Treatment with Apocynin Limits the Development of Acute Graft-versus-Host Disease in Mice

Rezende, Bárbara Antunes; Bernardes, Priscila T. T.; Gonçalves, William; Resende, Carolina Braga de; Athayde, Rayssa Maciel; Ávila, Thiago Vinicius; Martins, Débora Gonzaga; Castor, Marina Gomes Miranda e; Teixeira, Mauro M.; Pinho, Vanessa

doi:10.1155/2019/9015292

Cited by 8 publications

(5 citation statements)

References 66 publications

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“…Our previous research has shown the presence of an imbalance in redox metabolism during the development of GVHD [ 7 , 10 , 11 ]. To further explore the regulatory effects of hPMSCs on redox metabolism in GVHD, the MDA levels and SOD activity in the serum of GVHD patients and the levels of GSH and carbonyl and the activity of GCL and SOD were measured in the liver and spleen in the mouse model.…”

Section: Resultsmentioning

confidence: 99%

“…Several studies have confirmed that the activation and proliferation of T cells during the development of GVHD is accompanied by a marked increase in energy metabolism. During this process, the levels of reactive oxygen species (ROS), carbonylation, and malondialdehyde (MDA) increase remarkably, which lead to the development of cell and liver damage [ 10 , 11 ]. Enzymes and nonenzymatic antioxidants, such as glutathione (GSH) and superoxide dismutase (SOD), play important roles in the maintenance of normal physiological functions.…”

Section: Introductionmentioning

confidence: 99%

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hPMSCs inhibit the expression of PD-1 in CD4+IL-10+ T cells and mitigate liver damage in a GVHD mouse model by regulating the crosstalk between Nrf2 and NF-κB signaling pathway

Zhang

et al. 2021

Stem Cell Res Ther

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Background The activation of T cells and imbalanced redox metabolism enhances the development of graft-versus-host disease (GVHD). Human placenta-derived mesenchymal stromal cells (hPMSCs) can improve GVHD through regulating T cell responses. However, whether hPMSCs balance the redox metabolism of CD4+IL-10+ T cells and liver tissue and alleviate GVHD remains unclear. This study aimed to investigate the effect of hPMSC-mediated treatment of GVHD associated with CD4+IL-10+ T cell generation via control of redox metabolism and PD-1 expression and whether the Nrf2 and NF-κB signaling pathways were both involved in the process. Methods A GVHD mouse model was induced using 6–8-week-old C57BL/6 and Balb/c mice, which were treated with hPMSCs. In order to observe whether hPMSCs affect the generation of CD4+IL-10+ T cells via control of redox metabolism and PD-1 expression, a CD4+IL-10+ T cell culture system was induced using human naive CD4+ T cells. The percentage of CD4+IL-10+ T cells and their PD-1 expression levels were determined in vivo and in vitro using flow cytometry, and Nrf2, HO-1, NQO1, GCLC, GCLM, and NF-κB levels were determined by western blotting, qRT-PCR, and immunofluorescence, respectively. Hematoxylin-eosin, Masson’s trichrome, and periodic acid-Schiff staining methods were employed to analyze the changes in hepatic tissue. Results A decreased activity of superoxide dismutase (SOD) and a proportion of CD4+IL-10+ T cells with increased PD-1 expression were observed in GVHD patients and the mouse model. Treatment with hPMSCs increased SOD activity and GCL and GSH levels in the GVHD mouse model. The percentage of CD4+IL-10+ T cells with decreased PD-1 expression, as well as Nrf2, HO-1, NQO1, GCLC, and GCLM levels, both in the GVHD mouse model and in the process of CD4+IL-10+ T cell generation, were also increased, but NF-κB phosphorylation and nuclear translocation were inhibited after treatment with hPMSCs, which was accompanied by improvement of hepatic histopathological changes. Conclusions The findings suggested that hPMSC-mediated redox metabolism balance and decreased PD-1 expression in CD4+IL-10+ T cells were achieved by controlling the crosstalk between Nrf2 and NF-κB, which further provided evidence for the application of hPMSC-mediated treatment of GVHD.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

hPMSCs inhibit the expression of PD-1 in CD4+IL-10+ T cells and mitigate liver damage in a GVHD mouse model by regulating the crosstalk between Nrf2 and NF-κB signaling pathway

Zhang

et al. 2021

Stem Cell Res Ther

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“…The specific situation has been marked with different labels. Meanwhile, an intensive reading part of recently published literatures was shown in Table 2 with appropriate and detailed descriptions [19][20][21][22].…”

Section: Discussionmentioning

confidence: 99%

A Novel Scientometrics Research on the Interaction between Oxidative Stress and Hematopoietic Stem Cell Transplantation Complications: From Graft-versus-Host Disease to Sepsis

