Research Promotion and Support Headquarters, Fujita Health University, Toyoake, Aichi 470‑1192, Japan.
Department of Informative Clinical Medicine, Fujita Health University Graduate School of Health Sciences, Toyoake, Aichi 470‑1192, Japan.
Mol Med Rep. 2023 Feb;27(2). doi: 10.3892/mmr.2022.12911. Epub 2022 Dec 9.
The partial loss of liver due to liver transplantation or acute liver failure induces rapid liver regeneration. Recently, we reported that the selective inhibition of indoleamine 2,3‑dioxygenase (Ido) 1 promotes early liver regeneration. However, the role of Ido2 in liver regeneration remains unclear. Wild‑type (WT) and Ido2‑deficient (Ido2‑KO) mice were subjected to 70% partial hepatectomy (PHx). Hepatocyte growth was measured using immunostaining. The mRNA expression of inflammatory cytokines and production of kynurenine in intrahepatic mononuclear cells (MNCs) were analyzed using reverse transcription‑quantitative PCR and high‑performance liquid chromatography. The activation of NF‑κB was determined by both immunocytochemistry and western blotting analysis. The ratio of liver to body weight and the frequency of proliferation cells after PHx were significantly higher in Ido2‑KO mice compared with in WT mice. The expression of IL‑6 and TNF‑α in MNCs were transiently increased in Ido2‑KO mice. The nuclear transport of NF‑κB was significantly higher in peritoneal macrophages of Ido2‑KO mice compared with WT mice. These results suggested that Ido2 deficiency resulted in transiently increased production of inflammatory cytokines through the activation of NF‑kB, thereby promoting liver regeneration. Therefore, the regulation of Ido2 expression in MNCs may play a therapeutic role in liver regeneration under injury and disease conditions.
由于肝移植或急性肝衰竭导致部分肝脏丧失,会引发快速的肝脏再生。最近,我们报道了吲哚胺 2,3-双加氧酶(Ido)1 的选择性抑制可促进早期肝脏再生。然而,Ido2 在肝脏再生中的作用仍不清楚。野生型(WT)和 Ido2 缺陷型(Ido2-KO)小鼠接受 70%部分肝切除术(PHx)。使用免疫染色测量肝细胞生长。使用逆转录定量 PCR 和高效液相色谱法分析肝内单核细胞(MNC)中炎症细胞因子的 mRNA 表达和犬尿氨酸的产生。通过免疫细胞化学和 Western blot 分析测定 NF-κB 的激活。与 WT 小鼠相比,Ido2-KO 小鼠的肝重与体重比以及 PHx 后增殖细胞的频率明显更高。Ido2-KO 小鼠 MNC 中 IL-6 和 TNF-α 的表达短暂增加。与 WT 小鼠相比,Ido2-KO 小鼠腹腔巨噬细胞中 NF-κB 的核转运明显更高。这些结果表明,Ido2 缺乏通过激活 NF-κB 导致炎症细胞因子的短暂产生增加,从而促进肝脏再生。因此,调节 MNC 中 Ido2 的表达可能在损伤和疾病状态下对肝脏再生具有治疗作用。