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A DPP-4 inhibitor suppresses fibrosis and inflammation on experimental autoimmune myocarditis in mice.

Hirakawa H, Zempo H, Ogawa M, Watanabe R, Suzuki J, Akazawa H, Komuro I, Isobe M - PLoS ONE (2015)

Bottom Line: No specific or effective treatment has been established.DPP-4 inhibitors have salutary effects not only on type 2 diabetes but also on certain cardiovascular diseases.Lymphocyte proliferation assay showed that treatment with the DPP-4 inhibitor had no effect on antigen-induced spleen cell proliferation.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.

ABSTRACT
Myocarditis is a critical inflammatory disorder which causes life-threatening conditions. No specific or effective treatment has been established. DPP-4 inhibitors have salutary effects not only on type 2 diabetes but also on certain cardiovascular diseases. However, the role of a DPP-4 inhibitor on myocarditis has not been investigated. To clarify the effects of a DPP-4 inhibitor on myocarditis, we used an experimental autoimmune myocarditis (EAM) model in Balb/c mice. EAM mice were assigned to the following groups: EAM mice group treated with a DPP-4 inhibitor (linagliptin) (n = 19) and those untreated (n = 22). Pathological analysis revealed that the myocardial fibrosis area ratio in the treated group was significantly lower than in the untreated group. RT-PCR analysis demonstrated that the levels of mRNA expression of IL-2, TNF-α, IL-1β and IL-6 were significantly lower in the treated group than in the untreated group. Lymphocyte proliferation assay showed that treatment with the DPP-4 inhibitor had no effect on antigen-induced spleen cell proliferation. Administration of the DPP-4 inhibitor remarkably suppressed cardiac fibrosis and reduced inflammatory cytokine gene expression in EAM mice. Thus, the agents present in DPP-4 inhibitors may be useful to treat and/or prevent clinical myocarditis.

No MeSH data available.


Related in: MedlinePlus

Pathological analysis revealed that a DPP-4 inhibitor prevented cardiac fibrosis in EAM.A, Representative pathological images stained with HE staining and Mallory staining in low (× 20) power microscopic field are presented. B, Quantitative analysis of the cell infiltration area in myocardium. There is no significant difference between the untreated group and the treated group. C, Quantitative analysis of the fibrotic area in myocardium. The untreated group showed severe fibrosis, however, the treated group showed a smaller fibrotic area. *P < 0.05, Fisher’s PLSD. Values are mean ± SEM. Scale bars = 1mm
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pone.0119360.g001: Pathological analysis revealed that a DPP-4 inhibitor prevented cardiac fibrosis in EAM.A, Representative pathological images stained with HE staining and Mallory staining in low (× 20) power microscopic field are presented. B, Quantitative analysis of the cell infiltration area in myocardium. There is no significant difference between the untreated group and the treated group. C, Quantitative analysis of the fibrotic area in myocardium. The untreated group showed severe fibrosis, however, the treated group showed a smaller fibrotic area. *P < 0.05, Fisher’s PLSD. Values are mean ± SEM. Scale bars = 1mm

Mentions: The fibrosis area ratio of myocardium in the treated group (2.0 ± 0.1%) was lower than the untreated group (4.6 ± 1.0%, P<0.05). Regarding the cell infiltration area in myocardium, there was no significant difference between the treated group (1.75 ± 0.57) and the untreated group (3.04 ± 0.58) (p = 0.27). (Fig. 1)


A DPP-4 inhibitor suppresses fibrosis and inflammation on experimental autoimmune myocarditis in mice.

Hirakawa H, Zempo H, Ogawa M, Watanabe R, Suzuki J, Akazawa H, Komuro I, Isobe M - PLoS ONE (2015)

Pathological analysis revealed that a DPP-4 inhibitor prevented cardiac fibrosis in EAM.A, Representative pathological images stained with HE staining and Mallory staining in low (× 20) power microscopic field are presented. B, Quantitative analysis of the cell infiltration area in myocardium. There is no significant difference between the untreated group and the treated group. C, Quantitative analysis of the fibrotic area in myocardium. The untreated group showed severe fibrosis, however, the treated group showed a smaller fibrotic area. *P < 0.05, Fisher’s PLSD. Values are mean ± SEM. Scale bars = 1mm
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4359137&req=5

pone.0119360.g001: Pathological analysis revealed that a DPP-4 inhibitor prevented cardiac fibrosis in EAM.A, Representative pathological images stained with HE staining and Mallory staining in low (× 20) power microscopic field are presented. B, Quantitative analysis of the cell infiltration area in myocardium. There is no significant difference between the untreated group and the treated group. C, Quantitative analysis of the fibrotic area in myocardium. The untreated group showed severe fibrosis, however, the treated group showed a smaller fibrotic area. *P < 0.05, Fisher’s PLSD. Values are mean ± SEM. Scale bars = 1mm
Mentions: The fibrosis area ratio of myocardium in the treated group (2.0 ± 0.1%) was lower than the untreated group (4.6 ± 1.0%, P<0.05). Regarding the cell infiltration area in myocardium, there was no significant difference between the treated group (1.75 ± 0.57) and the untreated group (3.04 ± 0.58) (p = 0.27). (Fig. 1)

Bottom Line: No specific or effective treatment has been established.DPP-4 inhibitors have salutary effects not only on type 2 diabetes but also on certain cardiovascular diseases.Lymphocyte proliferation assay showed that treatment with the DPP-4 inhibitor had no effect on antigen-induced spleen cell proliferation.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular Medicine, Tokyo Medical and Dental University, Tokyo, Japan.

ABSTRACT
Myocarditis is a critical inflammatory disorder which causes life-threatening conditions. No specific or effective treatment has been established. DPP-4 inhibitors have salutary effects not only on type 2 diabetes but also on certain cardiovascular diseases. However, the role of a DPP-4 inhibitor on myocarditis has not been investigated. To clarify the effects of a DPP-4 inhibitor on myocarditis, we used an experimental autoimmune myocarditis (EAM) model in Balb/c mice. EAM mice were assigned to the following groups: EAM mice group treated with a DPP-4 inhibitor (linagliptin) (n = 19) and those untreated (n = 22). Pathological analysis revealed that the myocardial fibrosis area ratio in the treated group was significantly lower than in the untreated group. RT-PCR analysis demonstrated that the levels of mRNA expression of IL-2, TNF-α, IL-1β and IL-6 were significantly lower in the treated group than in the untreated group. Lymphocyte proliferation assay showed that treatment with the DPP-4 inhibitor had no effect on antigen-induced spleen cell proliferation. Administration of the DPP-4 inhibitor remarkably suppressed cardiac fibrosis and reduced inflammatory cytokine gene expression in EAM mice. Thus, the agents present in DPP-4 inhibitors may be useful to treat and/or prevent clinical myocarditis.

No MeSH data available.


Related in: MedlinePlus