerging literature opens relevant preventative and therapeutic perspectives.

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Section: Microbiota and Gut-derived Inflammation In Mddmentioning

confidence: 93%

Gut Microbiota, Bacterial Translocation, and Interactions with Diet: Pathophysiological Links between Major Depressive Disorder and Non-Communicable Medical Comorbidities

Slyepchenko

Maes

Jacka

et al. 2016

Psychother Psychosom

219

136

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“…So, melatonin reduced in a concentrationdependent manner IL6 secretion in amyloid β peptidetreated brain slices (Clapp-Lilly et al 2001). Administration of melatonin in doses of 5 and 10 mg/kg were able to decrease lipopolysaccharide (LPS)-induced pro-inflammatory cytokines (TNFα, IL1β) and oxidative stress in different brain regions, including the hippocampus (Tyagi et al 2010). Choi et al (2008) reported that oestrogen-induced protection was associated with a decrease in IL1β and an increase in interleukin-1 receptor antagonist (IL1ra) expression in the ischemic hippocampus during early reperfusion periods, which suggests that the modulation of IL1β/ IL1ra might be part of the anti-inflammatory effects of oestrogens.…”

Section: Discussionmentioning

confidence: 99%

Melatonin and oestrogen treatments were able to improve neuroinflammation and apoptotic processes in dentate gyrus of old ovariectomized female rats

Kireev

Vara

Viña

et al. 2014

AGE

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The aim of this study was to determine the outcomes of oestrogen and melatonin treatments following long-term ovarian hormone depletion on neuroinflammation and apoptotic processes in dentate gyrus of hippocampi. Forty-six female Wistar rats of 22 months of age were used. Twelve of them remained intact, and the other 34 were ovariectomized at 12 months of age. Ovariectomized animals were divided into three groups and treated for 10 weeks with oestrogens, melatonin or saline. All rats were killed by decapitation at 24 months of age, and dentate gyri were collected. A group of 2 month-old intact female rats was used as young control. The levels of pro-inflammatory cytokines and heat shock protein 70 (HSP 70) were analysed by ELISA. The expressions of TNFα, IL1β, GFAP, nNOS, iNOS, HO-1, NFκB, Bax, Bad, AIF, Bcl2 and SIRT1 genes were detected by real-time (RT)-PCR. Western blots were used to measure the protein expression of NFκB p65, NFκB p50/105, IκBα, IκBβ, p38 MAPK, MAP-2 and synapsin I. We have assessed the ability of 17β-oestradiol and melatonin administration to downregulate markers of neuroinflammation in the dentate gyrus of ovariectomized female rats. Results indicated that 17β-oestradiol and melatonin treatments were able to significantly decrease expression of pro-inflammatory cytokines, iNOS and HO-1 in the hippocampus when compared to non-treated animals. A similar age-and long-term ovarian hormone depletion-related increase in GFAP was also attenuated after both melatonin and oestradiol treatments. In a similar way to oestradiol, melatonin decreased the activation of p38 MAPK and NFκB pathways. The treatments enhanced the levels of synaptic molecules synapsin I and MAP-2 and have been shown to modulate the pro-antiapoptotic ratio favouring the second and to increase SIRT1 expression. These findings support the potential therapeutic role of melatonin and oestradiol as protective antiinflammatory agents for the central nervous system during menopause.

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“…A number of studies attest to the anti-inflammatory activity of melatonin both in vivo and in vitro . Melatonin reduces oxidative damage and suppresses IL-6 mRNA expression after venous infusion of LPS and peptidoglycan in rats [28], and also diminishes the levels of TNF-α, IL-1β, and oxidative stress mediators in different regions of rat brains after intracerebroventricular administration of LPS [29]. In pregnant mice, melatonin reduces LPS-induced increases in TNF-α levels in the maternal serum and fetal brain [30].…”

Section: Introductionmentioning

confidence: 99%

The anti-inflammatory and antioxidant effects of melatonin on LPS-stimulated bovine mammary epithelial cells

et al. 2017

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Mastitis is the most prevalent disease in dairy cattle worldwide and not only causes huge economic losses in the dairy industry but also threatens public health. To evaluate the therapeutic potential of melatonin in mastitis, we examined the ability of melatonin to protect bovine mammary epithelial cells (bMECs) from the harmful effects of lipopolysaccharide (LPS). We found that melatonin inhibited the LPS-binding protein–CD14–TLR4 signaling pathway in bMECs, which had opposing effects on pro-inflammatory and anti-inflammatory mediators. Melatonin decreased LPS-induced expression of pro-inflammatory cytokines, chemokines, and positive acute-phase proteins (APPs), including tumor necrosis factor-α, interleukin (IL)-1β, IL-6, granulocyte-monocyte colony-stimulating factor, chemokine CC motif ligand (CCL)2, CCL5, serum amyloid A, haptoglobin, C-reactive protein, ceruloplasmin, and α-1 antitrypsin, and increased expression of the anti-inflammatory cytokine IL-1Ra and the negative APP fibrinogen. In addition, melatonin increased dityrosine levels but suppressed nitrite levels by upregulating the expression of Nrf2 and heme oxygenase-1 in the Nrf2 antioxidant defense pathway. Finally, melatonin administration increased the viability of LPS-stimulated bMECs. These results suggest that melatonin protects bMECs from LPS-induced inflammatory and oxidant stress damage and provide evidence that melatonin might have therapeutic utility in mastitis.

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Effect of melatonin on neuroinflammation and acetylcholinesterase activity induced by LPS in rat brain

Cited by 87 publications

References 36 publications

Gut Microbiota, Bacterial Translocation, and Interactions with Diet: Pathophysiological Links between Major Depressive Disorder and Non-Communicable Medical Comorbidities

Gut Microbiota, Bacterial Translocation, and Interactions with Diet: Pathophysiological Links between Major Depressive Disorder and Non-Communicable Medical Comorbidities

Melatonin and oestrogen treatments were able to improve neuroinflammation and apoptotic processes in dentate gyrus of old ovariectomized female rats

The anti-inflammatory and antioxidant effects of melatonin on LPS-stimulated bovine mammary epithelial cells

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