Shogaol but not gingerol has a neuroprotective effect on hemorrhagic brain injury: Contribution of the α, β-unsaturated carbonyl to heme oxygenase-1 expression

Ohnishi, Masatoshi; Ohshita, Mayu; Tamaki, Hideaki; Marutani, Yumi; Nakayama, Yuta; Akagi, Marina; Miyata, Marina; Maehara, Shoji; Hata, Toshiyuki; Inoue, Atsuko

doi:10.1016/j.ejphar.2018.10.029

Cited by 17 publications

(7 citation statements)

References 24 publications

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“…The thrombin‐induced activation of microglia is involved in ICH‐associated inflammation and neuronal injury, and microglia did not express iNOS after an ICH insult . These findings suggest a mixture of proinflammatory and other microglial populations in the brain, and drugs that only suppress proinflammatory microglia may be promising.…”

Section: Discussionmentioning

confidence: 85%

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Gadolinium causes M1 and M2 microglial apoptosis after intracerebral haemorrhage and exerts acute neuroprotective effects

Ohnishi

Kai

Shimizu

et al. 2020

Journal of Pharmacy and Pharmacology

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Objectives Gadolinium (Gd) affects microglial polarization during remyelination. We previously reported that the suppression of proinflammatory microglia was neuroprotective in intracerebral haemorrhage (ICH). The objective of the present study was to investigate the effects of Gd on microglial polarization and neuronal injury after ICH. Methods Gadolinium was intraperitoneally administered to ICH mice prepared by an intrastriatal microinjection of collagenase type VII. The polarization of M1, 2a, b and c microglia was evaluated by real‐time PCR using the respective markers. Changes in representative mRNAs were also confirmed by immunological methods. Neuroprotective effects were evaluated by counting NeuN‐positive cells and a behavioural analysis. Key findings One day after ICH, the mRNA levels of proinflammatory M1 microglial markers, such as inducible nitric oxide synthase (iNOS), and anti‐inflammatory M2 microglial markers, such as arginase1 (M2a, c), Ym1 (M2a), and transforming growth factor‐β (M2c), increased, while those of chemokine CCL1 (M2b) only increased after 3 days. Gd decreased the levels of all M1 and M2 markers. Arginase1 and iNOS protein levels also increased, and Gd reduced them due to apoptotic cell death. Gadolinium attenuated oedema, neuron loss, neurological deficits and the mortality rate without affecting haematoma sizes. Conclusions Gadolinium induced M1 and M2 microglial apoptosis and exerted acute neuroprotective effects after ICH.

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Section: Discussionmentioning

confidence: 85%

“…All of the animals were maintained under a 12‐h light/dark cycle at a constant ambient temperature of 22 ± 1 °C. The in vivo mouse model of ICH was created as described in our previous study . After being intraperitoneally (i.p.)…”

Section: Methodsmentioning

confidence: 99%

Gadolinium causes M1 and M2 microglial apoptosis after intracerebral haemorrhage and exerts acute neuroprotective effects

Ohnishi

Kai

Shimizu

et al. 2020

Journal of Pharmacy and Pharmacology

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“…Of course, increasing the M2/M1 phenotypic proportion of microglia usually brings more satisfactory results (Wang J. et al, 2018 ; Bai et al, 2020 ), and it has become the most frequently studied therapeutic method. Relying on the aforementioned targets, experimental therapeutic studies on the precise regulation on microglia phenotype are developing rapidly, and relevant drugs are summarized in Table 3 (Hu et al, 2011 ; Ohnishi et al, 2013 , 2019 ; Yang et al, 2014a , b , 2018 ; Iniaghe et al, 2015 ; Zhao et al, 2015a , b , 2018 ; Flores et al, 2016 ; Shi et al, 2016 ; Sukumari-Ramesh and Alleyne, 2016 ; Zhang et al, 2016 ; Anan et al, 2017 ; Chen-Roetling and Regan, 2017 ; Lan et al, 2017a ; Wang J. et al, 2017 ; Wei et al, 2017 ; Xu et al, 2017 ; Zeng et al, 2017 ; Chen C. et al, 2018 ; Chen S. et al, 2018 ; Fu et al, 2018 ; Han et al, 2018 ; Li X. et al, 2018 ; Qiao et al, 2018 ; Ren et al, 2018 ; Wang et al, 2018b ; Liang et al, 2019 ; Song and Zhang, 2019 ; Xi et al, 2019 ; Zhou F. et al, 2019 ; Cheng et al, 2020 ; Ding et al, 2020 ).…”

Section: Polarization Mechanism Of Microglia After Ichmentioning

confidence: 99%

Microglia Phenotype and Intracerebral Hemorrhage: A Balance of Yin and Yang

Fang

You

et al. 2021

Front. Cell. Neurosci.

