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Hesperidin (HDN) is a bioflavonoid that serves a role as an antioxidant in biological systems. However, although HDN has hydrogen radical- and hydrogen peroxide-removal activities, the role of HDN in liver ischemia/reperfusion (I/R) injury remains unknown. This study aimed to determine the role of HDN in liver I/R injury. Male C57BL/6J wild-type (WT) mice were subjected to warm partial liver I/R injury. Liver damage was evaluated by measuring serum alanine aminotransferase (ALT) levels, cytokine production, oxidative stress indicators, tissue hematoxylin-eosin staining and cell death. The Akt signaling pathway was examined to elucidate the underlying mechanisms. HDN had no effect on ALT levels and tissue damage in WT mice without liver I/R injury. However, HDN significantly ameliorated liver I/R injury as measured by serum ALT levels and necrotic tissue areas. HDN decreased malondialdehyde content, but increased the levels of superoxide dismutase, catalase, glutathione peroxidase and glutathione. In addition, HDN significantly attenuated the mRNA expression levels of TNF-α, IL-6 and IL-1β after liver I/R injury. Furthermore, HDN protected the liver against apoptosis in liver I/R injury by increasing the levels of Bcl-2 and decreasing the levels of cleaved-caspase 3. Mechanistically, the levels of phosphorylated Akt were elevated by HDN during liver I/R injury. In addition, HDN could induce Akt activation in hepatocytes in vitro. Most importantly, treatment with the Akt inhibitor LY294002 in WT mice blocked the hepatoprotective effects of HDN in liver I/R injury. In summary, the results of the present study suggested that HDN may protect against liver I/R injury through activating the Akt pathway by ameliorating liver oxidative stress, suppressing inflammation and preventing hepatocyte apoptosis. HDN may be a useful factor for liver injury protection and a potential therapeutic treatment for liver I/R injury in the future.

Hesperidin (HDN) has been reported to have hydrogen radical- and hydrogen peroxide-removal activities and to serve an antioxidant role in biological systems. However, whether HDN protects hepatocytes (HCs) against hypoxia/reoxygenation (H/R)-induced injury remains unknown. The present study aimed to explore the role of HDN in H/R-induced injury. HCs were isolated and cultured under H/R conditions with or without HDN treatment. HC damage was markedly induced under H/R, as indicated by cell viability, supernatant lactate dehydrogenase levels and alanine aminotransferase levels; however, HDN treatment significantly reversed HC injury. Oxidative stress markers (malondialdehyde, superoxide dismutase, glutathioneand reactive oxygen species) were increased markedly during H/R in HCs; however, this effect was significantly attenuated after exposure to HDN. Compared with those of the control group, the mRNA expression levels of IL-6 and TNF-α in HCs and the concentrations of IL-6 and TNF-α in the supernatants increased significantly following H/R, and HDN significantly ameliorated these effects. Western blotting demonstrated that microtubule-associated protein 1 light chain 3α (MAP1LC3A, also known as LC3) and Beclin-1 protein expression levels increased, while sequestosome 1 levels decreased during H/R following exposure to HDN. The number of GFP-LC3 puncta in HCs following exposure to HDN was increased compared with that observed in HCs without HDN exposure under the H/R conditions after bafilomycin A1 treatment. In summary, the present study demonstrated that HDN attenuated HC oxidative stress and inflammatory responses while enhancing autophagy during H/R. HDN may have a potential protective effect on HCs during H/R-induced injury.

Pulmonary contusion (PC) is very common in blunt chest trauma, and always results in negative pulmonary outcomes, such as pneumonia, acute respiratory distress syndrome (ARDS), respiratory failure or even death. However, there are no effective biomarkers which can be used to predict the outcomes in these patients. The present study aimed to determine the value of interleukin (IL)-17 and IL-22 in predicting the severity and outcomes of PC in trauma patients. All trauma patients admitted to The First Affiliated Hospital of Guangxi Medical University between January 2015 and December 2017, were studied. Patients aged >14 years old with a diagnosis of PC upon their admission to the emergency department were included. Patients with PC were enrolled as the PC group, patients without PC were enrolled as the non-PC group, and healthy individuals were selected as the control group. Clinical information, including sociodemographic parameters, clinical data, biological findings and therapeutic interventions were recorded for all patients who were enrolled. Blood samples were collected and stored according to the established protocols. PC volume was measured by computed tomography and plasma cytokine levels were assayed by ELISA. A total of 151 patients with PC (PC group) and 159 patients without PC (non-PC group) were included in the present study. In addition, 50 healthy individuals were used as the control group. The primary cause of PC was motor vehicle crashes. PC patients had more rib fractures, but similar injury severity scores compared with other patients. More patients received Pleurocan drainage treatment and had pneumonia complications in the PC group compared with the other two groups. PC patients had a high incidence of ARDS and admission to the intensive care unit (ICU). PC patients also experienced longer periods on mechanical ventilation and had longer stays in the ICU and hospital. PC volume was effective in predicting the outcomes of PC patients. IL-22 levels were similar in the PC group and non-PC group. However, IL-17 could be used as a biomarker to predict the severity of PC, and was strongly associated with PC volume. IL-17 was significantly associated with pro-inflammatory complications in PC patients and could be used as a biomarker for predicting in-patient outcomes of patients with PC. In conclusion, IL-17 is a potential biomarker for predicting the severity and outcomes of PC in trauma patients.