Decoding the role of tannic acid in wound healing: a dual‐action mechanism linking IL‐1β modulation and FGF‐driven tissue repair

Swastini, Dewa Ayu; Nugroho, Agung Endro; Martien, Ronny; Fachiroh, Jajah; Khafi, Muhammad; Putra, Komang Dian Aditya

doi:10.22146/ijbiotech.113925

Akses terbuka Jurnal SINTA 1

Decoding the role of tannic acid in wound healing: a dual‐action mechanism linking IL‐1β modulation and FGF‐driven tissue repair

Indonesian Journal of Biotechnology · Vol. 31 No. 1 (2026) · hlm. 9–17

DOI: 10.22146/ijbiotech.113925
ISSN: 2089-2241, 0853-8654
Terbit: 2026-03-31
Penerbit: Universitas Gadjah Mada
Bahasa: eng
Lisensi: creativecommons.org/licenses/by-sa/4.0

Abstrak

Tannic acid (TA) has been shown in a previous study to expedite cutaneous wound healing in rats; however, the precise mechanism by which it operates remains poorly understood. This research evaluates the effects of TA on wound healing using both in vitro and in silico methods. In vitro, its influence on the inflammatory cytokine interleukin‐1β (IL‐1β) and the growth factor fibroblast growth factor (FGF) throughout the healing process were assessed. In silico molecular docking was employed to predict direct ligand–protein interactions and to provide a mechanistic insight into whether these proteins represent primary molecular targets or downstream effects. Parameters evaluated included cell viability and proliferation, scratch assays, and the activity of pro‐inflammatory cytokines in the lipopolysaccharide (LPS)‐stimulated RAW 264.7 macrophage cell line, together with growth factors in the NIH 3T3 fibroblast cell line; all were evaluated using enzyme‐linked immunosorbent assay (ELISA). The results indicate that TA significantly facilitates wound closure by promoting NIH 3T3 fibroblast cell proliferation, enhancing FGF expression, and suppressing IL‐1ß synthesis in both in vitro and in silico approaches. These findings suggest that TA may hold considerable promise for wound‐healing management.

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Muhammadiyah University of Yogyakarta
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Rekan penulis	Organisasi	Artikel bersama
S. Sardjiman	Afiliasi tidak diketahui	1
Kazutaka Maeyama	Afiliasi tidak diketahui	1
S. Sismindari	Afiliasi tidak diketahui	1
Anggun Feranisa	Afiliasi tidak diketahui	1
Dewa Ayu Arimurni	Afiliasi tidak diketahui	1
Hilda Ismail	Afiliasi tidak diketahui	1
Anggi Laksmita Dewi	Afiliasi tidak diketahui	1
Dewi Kartikawati Paramita	Afiliasi tidak diketahui	1
Novia Tri Astuti	Afiliasi tidak diketahui	1
Suwijiyo Pramono	Afiliasi tidak diketahui	1
Putri Rachma Novitasari	Afiliasi tidak diketahui	1
Raymond Tjandrawinata	Afiliasi tidak diketahui	1
Edy Meiyanto	Afiliasi tidak diketahui	1
Anindyajati Anindyajati	Afiliasi tidak diketahui	1
Ika Nurzijah	Afiliasi tidak diketahui	1
Dita Brenna Septhea	Afiliasi tidak diketahui	1
Andita Pra Darma	Afiliasi tidak diketahui	1
Sugeng Riyanto	Muhammadiyah University of Yogyakarta	1
Puguh Noviarsito	Afiliasi tidak diketahui	1
Endang Lukitaningsih	Afiliasi tidak diketahui	1
Annik Megawati	Afiliasi tidak diketahui	1
Arief Nurrochmad	Afiliasi tidak diketahui	1
Prajona Marbun	Afiliasi tidak diketahui	1

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Sumber metadata: OAI-PMH (metadata jurnal) https://jurnal.ugm.ac.id/ijbiotech/oai, pertama di-harvest 8 Nov 2026, terakhir terlihat 8 Nov 2026.

Metadata asli (oai_dc)

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	<dc:title xml:lang="en-US">Decoding the role of tannic acid in wound healing: a dual‐action mechanism linking IL‐1β modulation and FGF‐driven tissue repair</dc:title>
	<dc:creator>Swastini, Dewa Ayu</dc:creator>
	<dc:creator>Nugroho, Agung Endro</dc:creator>
	<dc:creator>Martien, Ronny</dc:creator>
	<dc:creator>Fachiroh, Jajah</dc:creator>
	<dc:creator>Khafi, Muhammad</dc:creator>
	<dc:creator>Putra, Komang Dian Aditya</dc:creator>
	<dc:subject xml:lang="en-US">Growth factors; Inflammatory cytokines ; Mechanism; Tannic acid; Wound healing</dc:subject>
	<dc:description xml:lang="en-US">Tannic acid (TA) has been shown in a previous study to expedite cutaneous wound healing in rats; however, the precise mechanism by which it operates remains poorly understood. This research evaluates the effects of TA on wound healing using both in vitro and in silico methods. In vitro, its influence on the inflammatory cytokine interleukin‐1β (IL‐1β) and the growth factor fibroblast growth factor (FGF) throughout the healing process were assessed. In silico molecular docking was employed to predict direct ligand–protein interactions and to provide a mechanistic insight into whether these proteins represent primary molecular targets or downstream effects. Parameters evaluated included cell viability and proliferation, scratch assays, and the activity of pro‐inflammatory cytokines in the lipopolysaccharide (LPS)‐stimulated RAW 264.7 macrophage cell line, together with growth factors in the NIH 3T3 fibroblast cell line; all were evaluated using enzyme‐linked immunosorbent assay (ELISA). The results indicate that TA significantly facilitates wound closure by promoting NIH 3T3 fibroblast cell proliferation, enhancing FGF expression, and suppressing IL‐1ß synthesis in both in vitro and in silico approaches. These findings suggest that TA may hold considerable promise for wound‐healing management.</dc:description>
	<dc:publisher xml:lang="en-US">Universitas Gadjah Mada</dc:publisher>
	<dc:contributor xml:lang="en-US">Center for Education Financial Services (Puslapdik)</dc:contributor>
	<dc:contributor xml:lang="en-US">Indonesian Endowment Funds for Education Scholarship Program (Beasiswa Pendidikan Indonesia)</dc:contributor>
	<dc:date>2026-03-31</dc:date>
	<dc:type>info:eu-repo/semantics/article</dc:type>
	<dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
	<dc:type xml:lang="en-US">Original Research Articles</dc:type>
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	<dc:format>application/pdf</dc:format>
	<dc:identifier>https://journal.ugm.ac.id/ijbiotech/article/view/113925</dc:identifier>
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	<dc:source xml:lang="en-US">Indonesian Journal of Biotechnology; Vol 31, No 1 (2026); 9-17</dc:source>
	<dc:source>2089-2241</dc:source>
	<dc:source>0853-8654</dc:source>
	<dc:language>eng</dc:language>
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	<dc:rights xml:lang="en-US">Copyright (c) 2026 The Author(s)</dc:rights>
	<dc:rights xml:lang="en-US">http://creativecommons.org/licenses/by-sa/4.0</dc:rights>
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