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Data · dataset · 2026

Presentation 1_Apelin aggravates inflammatory response and hepatic steatosis in alcohol-associated liver disease via ERK signaling pathway.pptx

Listed in ZivaHub and Deakin Research Online — shown once because both records carry DOI 10.3389/fphar.2026.1912482.s001

Background<p>Though apelin is involved in cardiovascular, metabolic, and homeostasis disorders, its role in alcohol-associated liver disease (ALD) remains unclear.

Description

This study aimed to investigate the mechanism of apelin in promoting hepatic inflammation in ALD.</p>Methods<p>RAW 264.7 macrophages and a chronic alcohol-fed C57BL/6 mouse model were used. Apelin activated ERK1/2 phosphorylation, and PD98059 pretreatment attenuated apelin-induced MCP-1 and PCNA expression.

Inflammatory and proliferative markers (MCP-1, IL-6, PCNA) were assessed by qRT-PCR and western blot. ERK signaling was evaluated using the inhibitor PD98059. Liver pathology was examined by H&E and Oil Red O staining.</p>Results<p>Alcohol upregulated apelin expression in RAW 264.7 cells.

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Apelin-13 increased MCP-1 and PCNA expression in time- and dose-dependent manners. Apelin overexpression enhanced, while siRNA knockdown reduced, inflammatory and proliferative gene expression. Apelin activated ERK1/2 phosphorylation, and PD98059 pretreatment attenuated apelin-induced MCP-1 and PCNA expression.

In vivo, apelin overexpression exacerbated steatosis, ballooning degeneration, and inflammatory infiltration, with elevated MCP-1, IL-6, and PCNA levels.</p>Conclusion<p>Apelin aggravates inflammatory responses and hepatic steatosis in ALD via the ERK signaling pathway, suggesting that the apelin/APJ/p-ERK/inflammation axis may represent a novel therapeutic target for ALD.</p>

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Disease 75%
Provenance · 2 source records, 12 field assertions
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ZivaHuboai:figshare.com:article/3402946213 d agoJSON v1
Deakin Research Onlineoai:figshare.com:article/3402946213 d agoJSON v1
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