Abstract
This study aims to investigate the effect of epigallocatechin gallate on experimental burn wound progression. A deep second-degree burn was produced on male Wistar rats. Epigallocatechin gallate was systemically administrated as treatment intervention. The mitochondrial DNA level in serum and the level of proinflammatory cytokines in burn wounds were detected. The malonaldehyde content, the myeloperoxidase activity, and the nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 inflammasome level in the burn wounds were measured. The histopathological examination of burn wounds was performed, and the time to wound reepithelialization was recorded. Burn resulted in remarkably higher level of mitochondrial DNA release in serum and proinflammatory cytokines in burn wounds. Moreover, the malonaldehyde content, myeloperoxidase activity, and nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 inflammasome level in burn wounds were significantly higher than that of sham burn. Epigallocatechin gallate treatment significantly reduced mitochondrial DNA level in serum and inflammatory response in burn wounds. Furthermore, the burn wound depth of rats in epigallocatechin gallate group was markedly attenuated, and the wound reepithelialization time was accelerated. Epigallocatechin gallate ameliorated burn wound progression probably through inhibiting the mitochondrial DNA-induced inflammation and protecting wounds from inflammatory infiltration and oxidative damage.
Similar content being viewed by others
References
Salibian AA, Rosario ATD, Severo LAM, Nguyen L, Banyard DA, Toranto JD, Evans GRD, Widgerow AD (2016) Current concepts on burn wound conversion-a review of recent advances in understanding the secondary progressions of burns. Burns 42:1025–1035
Shupp JW, Nasabzadeh TJ, Rosenthal DS, Jordan MH, Fidler P, Jeng JC (2010) A review of the local pathophysiologic bases of burn wound progression. J Burn Care Res 31:849–873
Sadeghipour H, Torabi R, Gottschall J, Lujan-Hernandez J, Sachs DH, Moore FD Jr, Cetrulo CL Jr (2017) Blockade of IgM-mediated inflammation alters wound progression in a swine model of partial-thickness burn. J Burn Care Res 38:148–160
West AP, Shadel GS (2017) Mitochondrial DNA in innate immune responses and inflammatory pathology. Nat Rev Immunol 17:363–375
Stanojcic M, Abdullahi A, Rehou S, Parousis A, Jeschke MG (2018) Pathophysiological response to burn injury in adults. Ann Surg 267:576–584
Liu R, Xu F, Bi S, Zhao X, Jia B, Cen Y (2019) Mitochondrial DNA-induced inflammatory responses and lung injury in thermal injury murine model: protective effect of cyclosporine-A. J Burn Care Res 40:355–360
Carter DW, Prudovsky I, Kacer D, Soul T, Kumpel C, Pyburn K, Palmeri M, Kramer R, Rappold J (2019) Tranexamic acid suppresses the release of mitochondrial DAMPs and reduces lung inflammation in a murine burn model. J Trauma Acute Care Surg 86:617–624
Xiao J, Ho CT, Liong EC, Nanji AA, Leung TM, Lau TY, Fung ML, Tipoe GL (2014) Epigallocatechin gallate attenuates fibrosis, oxidative stress, and inflammation in non-alcoholic fatty liver disease rat model through TGF/SMAD, PI3 K/Akt/FoxO1, and NF-kappa B pathways. Eur J Nutr 53:187–199
Huang YW, Zhu QQ, Yang XY, Xu HH, Sun B, Wang XJ, Sheng J (2019) Wound healing can be improved by (-)-epigallocatechin gallate through targeting Notch in streptozotocin-induced diabetic mice. FASEB J 33:953–964
Lin YH, Lin JH, Li TS, Wang SH, Yao CH, Chung WY, Ko TH (2016) Dressing with epigallocatechin gallate nanoparticles for wound regeneration. Wound Repair Regen 24:287–301
Qin CY, Gu J, Fan JX, Zhang HW, Xu F, Liang HM, Fan KJ, Xiao ZH, Zhang EY, Hu J (2018) Epigallocatechin gallate attenuates mitochondrial DNA-induced inflammatory damage in the development of ventilator-induced lung injury. Phytomedicine 48:120–128
Liu R, Xu F, Si S, Zhao X, Bi S, Cen Y (2017) Mitochondrial DNA-induced inflammatory responses and lung injury in thermal injury rat model: protective effect of epigallocatechin gallate. J Burn Care Res 38:304–311
