Lipopolysaccharide-induced functional and structural injury of the mitochondria in the nigrostriatal pathway

Hunter, Randy L.; Ojha, Uttam; Bhurtel, Sunil; Bing, Guoying; Choi, Dong‐Young

doi:10.1016/j.neures.2016.09.007

Cited by 25 publications

(20 citation statements)

References 43 publications

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“…Dysfunction in mitochondria is associated with the impairment of osteogenesis [ 31 , 32 ]. The toxic effect produced by LPS was demonstrated to be associated with dysfunction in mitochondria [ 35 – 37 ]. In the present study, LPS reduced ATP production in mitochondria and MMP of MC3T3-E1 cells, while the superoxide production in mitochondria was increased.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Attenuates Lipopolysaccharides (LPS)-Induced Inhibition of Osteoblast Differentiation in MC3T3-E1 Cells

Zhu

Zhao

et al. 2018

Med Sci Monit

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BackgroundLPS-inhibited osteoblastic differentiation plays an important role in the pathogenesis of osteomyelitis. Thus, searching for drugs that affect LPS-mediated osteoblastic differentiation may be crucial in developing therapies for osteomyelitis. The purpose of this study was to investigate the role and mechanisms of resveratrol, a natural polyphenol present in red wine, on LPS-inhibited osteoblastic differentiation.Material/MethodsCell viability was measured by MMT assay. Mitochondrial ATP levels, membrane potential, and superoxide production were measured to evaluate the effects of LPS and resveratrol on mitochondrial functions in osteoblast-like MC3T3-E1 cells. Osteoblast-related genes, including ALP, OCN, OPN, and RUNX2, were measured by ELISA analysis and RT-PCR in differentiated osteoblast cells treated with LPS and resveratrol. Cellular Sirt1 and PCG-1α levels were measured by Western blot to probe the impact of resveratrol treatment in LPS-stimulated MC3T3-E1 osteoblasts.ResultsThe results showed that LPS caused significant mitochondrial dysfunctions of MC3T3-E1 cells in a dose-dependent manner, which were attenuated by resveratrol. Furthermore, LPS markedly decreased the expression of ALP, OCN, OPN, and RUNX2 in MC3T3-E1 cells cultivated in osteoblast differentiation medium, suggesting that LPS inhibited the osteoblastic differentiation of MC3T3-E1 cells. However, resveratrol obviously alleviated the suppressive impact of LPS on osteoblast differentiation. In addition, resveratrol increased expression of Sirt1 and PGC-1α in MC3T3-E1 cells treated with LPS.ConclusionsTaken together, these results show that resveratrol alleviated the suppression of LPS on osteoblast differentiation by improving, at least in part, mitochondrial function.

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Section: Discussionmentioning

confidence: 99%

Resveratrol Attenuates Lipopolysaccharides (LPS)-Induced Inhibition of Osteoblast Differentiation in MC3T3-E1 Cells

Zhu

Zhao

et al. 2018

Med Sci Monit

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“…It is more likely that all neuropeptides studied have been previously described as substances taking part in the protection of the nervous system against different damaging factors [ 4 , 5 , 8 ]. At the same time, LPS is a relatively well-known factor, which may be involved in neurodegenerative processes within the central and peripheral nervous system [ 60 , 61 ] and these effects are so intense that LPS is one of the substances used to chemically-induce Parkinson’s disease in animal models [ 62 ]. Thus, the changes observed during the present study may help protect the intestinal neuronal structures from the neurodegenerative activity of LPS, particularly through the participation of nerves supplying the gastrointestinal tract in reduction of LPS-induced pathological changes as described in previous studies [ 63 ].…”

Section: Discussionmentioning

confidence: 99%

Modulation of the main porcine enteric neuropeptides by a single low-dose of lipopolysaccharide (LPS) Salmonella Enteritidis

