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Epigallocatechin Gallate Prevents Burn Wound Progression Through Inhibiting Mitochondrial DNA-Induced Inflammation

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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.

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References

  1. 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

    Article  Google Scholar 

  2. 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

    Article  Google Scholar 

  3. 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

    Article  Google Scholar 

  4. West AP, Shadel GS (2017) Mitochondrial DNA in innate immune responses and inflammatory pathology. Nat Rev Immunol 17:363–375

    Article  CAS  Google Scholar 

  5. Stanojcic M, Abdullahi A, Rehou S, Parousis A, Jeschke MG (2018) Pathophysiological response to burn injury in adults. Ann Surg 267:576–584

    Article  Google Scholar 

  6. 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

    Article  Google Scholar 

  7. 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

    Article  CAS  Google Scholar 

  8. 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

    Article  CAS  Google Scholar 

  9. 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

    Article  CAS  Google Scholar 

  10. 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

    Article  Google Scholar 

  11. 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

    Article  CAS  Google Scholar 

  12. 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

    Article  Google Scholar 

  13. 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

    Article  CAS  Google Scholar 

  14. 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

    Article  Google Scholar 

  15. 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

    Article  CAS  Google Scholar 

  16. 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

    Article  Google Scholar 

  17. 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

    Article  CAS  Google Scholar 

  18. 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

    Article  Google Scholar 

  19. 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

    PubMed  PubMed Central  Google Scholar 

  20. 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

    Article  CAS  Google Scholar 

  21. 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

    Article  Google Scholar 

  22. 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

  23. 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

    Article  CAS  Google Scholar 

  24. 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

    Article  Google Scholar 

  25. 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

    Article  Google Scholar 

  26. 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

  27. 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

  28. 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

    Article  Google Scholar 

  29. 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

    Article  CAS  Google Scholar 

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Correspondence to Mengjing Xiao.

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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

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  • DOI: https://doi.org/10.1007/s12262-021-03101-9

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