Effects of dexamethasone on hepatic macrophages in normal livers and thioacetamide-induced acute liver lesions in rats

Resident and infiltrative macrophages play important roles in the development of pathological lesions. M1/M2 macrophage polarization with respective CD68 and CD163 expression remains unclear in chemically induced liver injury. This study was aimed at investigating the influence of macrophages on nor...

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Bibliographic Details
Published in:Journal of Toxicologic Pathology 2020, Vol.33(4), pp.237-246
Main Authors: Hada, Noa, Kuramochi, Mizuki, Izawa, Takeshi, Kuwamura, Mitsuru, Yamate, Jyoji
Format: Article
Language:English
Subjects:
CD163 antigen
Dexamethasone
Fibrosis
Homeostasis
Immunosuppressive agents
Injuries
Kupffer cells
Lesions
Liver
M1 macrophage
M2 macrophage
Macrophages
Original
Pretreatment
Steroids
Thioacetamide
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Summary:Resident and infiltrative macrophages play important roles in the development of pathological lesions. M1/M2 macrophage polarization with respective CD68 and CD163 expression remains unclear in chemically induced liver injury. This study was aimed at investigating the influence of macrophages on normal and chemically induced liver injury. For this, dexamethasone (DX), an immunosuppressive drug, was administered in normal rats and thioacetamide (TAA)-treated rats. Liver samples were collected and analyzed with immunohistochemical methods. Repeated injections of DX (0.5 or 1.0 mg/kg BW) for 3, 7 and 11 days reduced the number of CD163 positive hepatic resident macrophages (Kupffer cells) in normal livers, while increasing AST and ALT levels. In TAA (300 mg/kg BW)-treated rats injected with DX (0.5 mg/kg BW) pretreatment, the number of M1 and M2 macrophages showed a significant decrease compared with that of TAA-treated rats without DX treatment. Additionally, reparative fibrosis resulting from hepatocyte injury induced by TAA injection was suppressed by DX pretreatment. Our data suggested that macrophages could influence not only normal hepatic homeostasis (reflected by AST and ALT levels) but also chemically induced hepatic lesion development (reduced reparative fibrosis).
ISSN:0914-9198
1881-915X
1347-7404
DOI:10.1293/tox.2020-0016