Rubya Pereira Zaccaron, Laura de Roch Casagrande, Ligia Milanez Venturini, João Vitor Silvano Bittencourt, Camila da Costa, Ellen de Pieri, Anand Thirupathi, Gislaine Tezza Rezin, Ricardo Andrez Machado-de-Ávila, Paulo Cesar Lock Silveira
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This study aimed to investigate the effect of an IL-1β inhibitor molecule associated with PBM irradiation in a model of epithelial injury in diabetic mice. After the induction of the DM model with streptozotocin (STZ), the skin lesion model was implemented through surgical excision. Sixty C57BL/6 mice divided into five experimental groups (n = 12) were used: excisional wound (EW), DM + EW, DM + EW + DAP 1-2 (inhibitor peptide), DM + EW + PBM, and DM + EW + PBM + DAP 1-2. Treatment started 12 h after wound induction and was performed daily for 5 days. Twenty-four hours after the last application, the animals were euthanized and the outer edge of the wound was removed. The results obtained demonstrate that the DM + EW + PBM + DAP 1-2 group caused a reduction in the levels of pro-inflammatory cytokines, an increase in anti-inflammatory cytokines, and an increase in TGF-β and maintenance of the cellular redox state with a consequent reduction in levels of inflammatory infiltrate and concomitant stimulation of type III collagen gene expression, as well as a decrease in the size of the wound in square centimeter 6 days after the injury. Only the combination of therapies was able to favor the process of tissue regeneration due to the development of an approach capable of acting at different stages of the regenerative process, through the mechanisms of action of interventions on the inflammatory process by avoiding its stagnation and stimulating progression of regeneration.</p>","PeriodicalId":13524,"journal":{"name":"Inflammation","volume":null,"pages":null},"PeriodicalIF":4.5000,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"IL-1β Antagonist Receptor Peptide Associated with Photobiomodulation Accelerates Diabetic Wound Tissue Repair.\",\"authors\":\"Rubya Pereira Zaccaron, Laura de Roch Casagrande, Ligia Milanez Venturini, João Vitor Silvano Bittencourt, Camila da Costa, Ellen de Pieri, Anand Thirupathi, Gislaine Tezza Rezin, Ricardo Andrez Machado-de-Ávila, Paulo Cesar Lock Silveira\",\"doi\":\"10.1007/s10753-024-01974-y\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Chronic hyperglycemia caused by diabetes mellitus (DM) slows down the healing process due to prolonged inflammation which impedes the regeneration progression. 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引用次数: 0
摘要
糖尿病(DM)引起的慢性高血糖会导致炎症长期存在,阻碍再生进程,从而减缓愈合过程。光生物调节(PBM)被认为是一种非药物干预措施,具有抗炎和生物刺激作用,可加速愈合过程。目前发现的 IL-1β 抑制剂因其细胞毒性、用量过多和侵入性用药而难以使用,因此,在糖尿病伤口中应用这种肽是一种很有前景的干预措施,有助于解决炎症反应。本研究的目的是在糖尿病小鼠上皮损伤模型中研究与 PBM 照射相关的 IL-1β 抑制剂分子的效果。在用链脲佐菌素(STZ)诱导糖尿病小鼠模型后,通过手术切除实施皮肤损伤模型。60 只 C57BL/6 小鼠分为五个实验组(n = 12):切除伤口组(EW)、DM + EW 组、DM + EW + DAP 1-2 组(抑制肽)、DM + EW + PBM 组和 DM + EW + PBM + DAP 1-2 组。伤口诱导后 12 小时开始治疗,每天治疗一次,连续 5 天。最后一次施药 24 小时后,动物被安乐死,伤口外缘被切除。结果表明,DM + EW + PBM + DAP 1-2 组降低了促炎细胞因子的水平,增加了抗炎细胞因子,增加了 TGF-β,维持了细胞氧化还原状态,从而降低了炎症浸润的水平,同时刺激了 III 型胶原蛋白基因的表达,并在受伤 6 天后缩小了伤口的平方厘米。由于开发了一种能够在再生过程的不同阶段发挥作用的方法,通过对炎症过程进行干预的作用机制,避免炎症过程停滞并促进再生,因此只有综合疗法能够促进组织再生过程。
Chronic hyperglycemia caused by diabetes mellitus (DM) slows down the healing process due to prolonged inflammation which impedes the regeneration progression. Photobiomodulation (PBM) is considered a non-pharmacological intervention and has anti-inflammatory and biostimulatory effects that accelerate the healing process. Currently found IL-1β inhibitors are difficult to implement due to their cytotoxic potential, excessive amounts, and invasive administration, and therefore, the application of this peptide in diabetic wounds represents a promising intervention to help resolve the inflammatory response. This study aimed to investigate the effect of an IL-1β inhibitor molecule associated with PBM irradiation in a model of epithelial injury in diabetic mice. After the induction of the DM model with streptozotocin (STZ), the skin lesion model was implemented through surgical excision. Sixty C57BL/6 mice divided into five experimental groups (n = 12) were used: excisional wound (EW), DM + EW, DM + EW + DAP 1-2 (inhibitor peptide), DM + EW + PBM, and DM + EW + PBM + DAP 1-2. Treatment started 12 h after wound induction and was performed daily for 5 days. Twenty-four hours after the last application, the animals were euthanized and the outer edge of the wound was removed. The results obtained demonstrate that the DM + EW + PBM + DAP 1-2 group caused a reduction in the levels of pro-inflammatory cytokines, an increase in anti-inflammatory cytokines, and an increase in TGF-β and maintenance of the cellular redox state with a consequent reduction in levels of inflammatory infiltrate and concomitant stimulation of type III collagen gene expression, as well as a decrease in the size of the wound in square centimeter 6 days after the injury. Only the combination of therapies was able to favor the process of tissue regeneration due to the development of an approach capable of acting at different stages of the regenerative process, through the mechanisms of action of interventions on the inflammatory process by avoiding its stagnation and stimulating progression of regeneration.
期刊介绍:
Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.