Fang Ling, Wang Xuepan, Guan Wei
Department of Emergency Medicine, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, 441021 Xiangyang, Hubei, China.
Department of Critical Care Medicine, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, 441021 Xiangyang, Hubei, China.
Discov Med. 2025 May;37(196):841-849. doi: 10.24976/Discov.Med.202537196.74.
Sepsis-mediated acute lung injury (ALI) has a high mortality rate, and glycyrrhizic acid (GA) possesses diverse pharmacologic activities. Herein, we investigated the role of GA in attenuating sepsis-triggered ALI.
Septic ALI was induced by cecal ligation and puncture (CLP). Mice were assigned into 5 groups with varied treatments. Their time of death was recorded every 6 hours after surgery. The wet/dry (W/D) weight ratio of the lung was measured. Observation of lung tissues was conducted by hematoxylin and eosin (HE) staining. Protein concentration in bronchoalveolar lavage fluid (BALF), levels of inflammatory cytokines, and production of reactive oxygen species (ROS) were detected by bicinchoninic acid (BCA), enzyme-linked immunosorbent assay, and dihydroethidium (DHE) staining, respectively. Endoplasmic reticulum (ER) stress-related genes, heme oxygenase-1 (HO-1), Janus kinase 2 (JAK2), and signal transducer and activator of transcription 3 (STAT3) levels were quantified by western blot.
GA remarkably elevated survival rate and mitigated lung injury ( < 0.05). CLP markedly increased the W/D weight ratio and BALF protein concentration, while GA did the opposite ( < 0.05). CLP promoted interleukin-1β (IL-1β), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), phosphorylation of eIF2α (p-eIF2α), activating transcription factor 4 (ATF4), C/EBP homologous protein (CHOP), the phosphorylation level of JAK/STAT3, along with DHE intensity, while GA showed opposite effects ( < 0.01). Additionally, GA markedly enhanced the HO-1 level ( < 0.05).
GA holds promise for future improvements in treating sepsis-induced ALI.
脓毒症介导的急性肺损伤（ALI）死亡率很高，甘草酸（GA）具有多种药理活性。在此，我们研究了GA在减轻脓毒症引发的ALI中的作用。
通过盲肠结扎和穿刺（CLP）诱导脓毒症ALI。将小鼠分为5组，进行不同处理。术后每6小时记录一次它们的死亡时间。测量肺组织的湿/干（W/D）重量比。通过苏木精和伊红（HE）染色观察肺组织。分别采用二辛可宁酸（BCA）法、酶联免疫吸附测定法和二氢乙锭（DHE）染色检测支气管肺泡灌洗液（BALF）中的蛋白质浓度、炎症细胞因子水平和活性氧（ROS）的产生。通过蛋白质免疫印迹法对内质网（ER）应激相关基因、血红素加氧酶-1（HO-1）、Janus激酶2（JAK2）和信号转导子及转录激活子3（STAT3）的水平进行定量分析。
GA显著提高了生存率并减轻了肺损伤（<0.05）。CLP显著增加了W/D重量比和BALF蛋白质浓度，而GA则起到相反作用（<0.05）。CLP促进了白细胞介素-1β（IL-1β）、肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）、蛋白激酶R（PKR）样内质网激酶（PERK）、真核翻译起始因子2α（eIF2α）的磷酸化（p-eIF2α）、激活转录因子4（ATF4）、C/EBP同源蛋白（CHOP）、JAK/STAT3的磷酸化水平以及DHE强度，而GA则表现出相反的作用（<0.01）。此外，GA显著提高了HO-1水平（<0.05）。
GA有望为未来治疗脓毒症诱导的ALI带来改善。
