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Hypoxia-preconditioned mesenchymal stem cells attenuate peritoneal adhesion through TGF-β inhibition

Universa Medicina · Vol. 39 No. 2 (2020) · hlm. 97–104

DOI
10.18051/UnivMed.2020.v39.97-104
ISSN
2407-2230, 1907-3062
Terbit
2020-07-09
Penerbit
Faculty of Medicine, Universitas Trisakti
Bahasa
eng
Lisensi
creativecommons.org/licenses/by-nc-sa/4.0

Abstrak

BackgroundPeritoneal adhesions (PAs) are generally described as fibrous bands between intra-abdominal organs following an abdominal surgical operation. The definitive treatments of PAs are currently ineffective yet. Hypoxia-mesenchymal stem cells (H-MSCs) have a higher capability to survive at the site of injury than normoxia-MSCs (N-MSCs) to repair injured tissue without fibrosis. This study aimed to analyze the effect of H-MSCs in controlling formation of PAs by reducing TGF-β level in a rat model. Methods A study of post-test only control group design was conducted, involving eighteen PA rat models weighing 250 ± 25 g that were randomly assigned into 3 groups, comprising control group (C), and groups T1 and T2 receiving H-MSC treatment at doses of 3 x 106 and 1.5 x 106, respectively. To induce H-MSCs, MSCs were incubated in hypoxic conditions at 5% O2 and 37oC for 24 hours. Expression level of TGF-β was analyzed by enzyme-linked immunosorbent assay (ELISA) at 450 nm and adhesion formation was described macroscopically. The Kruskal-Wallis variance analysis was used to analyze significant differences among the groups.ResultsThe results of this study showed that H-MSCs in group T1 inhibited TGF-β expression significantly on day 8 (p<0.001) and day 14 (p<0.05). Moreover, there was almost no adhesion apparent following H-MSC administration in group T1. ConclusionsBased on this study, we conclude that H-MSCs may attenuate PA formation following inhibition of TGF-β expression in the PA rat model.

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  • Sultan Agung Islamic University
  • Universitas Sumatera Utara
  • State University of Semarang
  • University of Mataram
  • Soegijapranata Catholic University
  • Diponegoro University
  • Universitas Prima Indonesia
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Rekan penulisOrganisasiArtikel bersama
Nur Dina AmalinaState University of Semarang4
Nurul HidayahSultan Agung Islamic University4
Titiek SumarawatiSultan Agung Islamic University3
Nurul HidayahSultan Agung Islamic University3
Iffan AlifSultan Agung Islamic University3
Risky Chandra Satria IrawanSultan Agung Islamic University3
Chodijah ChodijahSultan Agung Islamic University2
Bayu Tirta DirjaUniversity of Mataram2
Salma Yasmine AzzaharaSultan Agung Islamic University2
Yulice Soraya Nur IntanSultan Agung Islamic University2
Citra Primavita MayangsariSultan Agung Islamic University2
Rita Kartika SariSultan Agung Islamic University2
Faizal MukharimSultan Agung Islamic University2
Dedy HermansyahUniversitas Sumatera Utara2
Nur Anna Chalimah Sa'dyahAfiliasi tidak diketahui2
Chodidjah ChodidjahSultan Agung Islamic University2
Hadi SunartoSultan Agung Islamic University2
Arya TjiptaUniversitas Sumatera Utara2
Sugeng IbrahimSoegijapranata Catholic University1
Alisia Martha DewiSultan Agung Islamic University1
Setyo TrisnasiSultan Agung Islamic University1
Hadi SarosaSultan Agung Islamic University1
Sri Priyantini MulyaniSultan Agung Islamic University1
Yan Wisnu PrajokoDiponegoro University1
Pangesti DrawinaSultan Agung Islamic University1
Taufiqurrachman NasihunSultan Agung Islamic University1
Riska RachmaniaSultan Agung Islamic University1
Sofian Azalia HusainAfiliasi tidak diketahui1
Ade Indra MuktiUniversitas Prima Indonesia1
Reynaldi SuryajayaAfiliasi tidak diketahui1
Imam Djamaluddin MashoediSultan Agung Islamic University1
Dwi Fikha AprilyantiSultan Agung Islamic University1
RinawatiAfiliasi tidak diketahui1
Andhika Dwi AnggaraSultan Agung Islamic University1
Iwang YusufSultan Agung Islamic University1
Aditya NugrahaSultan Agung Islamic University1

