Wound Healing of Quinic Acid in Human Dermal Fibroblasts by Regulating Expression of FN1 and COL1A1 Gene

Yıl 2022, Cilt: 11 Sayı: 4, 63 - 69, 28.12.2022

Sıdıka Genç , Yeşim Yeni , Betül Çiçek , Ahmet Hacımüftüoğlu

https://doi.org/10.46810/tdfd.1186878

Cited By: 5

Öz

Quinic acid (QA) is an alicyclic organic acid widely found in plants. It accumulates in varying concentrations of plant species and is actively metabolized throughout the plant's life cycle. Wound healing after skin injury involves a complex interaction of many cells, fibroblasts, endothelial cells, and regenerated immune cells and their interrelating extracellular matrix. In our study, the healing effect of QA on scar tissue was studied. For this aim, oxidative stress, and changes in FN1 and Collogen1α gene levels were examined. For this purpose, fibroblast cells were seeded in 24, 96 and well plates for wound healing, MTT analysis and Real-Time PCR testing (respectively). Wells were drawn with a 100 µL pipette tip for wound line. As a conclusion of our study, it was determined that cell viability increased significantly, especially in the QA 20 µg-ml group at the end of 48 hours. Increased cell viability and antioxidant capacity resulted in increased cell proliferation. Both FN1 and COL1A1 gene expression levels were up regulated in the QA groups compared to the control group. Our findings show for the first time that quinic acid promotes migration and/or proliferation of fibroblasts by regulating oxidative stress and the FN1A and COL1A1 genes. This activity may be related to the production of FN1A and COL1A1, which are considered important targets for modulation of the tissue repair process.

Anahtar Kelimeler

FN1A, COL1A1, 8OHdG

Destekleyen Kurum

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Proje Numarası

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Teşekkür

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Wound Healing of Quinic Acid in Human Dermal Fibroblasts by Regulating Expression of FN1 and COL1A1 Gene

Öz

Quinic acid (QA) is an alicyclic organic acid widely found in plants. It accumulates in varying concentrations of plant species and is actively metabolized throughout the plant's life cycle. Wound healing after skin injury involves a complex interaction of many cells, fibroblasts, endothelial cells, and regenerated immune cells and their interrelating extracellular matrix. In our study, the healing effect of QA on scar tissue was studied. For this aim, oxidative stress, and changes in FN1 and Collogen1α gene levels were examined. For this purpose, fibroblast cells were seeded in 24, 96 and well plates for wound healing, MTT analysis and Real-Time PCR testing (respectively). Wells were drawn with a 100 µL pipette tip for wound line. As a conclusion of our study, it was determined that cell viability increased significantly, especially in the QA 20 µg-ml group at the end of 48 hours. Increased cell viability and antioxidant capacity resulted in increased cell proliferation. Both FN1 and COL1A1 gene expression levels were up regulated in the QA groups compared to the control group. Our findings show for the first time that quinic acid promotes migration and/or proliferation of fibroblasts by regulating oxidative stress and the FN1A and COL1A1 genes. This activity may be related to the production of FN1A and COL1A1, which are considered important targets for modulation of the tissue repair process.

