Redox evaluation in sepsis model mice by the in vivo ESR technique using acyl-protected hydroxylamine

Okazaki, Shoko; Tachibana, Yoshihisa; Koga‐Ogawa, Yukari; Takeshita, Keizo

doi:10.1016/j.freeradbiomed.2013.11.011

Cited by 11 publications

(7 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…iNOS contributes to the production of NO and the latter interacts with superoxide to form peroxynitrite (Ferdinandy et al, ). Peroxynitrite is a potent oxidant and could cause deleterious effects on cardiac function (Ferdinandy et al, ). In vivo electron spin resonance spectroscopy has recently been used to determinate the oxidative stress level in LPS induced mouse model (Okazaki, Tachibana, Koga‐Ogawa, & Takeshita, ), and the experimental data presented that LPS‐treated mouse undergoes severe oxidative stress (Okazaki et al, ). In this study, our data demonstrated that LPS induced the overexpression of iNOS, which can be inhibited with myricetin treatment.…”

Section: Discussionmentioning

confidence: 99%

Myricetin attenuated LPS induced cardiac injury in vivo and in vitro

Zhang

Hong

Liao

et al. 2017

Phytotherapy Research

View full text Add to dashboard Cite

Sepsis induced myocardial dysfunction (SIMD) is a common complication and leads to an increased mortality. SIMD is closely related to inflammation and oxidative stress. Myricetin exhibits strong capacities of anti-inflammation and anti-oxidative stress, but its pharmacological effects for lipopolysaccharide (LPS) induced cardiac injury remains undefined. This study aimed to explore whether myricetin was efficient to alleviate SIMD in mice and neonatal rat cardiomyocytes injury. Mice administrated with myricetin (100 mg/kg, po, bid) or vehicle groups were challenged with LPS (10 mg/kg, ip), and cardiac functions examined by echocardiography after 12 hr LPS exposure. LPS markedly impaired mouse cardiac functions, which were significantly attenuated by myricetin administration. Myricetin significantly reduced the production of inflammatory cytokines both in serum and cardiac tissue. Myricetin could inhibit the nuclear translocation of p65, degradation of IκBα, and cellular apoptosis in vivo and in vitro. Myricetin also prevented overexpression of iNOS and reduction of oxidoreductase (SOD and GPx) activity. Besides, Myricetin treatment could attenuate production of inflammatory cytokines of peritoneal macrophages stimulated with LPS in vitro. Thus we concluded that myricetin could attenuate the LPS induced cardiac inflammation injury in vivo and in vitro. Myricetin may be a potential therapy or adjuvant therapy for SIMD.

show abstract

Section: Discussionmentioning

confidence: 99%

Myricetin attenuated LPS induced cardiac injury in vivo and in vitro

Zhang

Hong

Liao

et al. 2017

Phytotherapy Research

View full text Add to dashboard Cite

show abstract

“…Peripheral administration of highdose LPS leads to a potent inflammatory response, via TLR-4 binding and subsequent NF-jB pathway activation. These LPS treatments mimic many of the clinical features of sepsis and results in a hyper-inflammatory response, accompanied by depressed EEG rhythmicity, low blood pressure, oxidative stress, multiple organ failure and a significant mortality rate (Chang et al, 2013;Lin et al, 2010;Okazaki et al, 2014). Following recovery from the acute effects of LPS-induced sepsis, an increased level microglial activation persists in the CNS, accompanied by prolonged over-expression of pro-inflammatory cytokines as well as time and dose dependent neuronal degeneration (Bossù et al, 2012;Weberpals et al, 2009;Qin et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide-induced sepsis induces long-lasting affective changes in the mouse

