2020
DOI: 10.1007/s00011-020-01426-x
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Burn injury induces elevated inflammatory traffic: the role of NF-κB

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Cited by 22 publications
(12 citation statements)
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“…The transcription factor NF-κB and the multifunctional cytokine TNF-α are potent inflammatory mediators that actively play predominant roles in cellular events such as cell survival, proliferation, differentiation, and death 61 . Researchers have well-established quercetin as a model medication for improving wound healing 53 , 56 , and the current study highlights the beneficial effects of the quercetin-supplemented GbH in the recovery of second-degree burn wounds in rat models.…”
Section: Resultsmentioning
confidence: 99%
“…The transcription factor NF-κB and the multifunctional cytokine TNF-α are potent inflammatory mediators that actively play predominant roles in cellular events such as cell survival, proliferation, differentiation, and death 61 . Researchers have well-established quercetin as a model medication for improving wound healing 53 , 56 , and the current study highlights the beneficial effects of the quercetin-supplemented GbH in the recovery of second-degree burn wounds in rat models.…”
Section: Resultsmentioning
confidence: 99%
“…20 It can reflect the inflammatory response in the body and is an important indicator of inflammatory infection and poor prognosis. 20 The study by George 21 pointed out that the levels of inflammatory The growth of granulation tissue at the wound surface indicates that the wound is repairing itself, and the granulation tissue can fill the defect tissue, help the wound to shrink, and improve the anti-infection ability of the wound. 24 However, the growth of granulation tissue is closely related to the oxygen environment of the wound tissue.…”
Section: Discussionmentioning
confidence: 99%
“…The results of Gene Ontology analysis showed that DEGs after burn were related to immune system function, metabolic process, and cellular biological regulation. The results of KEGG pathway enrichment analysis showed that DEGs after burn were mainly located in the Toll-like receptor [ 22 ], p53 [ 23 ], PD-1/PD-L1 [ 24 ], and NF- κ B [ 25 ]. Toll-like receptor signaling pathway can activate bacterial membrane components and promote the activation of MAPK signaling pathway, which in turn triggers the body's inherent immune response and increases the production of proinflammatory factors [ 26 ].…”
Section: Discussionmentioning
confidence: 99%