Ma Jing, Zhang Junhe, Xi Lingling, Qu Junxing, Ma Shuangping, Yao Sanqiao, Liu Jie, Ren Wenjie
The Third Affiliated Hospital of Xinxiang Medical University, No. 83 Hualan Road, Xinxiang, 453003, Henan, China.
Xinxiang Key Laboratory for Tumor Drug Screening and Targeted Therapy, Institutes of Health Central Plains, Xinxiang Medical University, Xinxiang, 453003, Henan, China.
Sci Rep. 2025 Apr 8;15(1):11987. doi: 10.1038/s41598-025-97096-y.
Gas explosion is a recurrent event in coal mining that cause severe spleen damage. This study aimed to investigate the role and mechanism of oxidative stress in gas explosion-induced spleen injury. 120 male Sprague-Dawley (SD) rats were randomly divided into a control group (NC), a gas explosion-induced spleen injury model group (Model), an Nrf2 inhibitor group (Model + ATRA), and an Nrf2 induction group (Model + TBHQ). After explosion, the rats of the inhibitor group and induction group were immediately given intraperitoneal injection of all-trans-retinoicacid (ATRA, 5 mg/kg) or tertiary butylhydro-quinone (TBHQ, 1 mg/kg) once. Then, the rats were anesthetized with blood taken from the abdominal aorta at 24 h, 72 h and 7 days. The results showed that gas explosion reduced the spleen index. The expression of oxidative stress-related genes and proteins Nrf2, HO-1, COX2 and GPX4 were increased significantly (P < 0.05) after gas explosion. Compared with the model group, TBHQ improved the spleen index, and reduced inflammation. Moreover, the expression of inflammatory factor IL-6 and ROS was decreased (P < 0.05), HMOX1 and the expression of oxidative stress-related genes and proteins were increased (P < 0.05), but the opposite results were observed in the inhibitor group. Taken together, we firstly found that TBHQ may regulate the degree of oxidative stress in spleen injury induced by gas explosion through the Nrf2/HO-1 signaling pathway.
瓦斯爆炸是煤矿开采中经常发生的事件，会导致严重的脾脏损伤。本研究旨在探讨氧化应激在瓦斯爆炸所致脾脏损伤中的作用及机制。将120只雄性Sprague-Dawley（SD）大鼠随机分为对照组（NC）、瓦斯爆炸致脾脏损伤模型组（Model）、Nrf2抑制剂组（Model + ATRA）和Nrf2诱导组（Model + TBHQ）。爆炸后，立即对抑制剂组和诱导组大鼠腹腔注射一次全反式维甲酸（ATRA，5 mg/kg）或叔丁基对苯二酚（TBHQ，1 mg/kg）。然后，在24小时、72小时和7天时对大鼠进行麻醉并采集腹主动脉血。结果显示，瓦斯爆炸降低了脾脏指数。瓦斯爆炸后，氧化应激相关基因和蛋白Nrf2、HO-1、COX2和GPX4的表达显著增加（P < 0.05）。与模型组相比，TBHQ改善了脾脏指数，并减轻了炎症。此外，炎症因子IL-6和ROS的表达降低（P < 0.05），HMOX1以及氧化应激相关基因和蛋白的表达增加（P < 0.05），但在抑制剂组中观察到相反的结果。综上所述，我们首次发现TBHQ可能通过Nrf2/HO-1信号通路调节瓦斯爆炸所致脾脏损伤中的氧化应激程度。
