Kupffer cell depletion by gadolinium chloride aggravates liver injury after brain death in rats.

Molecular Medicine Reports
Rongtao ZhuShuijun Zhang

Abstract

Brain death (BD) impairs liver function in potential donors, and is associated with hormonal and metabolic changes or molecular effects with pro‑inflammatory activation. Resident macrophages in the liver named Kupffer cells (KCs) undergo pro‑ or anti‑inflammatory pathway activation, which affects liver function. However, the role of the KCs in liver dysfunction following BD has not been fully elucidated. The aim of the present study was to investigate the role of KCs in liver dysfunction in the context of BD and the effects of their inhibition by gadolinium chloride (GdCl3). Rats were randomly divided into the following groups: Control, BD with GdCl3 pretreatment and BD with normal saline pretreatment. Liver function, hepatic pathological histology and cytokine levels in the liver were assessed. Apoptosis and apoptosis‑related proteins [cleaved caspase‑3, caspase‑3 and apoptosis regulator Bcl‑2 (Bcl‑2)] were evaluated. GdCl3 significantly aggravated liver injury by elevating alanine aminotransferase and aspartate aminotransferase levels (P<0.05) by inhibiting KCs. Interleukin (IL)‑1β and tumor necrosis factor α levels in the GdCl3 group were significantly increased compared with those in the control and saline groups (P<0.01). ...Continue Reading

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Citations

Nov 18, 2018·International Journal of Molecular Sciences·Andrés D KleinSilvana Zanlungo
Nov 5, 2020·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Tatiana A KorolenkoVaclav Vetvicka
Aug 14, 2021·Frontiers in Immunology·Takuya YamaguchiTakeshi Takahashi

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Methods Mentioned

BETA
light microscopy
X-ray
ELISA

Software Mentioned

Quantity One
SPSS

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