Ma Haoyang, Liu Jiaye, Du Yang, Zhang Shengnan, Cao Weidong, Jia Zhanjun, Gong Wei, Zhang Aihua
Department of Pediatrics, School of Medicine, Southeast University, Nanjing, China.
Department of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing, China.
Front Pharmacol. 2021 Apr 23;12:626166. doi: 10.3389/fphar.2021.626166. eCollection 2021.
Sepsis-associated liver dysfunction remains a challenge in clinical practice with high mortality and limited specific therapies. DY131 is a pharmacological agonist of the orphan receptor estrogen-related receptor (ERR) γ which plays a crucial role in regulating energy generation, oxidative metabolism, cell apoptosis, inflammatory responses, etc. However, its role in acute liver injury is unknown. In this study, we evaluated the effect of DY131 on lipopolysaccharide (LPS)-induced liver injury. Mice were pretreated with DY131 through intraperitoneal injection at a dose of 5 mg/kg/day for 3 days prior to LPS challenge (10 mg/kg). 24 h later, they were anesthetized and sacrificed. Blood and liver tissues were collected for further studies. In a separate experiment, mice were treated with saline (vehicle) or DY131 for 3 days to evaluate the toxicity of DY131. We found that ERRγ was downregulated in the liver tissues from LPS-treated mice. Pretreatment with DY131 ameliorated LPS-induced liver injury as demonstrated by reduced liver enzyme release (ALT, AST, and LDH), improved liver morphological damage, and attenuated oxidative stress, inflammation and apoptosis. Meanwhile, DY131 had no significant side effects on hepatic and renal functions in mice. Finally, transcriptomics analysis revealed that the dysregulated pathways associated with inflammation and metabolism were significantly reversed by DY131 in LPS-treated mice, providing more evidence in favor of the protective effect of DY131 against LPS-induced liver injury. Altogether, these findings highlighted the protective effect of DY131 on LPS-induced hepatotoxicity possibly via suppressing oxidative stress, inflammation, and apoptosis.
脓毒症相关的肝功能障碍在临床实践中仍然是一个挑战,死亡率高且特异性治疗有限。DY131是孤儿受体雌激素相关受体(ERR)γ的一种药理学激动剂,ERRγ在调节能量产生、氧化代谢、细胞凋亡、炎症反应等方面发挥着关键作用。然而,其在急性肝损伤中的作用尚不清楚。在本研究中,我们评估了DY131对脂多糖(LPS)诱导的肝损伤的影响。在LPS攻击(10mg/kg)前3天,通过腹腔注射以5mg/kg/天的剂量用DY131预处理小鼠。24小时后,将它们麻醉并处死。收集血液和肝组织用于进一步研究。在另一个实验中,用生理盐水(赋形剂)或DY131处理小鼠3天以评估DY131的毒性。我们发现LPS处理的小鼠肝组织中ERRγ下调。用DY131预处理可改善LPS诱导的肝损伤,表现为肝酶释放(ALT、AST和LDH)减少、肝形态损伤改善以及氧化应激、炎症和细胞凋亡减轻。同时,DY131对小鼠的肝肾功能没有明显副作用。最后,转录组学分析显示,DY131在LPS处理的小鼠中显著逆转了与炎症和代谢相关的失调途径,为DY131对LPS诱导的肝损伤的保护作用提供了更多证据。总之,这些发现突出了DY131对LPS诱导的肝毒性的保护作用,可能是通过抑制氧化应激、炎症和细胞凋亡来实现的。