Aerobic exercise attenuates LPS-induced cognitive dysfunction by reducing oxidative stress, glial activation, and neuroinflammation

Choi, Jae-Won; Jo, Sang-Woo; Kim, Dae-Eun; Paik, Il-Young; Balakrishnan, Rengasamy

doi:10.1016/j.redox.2024.103101

Cited by 25 publications

(1 citation statement)

References 66 publications

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“…Moreover, dobutamine effectiveness was also demonstrated in ischemic conditions both "in vitro" and "in vivo" through the stimulation of antioxidant genes [46,47]. Oxidative stress may be induced by pathogen-associated molecular patterns (PAMPs), such as LPS, that may activate different molecular pathways, including the NF-κB/NLRP3 pathway, thus playing a role in the pathogenesis of different diseases and also in neuroinflammation, well miming the consequences of hypovolemic shock in the CNS [48][49][50][51].…”

Section: Discussionmentioning

confidence: 99%

Levosimendan and Dobutamin Attenuate LPS-Induced Inflammation in Microglia by Inhibiting the NF-κB Pathway and NLRP3 Inflammasome Activation via Nrf2/HO-1 Signalling

Mannino,

Urzì Brancati,

Lauro

et al. 2024

Biomedicines

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Hypovolemic shock is a circulatory failure, due to a loss in the effective circulating blood volume, that causes tissue hypoperfusion and hypoxia. This condition stimulates reactive oxygen species (ROS) and pro-inflammatory cytokine production in different organs and also in the central nervous system (CNS). Levosimendan, a cardioprotective inodilator, and dobutamine, a β1-adrenergic agonist, are commonly used for the treatment of hypovolemic shock, thanks to their anti-inflammatory and antioxidant effects. For this reason, we aimed at investigating levosimendan and dobutamine’s neuroprotective effects in an “in vitro” model of lipopolysaccharide (LPS)-induced neuroinflammation. Human microglial cells (HMC3) were challenged with LPS (0.1 µg/mL) to induce an inflammatory phenotype and then treated with levosimendan (10 µM) or dobutamine (50 µM) for 24 h. Levosimendan and dobutamine significantly reduced the ROS levels and markedly increased Nrf2 and HO-1 protein expression in LPS-challenged cells. Levosimendan and dobutamine also decreased p-NF-κB expression and turned off the NLRP3 inflammasome together with its downstream signals, caspase-1 and IL-1β. Moreover, a reduction in TNF-α and IL-6 expression and an increase in IL-10 levels in LPS-stimulated HMC3 cells was observed following treatment. In conclusion, levosimendan and dobutamine attenuated LPS-induced neuroinflammation through NF-κB pathway inhibition and NLRP3 inflammasome activation via Nrf2/HO-1 signalling, suggesting that these drugs could represent a promising therapeutic approach for the treatment of neuroinflammation consequent to hypovolemic shock.

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Section: Discussionmentioning

confidence: 99%

Levosimendan and Dobutamin Attenuate LPS-Induced Inflammation in Microglia by Inhibiting the NF-κB Pathway and NLRP3 Inflammasome Activation via Nrf2/HO-1 Signalling

Mannino,

Urzì Brancati,

Lauro

et al. 2024

Biomedicines

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Pulmonary Flora‐Derived Lipopolysaccharide Mediates Lung‐Brain Axis through Activating Microglia Involved in Polystyrene Microplastic‐Induced Cognitive Dysfunction

Kang,

Huang,

Zhang

et al. 2024

Advanced Science

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Microplastics (MPs) have been detected in the atmospheric and the human respiratory system, indicating that the respiratory tract is a significant exposure route for MPs. However, the effect of inhaled MPs on cognitive function has not been adequately studied. Here, a C57BL/6 J mouse model of inhalation exposure to polystyrene MPs (PS‐MPs, 5 µm, 60 d) is established by intratracheal instillation. Interestingly, in vivo fluorescence imaging and transmission electron microscopy reveal that PS‐MPs do not accumulate in the brain. However, behavioral experiments shows that cognitive function of mice is impaired, accompanied by histopathological damage of lung and brain tissue. Transcriptomic studies in hippocampal and lung tissue have demonstrated key neuroplasticity factors as well as cognitive deficits linked to lung injury, respectively. Mechanistically, the lung‐brain axis plays a central role in PS‐MPs‐induced neurological damage, as demonstrated by pulmonary flora transplantation, lipopolysaccharide (LPS) intervention, and cell co‐culture experiments. Together, inhalation of PS‐MPs reduces cognitive function by altering the composition of pulmonary flora to produce more LPS and promoting M1 polarization of microglia, which provides new insights into the mechanism of nerve damage caused by inhaled MPs and also sheds new light on the prevention of neurotoxicity of environmental pollutants.

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Gallic acid ameliorates LPS-induced memory decline by modulating NF-κB, TNF-α, and Caspase 3 gene expression and attenuating oxidative stress and neuronal loss in the rat hippocampus

Dastan,

Rajaei,

Sharifi

et al. 2024

Metab Brain Dis

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Aerobic exercise attenuates LPS-induced cognitive dysfunction by reducing oxidative stress, glial activation, and neuroinflammation

Cited by 25 publications

References 66 publications

Levosimendan and Dobutamin Attenuate LPS-Induced Inflammation in Microglia by Inhibiting the NF-κB Pathway and NLRP3 Inflammasome Activation via Nrf2/HO-1 Signalling

Levosimendan and Dobutamin Attenuate LPS-Induced Inflammation in Microglia by Inhibiting the NF-κB Pathway and NLRP3 Inflammasome Activation via Nrf2/HO-1 Signalling

Pulmonary Flora‐Derived Lipopolysaccharide Mediates Lung‐Brain Axis through Activating Microglia Involved in Polystyrene Microplastic‐Induced Cognitive Dysfunction

Gallic acid ameliorates LPS-induced memory decline by modulating NF-κB, TNF-α, and Caspase 3 gene expression and attenuating oxidative stress and neuronal loss in the rat hippocampus

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