Melola Discovery

← Melola Discovery

Akses terbuka Jurnal SINTA 1

Hypoxic mesenchymal stem cell-derived secretome and alkaline water synergistically reduce apoptosis and insulin resistance in type 2 diabetes mellitus rat model

Universa Medicina · Vol. 44 No. 3 (2025) · hlm. 310–317

DOI
10.18051/UnivMed.2025.v44.310-317
ISSN
2407-2230, 1907-3062
Terbit
2025-11-11
Penerbit
Faculty of Medicine, Universitas Trisakti
Bahasa
eng
Lisensi
creativecommons.org/licenses/by-nc-sa/4.0

Abstrak

BACKGROUNDType 2 Diabetes Mellitus (T2DM) is characterized by chronic inflammation and insulin resistance. These factors contribute to pancreatic β-cell apoptosis, reducing insulin production and impairing glucose homeostasis. This study aims to evaluate the protective effects of hypoxic mesenchymal stem cell-derived secretome (HMSCS) and alkaline water on inflammation, apoptosis, and insulin resistance in a T2DM rat model. METHODSAn experimental study was conducted involving 24 male Wistar T2DM model rats (aged 6-8 weeks, 200-250g). They were randomized into four groups: T2DM rats only as negative control (K-), T2DM rats with metformin as positive control (K+), HMSCS treatment (P1), and HMSCS plus alkaline water group (P2). Caspase-3 expression was measured to assess apoptosis levels using RT-PCR, while homeostatic model assessment for insulin resistance (HOMA-IR) was measured using ELISA. One way ANOVA followed by a post hoc LSD test were used to analyse the data. RESULTSThe P1 group (3.03 ± 1.26 a.u) and P2 group (2.93 ± 0.52 a.u.) had significantly lower caspase-3 expression compared to K- group (6.66 ± 2.76 a.u.) (p 0.05). Additionally, P2 group (6.76 ± 0.96) had a significantly lower HOMA-IR than K- group (18.92 ± 2.63) and K+ group (10.85 ± 1.39) (p<0.05), and similarly the P1 (7.71 ± 0.53) group also showed significant difference from K- and K+ groups (p<0.05). CONCLUSIONHigher doses of HMSCS and alkaline water are associated with reduced pancreatic β-cell apoptosis and improved insulin sensitivity, highlighting its potential as a novel therapeutic approach for T2DM.

Kata kunci

Jaringan kolaborasi para penulis

31 penulis · 62 tautan kepenulisan bersama · 23 lintas organisasi

Arahkan kursor atau ketuk sebuah nama untuk menyorot rekan penulisnya. Klik dua kali untuk membuka halaman penulis.

  • Sultan Agung Islamic University
  • University of Brawijaya
  • Universitas Gadjah Mada
  • Universitas Islam Indragiri
  • State University of Semarang
  • Padjadjaran University
  • Soegijapranata Catholic University
  • Organisasi lain
  • Afiliasi tidak diketahui
  • Organisasi berbeda
  • Organisasi sama
  • Afiliasi tidak diketahui
  • Garis lebih tebal = lebih banyak artikel bersama · lingkaran lebih besar = lebih banyak artikel
Tampilkan sebagai tabel
Rekan penulisOrganisasiArtikel bersama
Hurriyatul FitriyahUniversity of Brawijaya2
Agung Setia BudiUniversity of Brawijaya2
Rizal MaulanaUniversity of Brawijaya2
Muhammad Rheza CaesardiUniversity of Brawijaya1
Jeffry Atur FirdausUniversity of Brawijaya1
Sabriansyah Rizqika AkbarUniversity of Brawijaya1
Agung SetiabudiUniversitas Islam Indragiri1
Fahmi ErzaUniversity of Brawijaya1
Rakhmadhany PrimanandaUniversity of Brawijaya1
Naufal Mohamad GhifaryAfiliasi tidak diketahui1
Cleveria JessikaSultan Agung Islamic University1
Titiek SumarawatiSultan Agung Islamic University1
Carolina Kiwik RahardjaSultan Agung Islamic University1
Sri Priyantini MulyaniSultan Agung Islamic University1
Y. Titik HaryatiState University of Semarang1
Lakkana SuwannoiAfiliasi tidak diketahui1
Preecha MontakantikulAfiliasi tidak diketahui1
Busba ChindavijakAfiliasi tidak diketahui1
Mas Rizky A. A. SyamsunarnoPadjadjaran University1
Tarrayuana Rhamadia HasannuriSultan Agung Islamic University1
Riris Istighfari JenieUniversitas Gadjah Mada1
Muthi IkawatiUniversitas Gadjah Mada1
Iffan AlifSultan Agung Islamic University1
Agung PutraSultan Agung Islamic University1
Yeni FristianiSultan Agung Islamic University1
Dodik Tugasworo Pramukarso PramukarsoDiponegoro University1
Sugeng IbrahimSoegijapranata Catholic University1
Titiek SumarawatiSultan Agung Islamic University1

Afiliasi berasal dari OpenAlex; metadata OAI-PMH jurnal tidak memuatnya. Penulis tanpa ID OpenAlex dicocokkan berdasarkan nama, sehingga dua orang bisa tergabung atau satu orang bisa terpisah.

