ArticleMolecular medicine reports2018
Kupffer cell depletion by gadolinium chloride aggravates liver injury after brain death in rats.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- The FDA-approved excipient N,N-dimethylacetamide improves survival and attenuates inflammatory pathways in a murine model of endotoxemia.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Alpha Ketoglutaric Acid attenuates LPS Induced Inflammatory Response by Inhibiting the PKCε/MAPK/P65 Signaling Pathway and Inhibit Oxidative Stress in Kupffer Cells.Inflammation · 2025Article
- Gadolinium chloride pre-treatment reduces the inflammatory response and preserves intestinal barrier function in a rat model of sepsis.Experimental and therapeutic medicine · 2021Article
- Functional interaction between macrophages and hepatocytes dictate the outcome of liver fibrosis.Life science alliance · 2021Article
- Generation of Novel Human Red Blood Cell-Bearing Humanized Mouse Models Based on C3-Deficient NOG Mice.Frontiers in immunology · 2021Article
- Understanding, predicting and achieving liver transplant tolerance: from bench to bedside.Nature reviews. Gastroenterology & hepatology · 2020Review
- Lysosomotropic Features and Autophagy Modulators among Medical Drugs: Evaluation of Their Role in Pathologies.Molecules (Basel, Switzerland) · 2020Review
- Gadolinium Chloride Restores the Function of the Gap Junctional Intercellular Communication between Hepatocytes in a Liver Injury.International journal of molecular sciences · 2019Article
- Gadolinium Chloride Rescues Niemann⁻Pick Type C Liver Damage.International journal of molecular sciences · 2018Article
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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). However, IL‑10 levels in the GdCl3 group were significantly reduced compared with those in the saline group (P<0.05). Caspase‑3 and cleaved caspase‑3 activation, and apoptosis induction in the context of BD were also significantly aggravated by the depletion of KCs, whereas Bcl‑2 was significantly suppressed by the administration of GdCl3. The present study indicated that GdCl3 efficiently inhibits the activity of KCs, and is involved in the onset of liver injury through its effects on pro‑inflammatory and anti‑inflammatory activation. KCs are protective in the liver in the context of BD. This protection appears to be due to KCs secretion of the potent anti‑inflammatory cytokine IL‑10, suggesting that KCs are an attractive target for the prevention and treatment of liver injury in the context of BD in rats.
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