Cavagnaro

Shi

2023

Oxidative Medicine and Cellular Longevity

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As major and serious complications after hematopoietic stem cell transplantation (HSCT), graft-versus-host disease (GVHD) and sepsis are the chief causes of low survival rates as well as mortality and for HSCT recipients. Although the overall treatment outcomes of HSCT have improved significantly in recent years, there is still an increased incidence rate of complications and mortality after transplantation. In the immediate past, with a deeper understanding of oxidative stress, more and more shreds of evidence have shown that it is closely related to transplantation-related sepsis. However, there is currently a precious little research on the interaction between oxidative stress and complications after HSCT, and the major mechanism has not yet been clarified. The objective of this study was to assess the internal connection between and potential mechanisms as well as visualized the scientometrics results of all important literature related to the topic. Through exhaustive scientometrics analysis, we searched and carefully screened 286 related publications from the Web of Science Core Collection (WoSCC) with “((HSCT) OR (hematopoietic stem cell transplantation)) AND (oxidative stress)” as the search strategy. Then, detailed visualization of the overall information analysis was made by scientific and rigorous bibliometrics software or website. Next, we analyzed retrieved articles extensively and then 59 publications that are relevant to this topic were selected for nuanced analysis and summary. The assessment of these studies proved the validity of the interaction between oxidative stress and complications after HSCT objectively and directly.

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“…Apocynin pharmacokinetics and pharmacodynamics are characterized by the inhibition of ROS production in major organs [ 33 ]. In a study, it was demonstrated that ROS plays an important role in mediating Graft-Versus-Host Disease [ 34 ]. One of the important parameters showing liver regeneration is the number of Ki–67 in the cells.…”

Section: Discussionmentioning

confidence: 99%

Does apocynin increase liver regeneration in the partial hepatectomy model?

Bilgiç¹,

Kanat²,

Özhan³

et al. 2023

Turkish Journal of Medical Sciences

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Background/aim Hepayocyte loss may develop secondary to liver surgery and at this point liver regeneration plays a significant act in terms of liver reserve. The purpose of this research was to investigate the efficacy of apocynin on liver regeneration and preservation after partial hepatectomy in rats. Materials and methods A total of 32 rats, have been divided into 4 groups (n: 8) for hepatectomy model. Inflammatory and antiinflammatory parameters were measured from blood and liver tissue samples. In addition, the effects of apocynin were examined immunohistochemically and histopathologically from liver tissue. Results In liver tissue samples, a significant difference has been found in glutathione peroxidase, total nitrite, catalase, oxidative stress index, total antioxidant and total oxidant status between sham and hepatectomy groups. A significant difference has been achieved between hepatectomy and posthepatectomy-Apocynin in terms of glutathione peroxidase and oxidative stress index. Total antioxidant status, oxidative stress index, and total oxidant status were significantly different only between the sham and the hepatectomy groups. Statistical differences were found between sham and hepatectomy groups and between hepatectomy and pre+post-hepatectomy-Apocynin groups in terms of serum glutathione, malondialdehyde, total nitrite, and L-Arginine. There were significant differences between the sham and hepatectomy groups, between hepatectomy and posthepatectomy-apocynin groups, between posthepatctomy-apocynin and pre+posthepatectomy-apocynin groups in terms of sinusoidal dilatation, intracytoplasmic vacuolization and glycogen loss (p < 0.001), in all histopathologic parameters except sinusoidal dilatation (p < 0.05). However, significant Ki–67 increases have been elaborated in hepatectomy, posthepatectomy-apocynin, and pre+posthepatectomy-apocynin groups compared to sham group (p < 0.001), in pre+posthepatectomy apocynin group compared to hepatectomy and posthepatectomy-apocynin groups (p < 0.001). Conclusion Histopathology, immunohistochemistry, and biochemistry results of this study revealed that apocynin has a protective effect on enhancing liver regeneration in partial hepatectomy cases in rats.

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Treatment with Apocynin Limits the Development of Acute Graft-versus-Host Disease in Mice

Cited by 8 publications

References 66 publications

hPMSCs inhibit the expression of PD-1 in CD4+IL-10+ T cells and mitigate liver damage in a GVHD mouse model by regulating the crosstalk between Nrf2 and NF-κB signaling pathway

hPMSCs inhibit the expression of PD-1 in CD4+IL-10+ T cells and mitigate liver damage in a GVHD mouse model by regulating the crosstalk between Nrf2 and NF-κB signaling pathway

A Novel Scientometrics Research on the Interaction between Oxidative Stress and Hematopoietic Stem Cell Transplantation Complications: From Graft-versus-Host Disease to Sepsis

Does apocynin increase liver regeneration in the partial hepatectomy model?

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