Yang Xinyue, Li Jiajia, Liang Feixing, Qu Jinquan, Dong Xiang, Liu Jiangwei
Graduate School of Xinjiang Medical University, Urumqi, 830000, Xinjiang province, China.
Key Laboratory of Special Environmental Medicine of Xinjiang, Urumqi, 830000, Xinjiang Province, China.
Sci Rep. 2025 Apr 28;15(1):14833. doi: 10.1038/s41598-025-93853-1.
We established a swine model of traumatic hemorrhagic shock to assess secondary renal injury under dry-heat conditions to clarify the roles of cell pyroptosis and inflammatory response in traumatic hemorrhagic shock development. Sixty-eight domestic Landrace piglets were divided into normothermic environment, dry-heat sham surgery, and dry-heat environment traumatic hemorrhagic shock groups (four subgroups: 3 h of environmental exposure and 60, 120, and 180 min after inducing traumatic hemorrhagic shock). The kidneys and blood were sampled at various time points. Univariate analysis of variance or non-parametric test was used for intergroup and intragroup comparisons, and the least significant difference test was used for multiple comparisons. The serum lipopolysaccharide, neutrophil gelatinase-associated lipocalin, kidney injury molecule 1, blood urea nitrogen, and creatinine levels, as well as various inflammatory factors, oxidative stress indicators, and Paller score, were significantly higher under dry-heat environment traumatic hemorrhagic shock than under normothermic environment and dry-heat sham surgery at 180 min. The histopathological damage in the dry-heat environment traumatic hemorrhagic shock group increased significantly at 180 min. Immunohistochemistry, western blotting, and terminal deoxynucleotidyl transferase dUTP nick end labeling assays showed that protein expression and apoptosis index values in the renal tissues of all three groups increased but were significantly higher under dry-heat environment traumatic hemorrhagic shock than under normothermic environment and dry-heat sham surgery at 180 min. The combination of dry-heat environment and traumatic hemorrhagic shock induces an aggravation of secondary renal injury, which may be related to cell pyroptosis, inflammatory response, apoptosis, and oxidative stress. Our findings may assist in the development of treatments for acute kidney injury.
我们建立了创伤性失血性休克猪模型,以评估干热条件下的继发性肾损伤,从而阐明细胞焦亡和炎症反应在创伤性失血性休克发展中的作用。68只国内长白仔猪被分为常温环境组、干热假手术组和干热环境创伤性失血性休克组(四个亚组:环境暴露3小时以及诱导创伤性失血性休克后60、120和180分钟)。在不同时间点采集肾脏和血液样本。采用单因素方差分析或非参数检验进行组间和组内比较,并使用最小显著差异检验进行多重比较。在180分钟时,干热环境创伤性失血性休克组的血清脂多糖、中性粒细胞明胶酶相关脂质运载蛋白、肾损伤分子1、血尿素氮和肌酐水平,以及各种炎症因子、氧化应激指标和帕勒评分,均显著高于常温环境组和干热假手术组。在180分钟时,干热环境创伤性失血性休克组的组织病理学损伤显著增加。免疫组织化学、蛋白质印迹法和末端脱氧核苷酸转移酶介导的dUTP缺口末端标记检测显示,三组肾组织中的蛋白表达和凋亡指数值均升高,但在180分钟时,干热环境创伤性失血性休克组显著高于常温环境组和干热假手术组。干热环境与创伤性失血性休克相结合会导致继发性肾损伤加重,这可能与细胞焦亡、炎症反应、凋亡和氧化应激有关。我们的研究结果可能有助于急性肾损伤治疗方法的开发。