Zhong Chi, Wang Guangyi, Zhou Jianda, Liu Yang, Li Zhelin, Zhang Jianfei, Shi Ke, Li Peiting, Qiu Xiaohui, Wu Xianrui, Chen Shuyue, Li Fuying, Zhao Zitong, Liang Geao, Xu Hui, Xu Dan
The Third Xiangya Hospital of Central South University No. 138, Tongzipo Road, Yuelu District, Changsha 410013, Hunan, China.
Burn Institute of PLA, Department of Burn Surgery, The First Affiliated Hospital of Naval Medical University, Research Unit of Key Techniques for Treatment of Burns and Combined Burns and Trauma Injury, Chinese Academy of Medical Sciences Shanghai 200433, China.
Int J Burns Trauma. 2025 Apr 25;15(2):64-76. doi: 10.62347/IQTK3162. eCollection 2025.
Sodium hydroxide (NaOH) is known to cause severe injuries through lipid saponification; however, the mechanisms underlying NaOH-induced skin injuries, particularly their effects on lipid metabolism and ferroptosis, are unclear. Here, we aimed to elucidate these mechanisms based on lipid profile evaluations and ferroptosis occurrence.
We used experimental rat models of NaOH-induced skin burns (skin exposed to 0.05% NaOH for 90 or 180 s) alongside a sham-treated control group. Skin morphology and integrity were assessed. Differentially expressed lipid profiles were monitored via untargeted lipidomics. Oxidative stress, lipid peroxidation, and iron metabolism were also assessed. The expression of ferroptosis-associated genes, including acyl-CoA synthetase long-chain family member 4 (), lysophosphatidylcholine acyltransferase 3 (), and glutathione peroxidase 4 (), was analysed using immunohistochemical and quantitative reverse transcription-polymerase chain reaction analyses.
NaOH exposure for 90 and 180 s caused second- and third-degree burns, respectively, leading to elevated and reduced levels of polyunsaturated and monosaturated fatty acid phospholipids, respectively. Both groups showed significant increases in reactive oxygen species, ferrous iron, and malondialdehyde levels and significant decreases in glutathione levels. and expression increased, and expression decreased.
NaOH-induced skin burns disrupt skin appendages, resulting in lipid metabolism alterations and ferroptosis induction. These findings could provide valuable insights for elucidating the precise mechanisms underlying ferroptosis in the context of NaOH burns and for identifying potential therapeutic strategies.
已知氢氧化钠（NaOH）通过脂质皂化作用会导致严重损伤；然而，NaOH诱导皮肤损伤的潜在机制，尤其是其对脂质代谢和铁死亡的影响尚不清楚。在此，我们旨在基于脂质谱评估和铁死亡的发生情况来阐明这些机制。
我们使用了NaOH诱导皮肤烧伤的实验大鼠模型（皮肤暴露于0.05% NaOH 90秒或180秒）以及假处理对照组。评估了皮肤形态和完整性。通过非靶向脂质组学监测差异表达的脂质谱。还评估了氧化应激、脂质过氧化和铁代谢。使用免疫组织化学和定量逆转录 - 聚合酶链反应分析来分析铁死亡相关基因的表达，包括酰基辅酶A合成酶长链家族成员4（）、溶血磷脂酰胆碱酰基转移酶3（）和谷胱甘肽过氧化物酶4（）。
暴露于NaOH 90秒和180秒分别导致二度和三度烧伤，分别导致多不饱和脂肪酸磷脂水平升高和单不饱和脂肪酸磷脂水平降低。两组的活性氧、亚铁和丙二醛水平均显著升高，谷胱甘肽水平显著降低。 和 表达增加， 表达降低。
NaOH诱导的皮肤烧伤破坏皮肤附属器，导致脂质代谢改变和铁死亡诱导。这些发现可为阐明NaOH烧伤背景下铁死亡的确切机制以及确定潜在治疗策略提供有价值的见解。