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Sumber metadata: OAI-PMH (metadata jurnal) https://univmed.org/ejurnal/index.php/medicina/oai, pertama di-harvest 10 Nov 2026, terakhir terlihat 10 Nov 2026.
Metadata asli (oai_dc) 
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	<dc:title xml:lang="en">Hypoxia-preconditioned mesenchymal stem cells attenuate peritoneal adhesion through TGF-β inhibition</dc:title>
	<dc:creator xml:lang="en">Trisnadi, Setyo</dc:creator>
	<dc:creator xml:lang="en">Muhar, Adi Muradi</dc:creator>
	<dc:creator xml:lang="en">Putra, Agung</dc:creator>
	<dc:creator xml:lang="en">Kustiyah, Azizah Retno</dc:creator>
	<dc:subject xml:lang="en">Peritoneal adhesions</dc:subject>
	<dc:subject xml:lang="en">hypoxia</dc:subject>
	<dc:subject xml:lang="en">mesenchymal stem cells</dc:subject>
	<dc:subject xml:lang="en">TGF-β</dc:subject>
	<dc:description xml:lang="en">BackgroundPeritoneal adhesions (PAs) are generally described as fibrous bands between intra-abdominal organs following an abdominal surgical operation. The definitive treatments of PAs are currently ineffective yet. Hypoxia-mesenchymal stem cells (H-MSCs) have a higher capability to survive at the site of injury than normoxia-MSCs (N-MSCs) to repair injured tissue without fibrosis. This study aimed to analyze the effect of H-MSCs in controlling formation of PAs by reducing TGF-β level in a rat model. Methods A study of post-test only control group design was conducted, involving eighteen PA rat models weighing 250 ± 25 g that were randomly assigned into 3 groups, comprising control group (C), and groups T1 and T2 receiving H-MSC treatment at doses of 3 x 106 and 1.5 x 106, respectively. To induce H-MSCs, MSCs were incubated in hypoxic conditions at 5% O2 and 37oC for 24 hours. Expression level of TGF-β was analyzed by enzyme-linked immunosorbent assay (ELISA) at 450 nm and adhesion formation was described macroscopically. The Kruskal-Wallis variance analysis was used to analyze significant differences among the groups.ResultsThe results of this study showed that H-MSCs in group T1 inhibited TGF-β expression significantly on day 8 (p&amp;lt;0.001) and day 14 (p&amp;lt;0.05). Moreover, there was almost no adhesion apparent following H-MSC administration in group T1. ConclusionsBased on this study, we conclude that H-MSCs may attenuate PA formation following inhibition of TGF-β expression in the PA rat model.</dc:description>
	<dc:publisher xml:lang="en">Faculty of Medicine, Universitas Trisakti</dc:publisher>
	<dc:date>2020-07-09</dc:date>
	<dc:type>info:eu-repo/semantics/article</dc:type>
	<dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
	<dc:format>application/pdf</dc:format>
	<dc:identifier>https://univmed.org/ejurnal/index.php/medicina/article/view/902</dc:identifier>
	<dc:identifier>10.18051/UnivMed.2020.v39.97-104</dc:identifier>
	<dc:source xml:lang="en">Universa Medicina; Vol. 39 No. 2 (2020); 97-104</dc:source>
	<dc:source>2407-2230</dc:source>
	<dc:source>1907-3062</dc:source>
	<dc:source>10.18051/UnivMed.2020.v39.i2</dc:source>
	<dc:language>eng</dc:language>
	<dc:relation>https://univmed.org/ejurnal/index.php/medicina/article/view/902/589</dc:relation>
	<dc:rights xml:lang="en">Copyright (c) 2020 Setyo Trisnadi, Agung Putra, Azizah Retno Kustiyah, Adi Muradi</dc:rights>
	<dc:rights xml:lang="en">https://creativecommons.org/licenses/by-nc-sa/4.0</dc:rights>
</oai_dc:dc>