Anahtar Kelimeler

FN1A, COL1A1, 8OHdG

Proje Numarası

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Kaynakça

• Referans1 Guo S, Dipietro LA. Factors affecting wound healing. J Dent Res, 2010. 89(3): 219-29.
• Referans2 Xue M, Jackson CJ. Extracellular Matrix Reorganization During Wound Healing and Its Impact on Abnormal Scarring. Adv Wound Care (New Rochelle), 2015. 4(3):119-136.
• Referans3 Broughton G, Janis JE, Attinger CE. Wound healing: an overview. Plast Reconstr Surg, 2006. 117(7):1e-S-32e-S.
• Referans4 Gonzalez AC, Costa TF, Andrade ZA, Ribeiro A, Medrado 5T096YREPOL….AP. Wound healing - A literature review. An Bras Dermatol, 2016. 91(5):614-620.
• Referans5 Midwood KS, Williams LV, Schwarzbauer JE. Tissue repair and the dynamics of the extracellular matrix. Int J Biochem Cell Biol, 2004. 36(6):1031-7.
• Referans6 Li J, Chen J, Kirsner R. Pathophysiology of acute wound healing. Clinics in Dermatology, 2007. 25(1):9-18.
• Referans7 Falanga V. The chronic wound: impaired healing and solutions in the context of wound bed preparation. Blood Cells Mol Dis, 2004. 32(1):88-94.
• Referans8 Trengove NJ, Stacey MC, MacAuley S, Bennett N, Gibson J, Burslem F, et al. Analysis of the acute and chronic wound environments: the role of proteases and their inhibitors. Wound Repair Regen, 1999. 7(6):442-52.
• Referans9 Alam U, Nelson AJ, Cuthbertson DJ, Malik AR. An update on vitamin D and B deficiency in the pathogenesis and treatment of diabetic neuropathy: a narrative review. Future Neurology, 2018. 13(3):135-142.
• Referans10 Rodriguez PG, Felix FN, Woodley DT, Shim EK. The role of oxygen in wound healing: a review of the literature. Dermatol Surg, 2008. 34(9):1159-69.
• Referans11 Deng L. Du C, Song P, Chen T, Rui S, Armstrong DG, et al. The Role of Oxidative Stress and Antioxidants in Diabetic Wound Healing. Oxid Med Cell Longev, 2021. 2021:8852759.
• Referans12 Pankov R. and Yamada KM. Fibronectin at a glance. J Cell Sci, 2002. 115(20):3861-3.
• Referans13 Grinnell F. Fibronectin and wound healing. J Cell Biochem, 1984. 26(2):107-16.
• Referans14 Marzotto M, Bonafini C, Olioso D, Baruzzi A, Bettinetti L, Leva FD, et al. Arnica montana Stimulates Extracellular Matrix Gene Expression in a Macrophage Cell Line Differentiated to Wound-Healing Phenotype. PLoS One, 2016. 11(11):e0166340.
• Referans15 Tarachiwin L, Ute K, Kobayashi A, Fukusaki E. 1H NMR based metabolic profiling in the evaluation of Japanese green tea quality. J Agric Food Chem, 2007. 55(23):9330-6.
• Referans16 Wei F, Furihata K, Hu F, Miyakawa T, Tanokura M. Complex mixture analysis of organic compounds in green coffee bean extract by two-dimensional NMR spectroscopy. Magn Reson Chem, 2010. 48(11):857-65.
• Referans17 Naranjo Pinta, M, Pinta MN, Montoliu I, Aura AM, Seppänen-Laakso T, Barron D, Moco S. In Vitro Gut Metabolism of [U-(13) C]-Quinic Acid, The Other Hydrolysis Product of Chlorogenic Acid. Mol Nutr Food Res, 2018. 62(22):e1800396.
• Referans18 Liang N, Kitts DD. Role of Chlorogenic Acids in Controlling Oxidative and Inflammatory Stress Conditions. Nutrients, 2015. 8(1).
• Referans19 Jiang Y, Kusama K, Satoh K, Takayama E, Watanabe S, Sakagami H. Induction of cytotoxicity by chlorogenic acid in human oral tumor cell lines. Phytomedicine, 2000. 7(6): p. 483-491.
• Referans20 Altinoz MA. Altinoz MA, Yilmaz A, Taghizadehghalehjoughi A, Genc S, Yeni Y, et al. Ulipristal-temozolomide-hydroxyurea combination for glioblastoma: in-vitro studies. J Neurosurg Sci, 2022.22:1-14
• Referans21 Yeni Y, Cakir Z, Hacimuftuoglu A, Taghizadehghalehjoughi A, Okkay U, Genc S. A Selective Histamine H4 Receptor Antagonist, JNJ7777120, Role on glutamate Transporter Activity in Chronic Depression. J Pers Med, 2022. 12(2).
• Referans22 Janis JE, Harrison B. Wound Healing: Part I. Basic Science. Plast Reconstr Surg, 2016. 138(3): 9-17.
• Referans23 Sen CK, Roy S. Redox signals in wound healing. Biochim Biophys Acta, 2008. 1780(11):1348-61.
• Referans24 Fitzmaurice SD, Sivamani RK, Isseroff RR. Antioxidant therapies for wound healing: a clinical guide to currently commercially available products. Skin Pharmacol Physiol, 2011. 24(3):13-26.
• Referans25 Kunkemoeller B, Kyriakides TR. Redox Signaling in Diabetic Wound Healing Regulates Extracellular Matrix Deposition. Antioxid Redox Signal, 2017. 27(12): p. 823-838.
• Referans26 Fayet, C, Bendeck MP, Gotlieb AI. Cardiac valve interstitial cells secrete fibronectin and form fibrillar adhesions in response to injury. Cardiovasc Pathol, 2007. 16(4): p. 203-11. Referans27 Lenselink EA. Role of fibronectin in normal wound healing. Int Wound J, 2015. 12(3):313-6.
• Referans28 Shi F, Sottile J. MT1-MMP regulates the turnover and endocytosis of extracellular matrix fibronectin. J Cell Sci, 2011. 124(23): 4039-50.