A Mixture of Fermented Schizandrae Fructus Pomace and Hoveniae Semen cum Fructus Extracts Synergistically Protects against Oxidative Stress-Mediated Liver Injury.

Schizandrae Fructus (SF) and Hoveniae Semen cum Fructus (HSCF) have long been used as medicinal herbs for treating various diseases in Asian traditional medicine. In the current study, we investigated the protective effect of fermented SF pomace and HSCF extract 1:1 (w:w) combination mixture (MSH) against carbon tetrachloride (CCl4)-induced acute liver injury mice. After MSH (50-200 mg/kg) oral administration for 7 consecutive days, animals were injected intraperitoneally with CCl4 (0.5 mL/kg). Histopathological observation revealed that administration of MSH synergistically decreased the degeneration of hepatocytes and the infiltration of inflammatory cells induced by CCl4. Moreover, MSH administration reduced the activities of alanine aminotransferase, aspartate aminotransferase, and γ-glutamyl transpeptidase in serum, and mitigated apoptotic cell death in hepatic parenchyma. In addition, MSH alleviated CCl4-mediated lipid peroxidation by restoring endogenous antioxidants capacities including glutathione contents, superoxide dismutase, and catalase activities. In vitro assessments using tert-butyl hydroperoxide-induced oxidative stress in HepG2 cells revealed that MSH protects hepatocytes by lowering ROS generation and lipid peroxidation via upregulating the transcriptional activity of nuclear factor erythroid-2-related factor 2 and the expression of antioxidant genes. Furthermore, MSH synergistically attenuated the expression of proinflammatory cytokines in CCl4-injured liver and lipopolysaccharide-stimulated RAW 264.7 cells. Taken together, these findings suggest that MSH has the potential to prevent acute liver damage by effectively suppressing oxidative stress and inflammation.

Effects of Trauma Center Establishment on the Clinical Characteristics and Outcomes of Patients with Traumatic Brain Injury : A Retrospective Analysis from a Single Trauma Center in Korea.

OBJECTIVE: To investigate the effects of trauma center establishment on the clinical characteristics and outcomes of trauma patients with traumatic brain injury (TBI). METHODS: We enrolled 322 patients with severe trauma and TBI from January 2015 to December 2016. Clinical factors, indexes, and outcomes were compared before and after trauma center establishment (September 2015). The outcome was the Glasgow outcome scale classification at 3 months post-trauma. RESULTS: Of the 322 patients, 120 (37.3%) and 202 (62.7%) were admitted before and after trauma center establishment, respectively. The two groups were significantly different in age (p=0.038), the trauma location within the city (p=0.010), the proportion of intensive care unit (ICU) admissions (p=0.001), and the emergency room stay time (p<0.001). Mortality occurred in 37 patients (11.5%). Although the preventable death rate decreased from before to after center establishment (23.1% vs. 12.5%), the difference was not significant. None of the clinical factors, indexes, or outcomes were different from before to after center establishment for patients with severe TBI (Glasgow coma scale score ≤8). However, the proportion of inter-hospital transfers increased and the time to emergency room arrival was longer in both the entire cohort and patients with severe TBI after versus before trauma center establishment. CONCLUSION: We confirmed that for patients with severe trauma and TBI, establishing a trauma center increased the proportion of ICU admissions and decreased the emergency room stay time and preventable death rate. However, management strategies for handling the high proportion of inter-hospital transfers and long times to emergency room arrival will be necessary.

Effects of sphingolipid synthesis inhibition on cholesterol gallstone formation in C57BL/6J mice.

BACKGROUND: Sphingolipids play a very important role in cell membrane formation, signal transduction and plasma lipoprotein metabolism. The first rate-limiting step in the sphingolipid biosynthetic pathway is catalyzed by serine palmitoyltransferase (SPT), and myriocin is a potent and specific inhibitor of SPT. We investigated the impact of SPT inhibition on cholesterol gallstone formation in C57BL/6J mice. METHODS: Three groups of eight-week-old C57BL/6J mice were utilized. Each group consisted of 20 mice; group A, B, and C were fed normal chow, lithogenic diet with phosphate buffered saline, and lithogenic diet with myriocin (0.3 mg/kg), respectively, for 6 weeks. The ceramide levels in both serum and bile were assessed by high performance liquid chromatography analysis. Protein expression of ERK, JNK and p38 in the extracted gallbladder were determined by Western-blot analysis. RESULTS: Myriocin treatment caused a significant decrease in the rate of cholesterol gallstone formation. The lithogenic diet mice (group B) showed the highest ceramide activities in both the serum and bile among all the tested groups and there was significant suppression of the ceramide levels in both the serum and bile of the myriocin-treated mice (group C, p < 0.05). Phosphorylation of p38 in the gallbladder was increased in the lithogenic-diet mice and the expression of phosphorylated p38 was significantly suppressed in the myriocin treated mice. CONCLUSIONS: SPT inhibition by myriocin suppressed gallstone formation and the levels of ceramide in both the serum and bile. p38 in the cellular signaling pathways might be associated with cholesterol gallstone formation.