2017

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BackgroundThe present research was conducted to investigate the influence of a low, single dose of LPS, which does not result in any clinical symptoms of intoxication on the expression of selected neuropeptides within the intestines of the domestic pig.MethodsThis experiment was conducted on immature female pigs of the Pitrain × Duroc breed (n = five per group). Seven days after the intravenous injection of 10 mL saline solution for control animals and 5 μg/kg b.w. (in 10 mL saline solution) LPS Salmonella Enteritidis for the experimental group, the excised segments of duodenum, jejunum, ileum, ileocecal valve, caecum, descending colon, transverse colon, ascending colon and rectum were prepared to extract the main enteric neuropeptides, including GAL, NPY, SOM, SP, VIP.ResultsThe results of this research indicate that single low-dose LPS S. Enteritidis produced changes in the content of the selected neuropeptides of the porcine intestine. The most visible changes were observed in the transverse colon, where LPS induced the increase of GAL expression from 19.41 ± 7.121 to 92.92 ± 11.447 ng/g tissue.ConclusionThe exact functions of the substances studied and mechanisms of responses to LPS action depend on the sections of the intestines. The mechanisms of observed changes are not fully understood, but fluctuations in neuronal active substance levels may be connected with neurodegenerative and/or pro-inflammatory activity of LPS.

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“…81 The important role of butyrate in mitochondrial functionality has been demonstrated in colonocytes. 86 Alternatively, decreased blood levels of LPS will decrease brain inflammatory status and facilitate mitochondrial function. 82 In the transcriptome and proteome studies of these mice, the butyrate metabolism pathway was reported altered.…”

Section: Intestinal Microbiota On Mitochondriamentioning

confidence: 99%

“…85 It has been demonstrated that infusion of LPS into the striatum of rats causes damage to neuronal mitochondria, leading to a deficit in mitochondrial respiration, damage to mitochondrial cristae, mitochondrial redox potential disruption, and nitration. 86 Alternatively, decreased blood levels of LPS will decrease brain inflammatory status and facilitate mitochondrial function. In a further animal model, LPS was shown to cause mouse depression-like behaviors and this was reduced with the administration of butyrate.…”

Section: Intestinal Microbiota On Mitochondriamentioning

confidence: 99%

Mitochondria could be a potential key mediator linking the intestinal microbiota to depression

Chen¹,

Vitetta

2019

J of Cellular Biochemistry

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The intestinal microbiota has been reported to affect depression, a common mental condition with severe health‐related consequences. However, what mediates the effect of the intestinal microbiota on depression has not been well elucidated. We summarize the roles of the mitochondria in eliciting beneficial effects on the gut microbiota to ameliorate symptoms of depression. It is well known that mitochondria play a key role in depression. An important pathogenic factor, namely inflammatory response, may adversely impact mitochondrial functionality to maintain cellular homeostasis. Dysfunction of mitochondria not only affects neuronal function but also reduces neuron cell numbers. We posit that the intestinal microbiota could affect neuronal mitochondrial function through short‐chain fatty acids such as butyrate. Brain inflammatory processes could also be affected through the modulation of gut permeability and blood lipopolysaccharide levels. Aberrant mitochondria functionality coupled to adverse cellular homeostasis could be a key mediator for the effect of the intestinal microbiota on the progression of depression.

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Lipopolysaccharide-induced functional and structural injury of the mitochondria in the nigrostriatal pathway

Cited by 25 publications

References 43 publications

Resveratrol Attenuates Lipopolysaccharides (LPS)-Induced Inhibition of Osteoblast Differentiation in MC3T3-E1 Cells

Resveratrol Attenuates Lipopolysaccharides (LPS)-Induced Inhibition of Osteoblast Differentiation in MC3T3-E1 Cells

Modulation of the main porcine enteric neuropeptides by a single low-dose of lipopolysaccharide (LPS) Salmonella Enteritidis

Mitochondria could be a potential key mediator linking the intestinal microbiota to depression

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