Li M, Xu J, Shi T, Yu H, Bi J, Chen G (2016) Epigallocatechin-3-gallate augments therapeutic effects of mesenchymal stem cells in skin wound healing. Clin Exp Pharmacol Physiol 43:1115–1124
Kim HL, Lee JH, Kwon BJ, Lee MH, Han DW, Hyon SH, Park JC (2014) Promotion of full-thickness wound healing using epigallocatechin-3-O-gallate/poly (lactic-co-glycolic acid) membrane as temporary wound dressing. Artif Organs 38:411–417
Leu JG, Chen SA, Chen HM, Wu WM, Hung CF, Yao YD, Tu CS, Liang YJ (2012) The effects of gold nanoparticles in wound healing with antioxidant epigallocatechin gallate and alpha-lipoic acid. Nanomedicine 8:767–775
Xiao M, Li L, Li C, Zhang P, Hu Q, Ma L, Zhang H (2014) Role of autophagy and apoptosis in wound tissue of deep second-degree burn in rats. Acad Emerg Med 21:383–391
Xiao M, Li L, Li C, Liu L, Yu Y, Ma L (2016) 3,4-Methylenedioxy-beta-nitrostyrene ameliorates experimental burn wound progression by inhibiting the NLRP3 inflammasome activation. Plast Reconstr Surg 137:566e-e575
Yuhua S, Ligen L, Jiake C, Tongzhu S (2012) Effect of poloxamer 188 on deepening of deep second-degree burn wounds in the early stage. Burns 38:95–101
Sun LT, Friedrich E, Heuslein JL, Pferdehirt RE, Dangelo NM, Natesan S, Christy RJ, Washburn NR (2012) Reduction of burn progression with topical delivery of (antitumor necrosis factor-alpha)-hyaluronic acid conjugates. Wound Repair Regen 20:563–572
Zhang Q, Raoof M, Chen Y, Sumi Y, Sursal T, Junger W, Brohi K, Itagaki K, Hauser CJ (2010) Circulating mitochondrial DAMPs cause inflammatory responses to injury. Nature 464:104–107
Rani M, Nicholson SE, Zhang Q, Schwacha MG (2017) Damage-associated molecular patterns (DAMPs) released after burn are associated with inflammation and monocyte activation. Burns 43:297–303
Schwacha MG, Rani M, Nicholson SE, Lewis AM, Holloway TL, Sordo S, Cap AP (2016) Dermal gammadelta T-cells can be activated by mitochondrial damage-associated molecular patterns. PLoS One 11:e0158993
Yao X, Wigginton JG, Maass DL, Ma L, Carlson D, Wolf SE, Minei JP, Zang QS (2014) Estrogen-provided cardiac protection following burn trauma is mediated through a reduction in mitochondria-derived DAMPs. Am J Physiol Heart Circ Physiol 306:H882–H894
Zhang JZ, Wang J, Qu WC, Wang XW, Liu Z, Ren JX, Han L, Sun TS (2017) Plasma mitochondrial DNA levels were independently associated with lung injury in elderly hip fracture patients. Injury 48:454–459
Hu Q, Ren J, Wu J, Li G, Wu X, Liu S, Wang G, Gu G, Li J (2017) Elevated levels of plasma mitochondrial DNA are associated with clinical outcome in intra-abdominal infections caused by severe trauma. Surg Infect (Larchmt) 18:610–618
Szczesny B, Brunyanszki A, Ahmad A, Olah G, Porter C, Toliver-Kinsky T, Sidossis L, Herndon DN, Szabo C (2015) Time-dependent and organ-specific changes in mitochondrial function, mitochondrial DNA integrity, oxidative stress and mononuclear cell infiltration in a mouse model of burn injury. PLoS One 10:e0143730
Lee HE, Yang G, Park YB, Kang HC, Cho YY, Lee HS, Lee JY (2019) Epigallocatechin-3-gallate prevents acute gout by suppressing NLRP3 inflammasome activation and mitochondrial DNA synthesis. Molecules 24
Kim H, Kawazoe T, Han DW, Matsumara K, Suzuki S, Tsutsumi S, Hyon SH (2008) Enhanced wound healing by an epigallocatechin gallate-incorporated collagen sponge in diabetic mice. Wound Repair Regen 16:714–720
Lin SY, Kang L, Chen JC, Wang CZ, Huang HH, Lee MJ, Cheng TL, Chang CF, Lin YS, Chen CH (2019) (-)-Epigallocatechin-3-gallate (EGCG) enhances healing of femoral bone defect. Phytomedicine 55:165–171
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Competing Interests
The authors declare no competing interests.
Additional information
Publisher's Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Rights and permissions
About this article
Cite this article
Zou, X., Xiao, M., Zhang, B. et al. Epigallocatechin Gallate Prevents Burn Wound Progression Through Inhibiting Mitochondrial DNA-Induced Inflammation. Indian J Surg 84, 765–771 (2022). https://doi.org/10.1007/s12262-021-03101-9
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s12262-021-03101-9