RESUMEN
OBJECTIVE To study the repair effect and mechanism of Zhixu burn ointment on deep second-degree burned model rats. METHODS The deep second-degree burned model was established with a temperature-controlled apparatus. The model rats were randomly divided into model group， Jingwanhong ointment group and Zhixu burn ointment high-dose， medium-dose and low-dose groups （specifications were 20 g core+20 mL wetting agent， 10 g core+20 mL wetting agent， 5 g core+20 mL wetting agent， respectively）. Another blank control group （only dehairing treatment， no modeling） was set up， with 10 rats in each group. The rats in each administration group were given corresponding drugs， the rats in the blank control group were not treated， and the rats in the model group were given normal saline once a day for 21 d. The healing of burn wounds and histomorphological changes of burned skin in each group of rats were observed， and the healing rate of wounds was calculated； the levels of vascular endothelial growth factor （VEGF）， interleukin-1β （IL-1β）， IL-6 and tumor necrosis factor-α（TNF-α） in the wound skin tissue of rats were detected by enzyme-linked immunosorbent assay； immunohistochemical method was used to detect the expression levels of VEGF and platelet endothelial cell adhesion molecule-1 （CD31） protein in burned skin tissue. RESULTS Compared with model group， the wound area of the rats in the Jingwanhong ointment and Zhixu burn ointment groups gradually decreased and healed significantly by day 21， and the wound healing rate was significantly higher （P＜0.05 or P＜0.01）； thicker new epidermal layer was seen in the skin tissue， and connective tissue and new blood vessels were significantly increased in the dermis； the expression levels of IL-1β， IL-6 and TNF-α were significantly decreased （P＜0.05 or P＜0.01）， and the expression levels of VEGF and CD31 protein were significantly increased （P＜0.05 or P＜0.01） in the burned skin tissue. CONCLUSIONS Zhixu burn ointment can repair the skin of deep second-degree burned model rats， and the mechanism may be related to reducing the inflammatory response of burn wound and promoting the angiogenesis.
RESUMEN
OBJECTIVE： To study early toxicity of paracetamol （APAP） to drug-induced liver injury in mice based on lipid metabonomics research， and to provide reference for finding potential biological marker. METHODS： Totally 20 mice were randomly divided into normal group and APAP liver injury group， with 10 mice in each group. APAP liver injury group was given intraperitoneal injection of APAP 300 mg/kg to establish acute liver injury model； normal group was given constant volume of normal saline intraperitoneally. 1 h later， the blood of mice was collected to isolate plasma. UPLC-Triple-TOF-MS method was used to detect plasma metabolites and perform metabonomics analysis. PCA， PLS-DA and OPLS-DA analysis distinguished the difference of metabolism profiles between groups. The lipid metabolites were screened and identified according to HMDB， Metlin and LIPID MAPS databases. Meanwhile， the changes of APAP level in plasma of mice were detected. The lipid metabolites with variable influence in the projection （VIP） greater than 1 and P＜0.05 in OPLS-DA analysis were identified as differential metabolites. The correlation between lipid differential metabolites and plasma APAP level was analyzed. RESULTS： PCA， PLS-DA and OPLS-DA results showed that sample points in normal group and APAP liver injury group were located in different areas with good differentiation. Compared with liver injury group and normal group， levels of 5 fatty acid metabolites were significantly increased or decreased； levels of 8 glycerophospholipids were significantly decreased and one sphingolipids was significantly increased. 9-thiastearic acid， tetradecanedioic acid， 9-hydrogen peroxide-10，12-octadecadienoic acid， L-myristoyl carnitine （fatty acid） and scyphostation A （sphingolipids） levels had a significant correlation with APAP level in plasma. CONCLUSIONS： The plasma lipid metabolomics showed abnormal changes 1 hour after acetaminophen exposure. A total of 14 related lipid differential metabolites are found， and 5 of which are significantly correlated with APAP level in plasma.