PhD Scientific Days 2026

Pharmaceutical Sciences and Health Technologies 2.

Lysophosphatidic Acid Receptor 5 (LPAR5) Protects Against Nonsteroidal Anti-Inflammatory Drug-Induced Enteropathy in Mice

Előadó neve

Zsidai, Anna, MSc

Neptune code

AB16X8

Előadó munkahelye

Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary

Előadó telefonszáma

06304272549

Előadó e-mail címe

zsidai.anna@semmelweis.hu

Az előadás címe

Lysophosphatidic Acid Receptor 5 (LPAR5) Protects Against Nonsteroidal Anti-Inflammatory Drug-Induced Enteropathy in Mice

Szerző(k) neve és munkahelye

Anna Zsidai^1,2, Zsuzsanna O. Demeter^1,2, Gerda Wachtl^1,2, Arezoo Haghighi^1,2, Lili Lengyel^1,2, Julian Steinhardt^1,2, Klára Gyires^1,2, Zoltán S. Zádori^1,2

1: Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary
2: Center for Pharmacology and Drug Research & Development, Semmelweis University, Budapest, Hungary

Bemutatás módja

Szóbeli

Szekció

Pharmaceutical Sciences and Health Technologies 2.

Language of the presentation

Hungarian

Preferred session

Pharmaceutical Sciences and Health Technologies

Összefoglaló szövege

Introduction: Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly prescribed medications. However, chronic use of NSAIDs can cause inflammation and ulcers in the small intestine (enteropathy), affecting up to 70% of patients. Enteropathy can not be treated by using antisecretory drugs, so new therapeutic targets must be identified. Lysophosphatidic acid receptor 5 (LPAR5) has high expression level in the small intestine and on immune cells, suggesting that this receptor could serve as a potential target for the treatment of enteropathy. Activation of LPAR5 has been shown to regulate the immune cell recruitment, cytokine release and the expression of tight junction proteins, but its role in regulating NSAID-induced enteropathy is unclear.
Aims: Our aim was to assess the role of LPAR5 in NSAID-induced enteropathy by using Lpar5 knockout (KO) mice.
Method: Enteropathy was induced with indomethacin (INDO, 40 mg/kg) in WT and Lpar5 KO mice and animals were terminated 24 hour after INDO treatment. The severity of small intestinal inflammation was detected macroscopically, and by measuring the tissue level of different inflammatory markers (Il6, Il10, Il1β, COX-2, MPO, PTX3) and tight junction proteins (Claudin-1 and Occludin) by using Western blot or qPCR. The expression and localisation of Lpar5 mRNA was determined using RNAscope technique.
Results: INDO induced severe enteropathy, characterised by intestinal shortening, increased level of the measured inflammatory markers and decreased expression of tight junction proteins. Enteropathy was also associated with decreased Lpar5 expression. Deletion of Lpar5 itself did not cause intestinal inflammation, but resulted a decrease in the small intestinal level of tight junction proteins, and exacerbated the intestinal inflammation caused by INDO.
Conclusion: Our study shows that LPAR5 plays an important role in regulating the expression of tight junction proteins, and protects against NSAID-induced enteropathy. Therefore, activating LPAR5 could be a potential treatment for NSAID-induced enteropathy.
Funding: NKFI FK 138842

University

Semmelweis University

Supervisor

Dr. Zoltán S. Zádori

Publication of my abstract

I do not give consent to the publication of my abstract on the website of the congress.

phd.section.field

in doctoral studies before complex exam (PhD)

Kind

Szabad

Status

elfogadva

Accepted presentation method

szóbeli

Előadás fájl jóváhagyás

nem hagyta jóvá

Előadó

9003

Start

10:45

End

10:55