Glycyrrhizic Acid Prevents Sepsis-Induced Acute Lung Injury and Mortality in Rats

Abstract

SummaryGlycyrrhizic acid (GA), an active ingredient in licorice, has multiple pharmacological activities. However, the effects of GA on sepsis-induced acute lung injury (ALI) have not been determined. Tthe aim of this study was to investigate the molecular mechanism involved in the effects of GA against sepsis-induced ALI in rats. We found that GA alleviated sepsis-induced ALI through improvements in various pathological changes, as well as decreases in the lung wet/dry weight ratio and total protein content in bronchoalveolar lavage fluid, and a significant increase in the survival rate of treated rats. Additionally, GA markedly inhibited sepsis-induced pulmonary inflammatory responses. Moreover, we found that treatment with GA inhibited oxidative stress damage and apoptosis in lung tissue induced by ALI. Finally, GA treatment significantly inhibited NF-κ B, JNK and P38 MAPK activation. Our data indicate that GA has a protective effect against sepsis-induced ALI by inhibiting the inflammatory response, damage from oxidative stress, and apoptosis via inactivation of NF-κB and MAPK signaling pathways, providing a molecular basis for a new medical treatment for sepsis-induced ALI. (J Histochem Cytochem 64:125-137, 2016)

Protective role of down-regulated microRNA-31 on intestinal barrier dysfunction through inhibition of NF-κB/HIF-1α pathway by binding to HMOX1 in rats with sepsis

“…The operation was carried out in accordance with the instructions. A total of 15 rats in each group were randomly selected in order to observe the physiological activities and the survival rate at 72 h, and the remaining rats in each group (10 rats for each group) were used for other experiments (Zhao et al 2016 ).…”

Acetylated Polysaccharides From Pleurotus geesteranus Alleviate Lung Injury Via Regulating NF-κB Signal Pathway

“…β-D-glucose pentaacetate (348.9 mg) was dissolved into 10 mL ethyl alcohol adequately, and then the solution was kept at a constant volume and shook up in 50 mL volumetric flask. The aforementioned β-D-glucose pentaacetate stock solution (1,2,3,4, 5, 6 mL) was removed from the volumetric flask (25 mL) and used at constant volume, respectively. The above solution (5 mL), 5 mL hydroxylamine hydrochloride (0.1 mol/L), 5 mL sodium hydroxide solution (1.5 mol/L), 5 mL hydrochloric acid solution (2 mol/L), and 10 mL ferric chloride (0.37 mol/L) were added successively at constant volume (50 mL) with deionized water.…”

“…Systemic inflammatory response syndrome (SIRS) is caused by the body's systemic uncontrolled inflammatory immune response due to a variety of severe stimulations or attacks including infection, hypoxia, trauma, necrosis, and reperfusion [1]. As a result of excessive inflammation, it is a serious disease with complex etiology and serious condition, resulting in acute organ injury, shock, and multiple organ dysfunction syndrome (MODS) [2], while acute lung injury (ALI) is the earliest, has the highest incidence, and is also one of the important causes of death [3]. On the account of the lung being the most vulnerable target organ when SIRS occurs, ALI is a severe inflammatory disease caused by uncontrolled oxidative stress and inflammatory process [4].…”

Modulation of mitogen-activated protein kinase attenuates sepsis-induced acute lung injury in acute respiratory distress syndrome rats

“…In a lipopolysaccharide (LPS)-stimulated ARDS mouse model, some drugs or compounds (including Decitabine, 5-azacitidine, Andrographolide sulfonate, Hydroxy-Jolkinolide B-1 and Astilbin) alleviated LPS-induced ARDS by suppressing LPS-induced activation of the MAPK signaling pathways by blocking the phosphorylation of JNK, ERK and p38 in lung tissues (16)(17)(18)(19). Previous studies indicated that glycyrrhizic acid and Losartan have a protective effect against sepsis-induced acute lung injury by inhibiting the inflammatory response, reducing damage from oxidative stress, and apoptosis via inactivation of JNK and p38 MAPK (20,21). The aforementioned studies indicated the effect of MAPK signaling, particularly the JNK and p38 MAPK on sepsis-induced ARDS.…”