Schiavoni Larissa Cristina, Baptista Vivianne Izabelle de Araújo, Quintana Hananiah Tardivo, Lazzarin Mariana Cruz, de Oliveira Flavia
Departamento de Biociências, Universidade Federal de São Paulo (UNIFESP) Santos, SP, Brazil.
Escola Multicampi de Ciências Médicas do Rio Grande do Norte, Universidade Federal do Rio Grande do Norte (UFRN) Caicó, RN, Brazil.
Int J Burns Trauma. 2025 Jun 15;15(3):115-124. doi: 10.62347/ANQA2365. eCollection 2025.
Burn injury (BI) represents a major epidemiologic problem worldwide, mostly in children. BIs greater than 40% of the total body surface, are considered severe, and entail a hepatic hypermetabolic response, which is associated with proteins depletions and prolonged hypermetabolism.
This study aims to evaluated the effects of short- and long-term insulin treatment on liver morphology and the use of a biomarker related to oxidative damage to DNA (8-OHdG) to better understand the anabolic action of this hormone in the liver.
Wistar rats aged 21 d were distributed into four groups: control (C), control with insulin (C+I), scald burn injury (SBI), and SBI with insulin (SBI+I). The SBI groups were subjected to a burn 45% total body surface area. The C+I and SBI+I groups received insulin (5 UI/Kg/d) for 4- or 14 d. The livers were analyzed for morphometric, histopathological, and immunohistochemical for 8-OHdG.
The main results showed that, in a short time, insulin increases the density of binucleated hepatocytes as an organ response to burn injury. In the long term, insulin increased the area of hepatocytes in the SBI+I group in relation to SBI, highlighting the similar values between the SBI+I and the control groups. Regarding sinusoidal cells, insulin was able to modulate this liver proliferative reaction. Insulin reduces 8-OHdG immunoexpression in short and long-term post-burn moments.
The insulin modulation of 8-OHdG makes us infer that a study about the control of 8-OHdG as a potential biomarker in patients could be an efficient precursor of the level of oxidative stress associated with hepatic dysfunction associated to extensive burn injury.
烧伤是全球主要的流行病学问题，在儿童中尤为常见。超过全身表面积40%的烧伤被认为是严重烧伤，会引发肝脏的高代谢反应，这与蛋白质消耗和长期的高代谢状态相关。
本研究旨在评估短期和长期胰岛素治疗对肝脏形态的影响，以及与DNA氧化损伤相关的生物标志物（8-羟基脱氧鸟苷，8-OHdG）的作用，以更好地理解该激素在肝脏中的合成代谢作用。
将21日龄的Wistar大鼠分为四组：对照组（C）、胰岛素对照组（C+I）、烫伤组（SBI）和胰岛素烫伤组（SBI+I）。SBI组大鼠接受45%体表面积的烧伤。C+I组和SBI+I组大鼠接受胰岛素（5 UI/Kg/d）治疗4天或14天。对肝脏进行形态计量学、组织病理学分析以及8-OHdG的免疫组织化学分析。
主要结果显示，短期内，胰岛素可增加双核肝细胞的密度，这是机体对烧伤损伤的一种反应。长期来看，与SBI组相比，SBI+I组胰岛素增加了肝细胞面积，突出了SBI+I组与对照组之间的相似数值。关于肝血窦细胞，胰岛素能够调节这种肝脏增殖反应。胰岛素在烧伤后的短期和长期均能降低8-OHdG的免疫表达。
胰岛素对8-OHdG的调节作用使我们推断，将8-OHdG作为潜在生物标志物在患者中进行控制的研究，可能是与大面积烧伤相关的肝功能障碍所伴随的氧化应激水平的有效预测指标。