Anderson

Commins

Moynagh

et al. 2015

Brain, Behavior, and Immunity

140

View full text Add to dashboard Cite

Post-septic encephalopathy is a poorly understood condition in survivors of sepsis that is characterised by cognitive and affective impairments. In this study we have sought to better understand this condition by undertaking a comprehensive behavioural and cognitive assessment of mice who had previously survived sepsis. Mice were treated with lipopolysaccharide (LPS; 5mg/kg) and one month after this assessed on a battery of tests. Post-septic animals were found to display significantly more immobility in the tail suspension test and show a significantly decreased sucrose preference. Acute fluoxetine treatment reversed the increase in immobility in the tail suspension test in post-septic animals. Post-septic animals also showed less overall exploratory behaviour in the novel object recognition task and also showed increased anxiety-like behaviour in the elevated plus maze. Post-septic mice did not show signs of cognitive impairment, as assessed in the Morris watermaze, the 8-arm radial maze or on preference for the novel object in the novel object recognition task. Immunohistochemical analysis revealed significant upregulation of the microglial marker CD-11b, F4/80 and IBA-1 in the hippocampus of post-septic animals, as well as significant downregulation of the plasticity-related immediate early gene products ARC and EGR1. We also observed a decrease in neural stem cell proliferation in the dentate gyrus of post-septic animals as judged by BrdU incorporation. Co-treatment with the NF-κB pathway inhibitor PDTC attenuated the long-lasting effects of LPS on most of the affected parameters, but not on neural stem cell proliferation. These results show that LPS-induced sepsis in the mouse is followed by long-lasting increases in depressive- and anxiety-like behaviours, as well as by changes in neuroinflammatory- and neural plasticity-associated factors, and that attenuation of the severity of sepsis by PDTC attenuates many of these effects.

show abstract

“…The liver is selectively enriched with macrophages, natural killer cells and natural killer T cells, which are key components of the innate immune system and play a significant role in maintaining homeostasis and health. In sepsis, LPS stimulates liver macrophages to produce reactive oxygen species (ROS), which in turn recruit and activate neutrophils, resulting in neutrophil accumulation, ROS overproduction and oxidative stress in liver (Bautista et al ; Ben‐Shaul et al ; Hsu et al ; Okazaki et al ). ROS overproduction turns on the redox sensitive transcription factor nuclear factor‐кB (NF‐кB) and subsequently results in an inflammatory response, as evidenced by a large production of proinflammatory cytokines and chemokines (Cadenas & Cadenas ; Macdonald et al ).…”

Section: Introductionmentioning

confidence: 99%

Forsythia suspensa extract attenuates lipopolysaccharide‐induced inflammatory liver injury in rats via promoting antioxidant defense mechanisms

Zhao

Piao

Pan

et al. 2016

Animal Science Journal

View full text Add to dashboard Cite

Reactive oxygen species (ROS) have been shown to have a role in inflammation. We investigated whether Forsythia suspensa extract (FSE) could exert its antioxidant potential against lipopolysaccharide (LPS)-induced inflammatory liver injury in rats. Rats were orally fed FSE once daily for 7 consecutive days prior to LPS (Escherichia coli, serotype O55:B5) injection. LPS treatment caused liver dysfunction as evidenced by massive histopathological changes and increased serum alanine aminotransferase and aspartate aminotransferase activities which were ameliorated by FSE pretreatment. FSE attenuated LPS-induced depletion of cytosolic nuclear factor-erythroid 2-related factor 2 (Nrf2) and suppression of Nrf2 nuclear translocation in liver, and the generation of ROS and malondialdehyde in serum and liver. FSE increased the Nrf2-mediated induction of heme oxygenase-1 in liver, as well as superoxide dismutase and glutathione peroxidase activities in serum and liver. Importantly, FSE attenuated LPS-induced nuclear factor-кB (NF-кB) nuclear translocation in liver, and subsequently decreased tumor necrosis factor-α, interleukin (IL)-1β and IL-6 levels in serum and liver, which were associated with FSE-induced activation of Nrf2 in liver. These results indicate that the protective mechanisms of FSE may be involved in the attenuation of oxidative stress and the inhibition of the NF-кB-mediated inflammatory response by modulating the Nrf2-mediated antioxidant response against LPS-induced inflammatory liver injury.

show abstract

Redox evaluation in sepsis model mice by the in vivo ESR technique using acyl-protected hydroxylamine

Cited by 11 publications

References 34 publications

Myricetin attenuated LPS induced cardiac injury in vivo and in vitro

Myricetin attenuated LPS induced cardiac injury in vivo and in vitro

Lipopolysaccharide-induced sepsis induces long-lasting affective changes in the mouse

Forsythia suspensa extract attenuates lipopolysaccharide‐induced inflammatory liver injury in rats via promoting antioxidant defense mechanisms

Contact Info

Product

Resources

About