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) 
<oai_dc:dc xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/  http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
	<dc:title xml:lang="en">Hypoxic mesenchymal stem cell-derived secretome and alkaline water synergistically reduce apoptosis and insulin resistance in type 2 diabetes mellitus rat model</dc:title>
	<dc:creator xml:lang="en">Mawarini, Melisa Septi</dc:creator>
	<dc:creator xml:lang="en">Setiawan, Eko</dc:creator>
	<dc:creator xml:lang="en">Putra, Agung</dc:creator>
	<dc:subject xml:lang="en">Caspase-3</dc:subject>
	<dc:subject xml:lang="en">HOMA-IR</dc:subject>
	<dc:subject xml:lang="en">inflammation</dc:subject>
	<dc:subject xml:lang="en">insulin resistance</dc:subject>
	<dc:subject xml:lang="en">HMSCS</dc:subject>
	<dc:subject xml:lang="en">T2DM</dc:subject>
	<dc:subject xml:lang="en">rats</dc:subject>
	<dc:description xml:lang="en">BACKGROUNDType 2 Diabetes Mellitus (T2DM) is characterized by chronic inflammation and insulin resistance. These factors contribute to pancreatic β-cell apoptosis, reducing insulin production and impairing glucose homeostasis. This study aims to evaluate the protective effects of hypoxic mesenchymal stem cell-derived secretome (HMSCS) and alkaline water on inflammation, apoptosis, and insulin resistance in a T2DM rat model.
METHODSAn experimental study was conducted involving 24 male Wistar T2DM model rats (aged 6-8 weeks, 200-250g). They were randomized into four groups: T2DM rats only as negative control (K-), T2DM rats with metformin as positive control (K+), HMSCS treatment (P1), and HMSCS plus alkaline water group (P2). Caspase-3 expression was measured to assess apoptosis levels using RT-PCR, while homeostatic model assessment for insulin resistance (HOMA-IR) was measured using ELISA. One way ANOVA followed by a post hoc LSD test were used to analyse the data.
RESULTSThe P1 group (3.03 ± 1.26 a.u) and P2 group (2.93 ± 0.52 a.u.) had significantly lower caspase-3 expression compared to K- group (6.66 ± 2.76 a.u.) (p&amp;lt;0.05), but were not significantly different from K+ group (3.83 ± 1.61 a.u.) (p&amp;gt;0.05). Additionally, P2 group (6.76 ± 0.96) had a significantly lower HOMA-IR than K- group (18.92 ± 2.63) and K+ group (10.85 ± 1.39) (p&amp;lt;0.05), and similarly the P1 (7.71 ± 0.53) group also showed significant difference from K- and K+ groups (p&amp;lt;0.05).
CONCLUSIONHigher doses of HMSCS and alkaline water are associated with reduced pancreatic β-cell apoptosis and improved insulin sensitivity, highlighting its potential as a novel therapeutic approach for T2DM.</dc:description>
	<dc:publisher xml:lang="en">Faculty of Medicine, Universitas Trisakti</dc:publisher>
	<dc:date>2025-11-11</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/1772</dc:identifier>
	<dc:identifier>10.18051/UnivMed.2025.v44.310-317</dc:identifier>
	<dc:source xml:lang="en">Universa Medicina; Vol. 44 No. 3 (2025); 310-317</dc:source>
	<dc:source>2407-2230</dc:source>
	<dc:source>1907-3062</dc:source>
	<dc:source>10.18051/UnivMed.2025.v44.i3</dc:source>
	<dc:language>eng</dc:language>
	<dc:relation>https://univmed.org/ejurnal/index.php/medicina/article/view/1772/842</dc:relation>
	<dc:rights xml:lang="en">Copyright (c) 2025 Melissa Septi Mawarini, Eko Setiawan, Agung Putra</dc:rights>
	<dc:rights xml:lang="en">https://creativecommons.org/licenses/by-nc-sa/4.0</dc:rights>
</oai_dc:dc>