The Pantothenic Acid Derivative Dexpanthenol Attenuates Liver Injury Induced by Lung Ischemia- Reperfusion Through Its Anti-Inflammatory Effect

Year 2026, Volume: 33 Issue: 1, 41 - 48, 21.03.2026

Bilal Turan , Halil Aşcı , İsa Karaca , Özlem Özmen

https://doi.org/10.17343/sdutfd.1817428

https://izlik.org/JA98RN29CH

Abstract

Objective
Pulmonary ischemia-reperfusion (IR) injury can lead
to liver damage through inflammation triggered by
hypoxic conditions. Dexpanthenol (DEX), known for
its anti-inflammatory properties in organs such as the
lung, liver, and kidney, may exert hepatoprotective
effects. This study investigates the potential of DEX in
mitigating hepatic injury following pulmonary IR.

Material and Method
A total of 40 rats were randomly allocated into four
experimental groups: control, ischemia-reperfusion
(IR), IR treated with dexpanthenol (IR+DEX; 500
mg/kg, intraperitoneally, single dose), and DEX
alone. Following left thoracotomy, non-traumatic
vascular occlusion was performed for 60 min,
followed by a 60-min reperfusion period. Upon
sacrification, liver tissues were harvested and fixed in
formaldehyde for subsequent histopathological and
immunohistochemical evaluation.

Results
Histological evaluation of liver sections from the
control and DEX groups revealed normal tissue
architecture. In contrast, the IR group exhibited
prominent pathological changes, including moderate
hyperemia, hepatocellular necrosis, inflammatory
cell infiltration, and mild hemorrhage, predominantly
around the central veins. Notably, liver sections
from the DEX-treated groups demonstrated marked
histological improvement compared to the IR group.
Immunohistochemical analysis revealed minimal
cytoplasmic expression of c-Fos, HIF-1α, and IL-6 in
the control group. In contrast, the IR group exhibited
a marked increase in the expression of all three
markers within liver tissue. DEX treatment notably
reduced the expression levels of c-Fos, HIF-1α, and
IL-6, suggesting a protective effect against IR-induced
hepatic injury. While inflammatory cells and bile duct
epithelial cells showed similar expression patterns,
hepatocytes were the primary source of these
immunoreactive signals. All marker expressions were
confined to the cytoplasm. These findings indicate that
DEX provides a protective effect against IR-induced
liver damage.

Conclusion
In the context of pulmonary IR, damage is likely to occur
not only in lung tissue but also in other secondary
organs. This is attributed to the dissemination of
immunomodulatory cytokines developed within the
tissue through the bloodstream to other organs. DEX,
a derivative of pantothenic acid recognized in the literature
for its tis-sue-protective effects and known
anti-inflammatory properties, mitigates inflammation
in liver damage resulting from lung IR injury, as evidenced
by alterations and changes in immunological
markers.

Keywords

Ischemia-reperfusion , Dexpanthenol , Liver , Lung ischemia

Ethical Statement

The experimental design adhered to the guidelines for animal research set forth by the National Institutes of Health and received approval from the Committee on Animal Research at Suleyman Demirel University before commencement of the study (Approval no: 06-538, Date: 12.06.2025).

Supporting Institution

This study was supported by the Scientific Research Projects Coordination Unit of Suleyman Demirel University, with project code TSG-2024-9515.

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