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Intracerebral hemorrhage (ICH) features extremely high rates of morbidity and mortality, with no specific and effective therapy. And local inflammation caused by the over-activated immune cells seriously damages the recovery of neurological function after ICH. Fortunately, immune intervention to microglia has provided new methods and ideas for ICH treatment. Microglia, as the resident immune cells in the brain, play vital roles in both tissue damage and repair processes after ICH. The perihematomal activated microglia not only arouse acute inflammatory responses, oxidative stress, excitotoxicity, and cytotoxicity to cause neuron death, but also show another phenotype that inhibit inflammation, clear hematoma and promote tissue regeneration. The proportion of microglia phenotypes determines the progression of brain tissue damage or repair after ICH. Therefore, microglia may be a promising and imperative therapeutic target for ICH. In this review, we discuss the dual functions of microglia in the brain after an ICH from immunological perspective, elaborate on the activation mechanism of perihematomal microglia, and summarize related therapeutic drugs researches.

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“…The role of oxidative stress in the development of AKI is being increasingly recognized (7,8). Several studies have suggested that heme oxygenase-1 (HO-1) plays an antioxidant role in the progression of acute organ injury (9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

Heme oxygenase-1 as a predictor of sepsis-induced acute kidney injury: a cross-sectional study

Xia¹,

Zhang²,

Liu³

et al. 2022

Ann Transl Med

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Background: Sepsis patients suffer from severe inflammation and poor prognosis. Oxidative stress and local inflammation that results from sepsis can trigger organ injury, including acute kidney injury (AKI).Previous studies have shown that heme oxygenase-1 (HO-1) is overexpressed in proximal tubular cells under oxidative stress and has significant cytoprotective and anti-inflammatory effects. Heme-induced inflammation in sepsis is antagonized by increased tissue expression of heme oxygenase-1 (HO-1), which impacts on AKI development. The investigators observed intrarenal HO-1 expression and corresponding potential increases in plasma and urinary HO-1 protein concentrations in four different AKI models. Since serum levels of HO-1 reflect HO-1 expression, we aimed to investigate whether serum HO-1 could predict the development of AKI in sepsis patient.Methods: A total of 83 sepsis patients were enrolled in this study including septic patients with AKI and sepsis patients without AKI. According to the definition of septic shock and the global kidney diagnostic criteria described in the Kidney Disease: Improving Global Outcomes (KDIGO), patients were allocated to the sepsis and septic shock groups with and without AKI, respectively. The serum levels of HO-1 were measured by enzyme-linked immunosorbent assays (ELISA). Statistical analyses were performed using SPSS software.Results: There were statistically significant differences between septic patients with AKI and sepsis patients without AKI in terms of Sequential Organ Failure Assessment (SOFA) score, hospitalization time, and laboratory indicators including serum HO-1, creatine kinase MB (CK-MB), troponin I (TnI), urea, myoglobin (MYO), serum creatinine (Scr), procalcitonin, and activated partial thromboplastin time. Serum levels of alkaline phosphatase (ALP), urea, MYO, Scr, procalcitonin, activated partial thromboplastin time, and prothrombin time exhibited significant differences among the four groups. The concentration of serum HO-1 was higher in sepsis-induced AKI compared with sepsis patients without AKI. Serum HO-1 levels were increased in patients with sepsis shock-induced AKI. The area under the receiver operating characteristic (ROC) curve for serum HO-1 combined with Scr was 0.885 [95% confidence interval (CI): 0.761-1.000].Conclusions: Serum HO-1 is positively correlated with sepsis-induced AKI. These findings suggest that measurement of serum HO-1 may play a diagnostic and prediction role in sepsis-induced AKI.

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Shogaol but not gingerol has a neuroprotective effect on hemorrhagic brain injury: Contribution of the α, β-unsaturated carbonyl to heme oxygenase-1 expression

Cited by 17 publications

References 24 publications

Gadolinium causes M1 and M2 microglial apoptosis after intracerebral haemorrhage and exerts acute neuroprotective effects

Gadolinium causes M1 and M2 microglial apoptosis after intracerebral haemorrhage and exerts acute neuroprotective effects

Microglia Phenotype and Intracerebral Hemorrhage: A Balance of Yin and Yang

Heme oxygenase-1 as a predictor of sepsis-induced acute kidney injury: a cross-sectional study

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