Iffan Alif
Stem Cell and Cancer Research (SCCR), Faculty of Medicine, Sultan Agung Islamic University (UNISSULA), Semarang, Indonesia

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Hypoxic mesenchymal stem cell‐conditioned medium accelerates wound healing by regulating IL‐10 and TGF‐β levels in a full‐thickness‐wound rat model Adi Muradi Muhar; Faizal Mukharim; Dedy Hermansyah; Agung Putra; Nurul Hidayah; Nur Dina Amalina; Iffan Alif
Indonesian Journal of Biotechnology Vol 27, No 4 (2022)
Publisher : Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.22146/ijbiotech.63914

Abstract

Full‐thickness wound healing is a complex process requiring a well‐orchestrated mechanism of various factors, including cytokines, particularly interleukin (IL)‐10 and transforming growth factor (TGF)‐β. IL‐10 and TGF‐β act as robust anti‐inflammatory cytokines in accelerating the wound healing process by regulating myofibroblasts. Hypoxic mesenchymal stem cell‐conditioned medium (hypMSC‐CM) containing cytokines potentially contribute to accelerate wound repair without scarring through the paracrine mechanism. This study aims to observe the role of hypMSC‐CM in controlling TGF‐β and IL‐10 levels to accelerate full‐thickness wound repair and regeneration. A total of 24 male Wistar rats were used in this study. Six healthy rats as a sham group and 18 rats were created as full‐thickness‐wound animal models using a 6 mm punch biopsy. The animals were randomly assigned into three groups (n = 6) consisting of two treatment groups treated with hypMSC‐CM at a low dose (200 µL hypMSC‐CM with 2 g water‐based gel added) and a high dose (400 µL hypMSC‐CM with 2 g water‐based gel added) and a control group (2 g water‐based gel only). The IL‐10 and TGF‐β levels were examined by ELISA. The results showed a significant increase in IL‐10 levels on day 3 after hypMSC‐CM treatment, followed by a decrease in platelet‐derived growth factor (PDGF) levels on days 6 and 9. In line with this finding, the TGF‐β levels also increased significantly on day 3 and then linearly decreased on days 6 and 9. HypMSC‐CM administra‐ tion may thus promote wound healing acceleration by controlling IL‐10 and TGF‐β levels in a full‐thickness‐wound rat model.
Moringa oleifera leaf extract ameliorates collagen degradation via the inhibition of MMP‐3 expression in UVB‐induced rats Riska Rachmania; Titiek Sumarawati; Agung Putra; Nurul Hidayah; Iffan Alif; Sofian Azalia Husain; Ade Indra Mukti; Reynaldi Suryajaya; Salma Yasmine Azzahara
Indonesian Journal of Biotechnology Vol 29, No 3 (2024)
Publisher : Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.22146/ijbiotech.77538

Abstract

Prolonged exposure to high‐intensity UVB induces the formation of reactive oxygen species (ROS) in skin tissue, triggering an increase in matrix metalloproteinase‐3 (MMP‐3) enzyme production and leading to collagen degradation. Moringa oleifera (MO) contains bioactive compounds known for ROS‐scavenging and anti‐inflammatory properties. However, the precise molecular mechanism of action remains unclear, requiring the inhibition of MMP‐3 activation and regulation of collagen deposition. This study aims to elucidate the potential effect of MO leaf extract‐based gel in restoring collagen deposition by reducing MMP‐3 activation in UVB irradiate‐induced collagen loss in rats. This study employed a completely randomized design, comprising four groups: a healthy group without UVB radiation, a negative control group subjected to UVB radiation and receiving a placebo, and two treatment groups exposed to UVB radiation with 5% or 10% moringa leaf extract‐based gel (MO‐5% or MO‐10%), respectively. Results showed that MO‐5% and MO‐10% significantly reduced MMP‐3 gene expression and increased collagen density compared to the negative control group (p < 0.05). Moringa oleifera leaf extract ameliorates collagen degradation by inhibiting MMP‐3 expression in UVB‐induced rats, suggesting its potential as a pharmacological and cosmetic agent for UVB‐induced skin damage.