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Objective To investigate whether lidocaine can reverse Kupffer cell dysfunction in diabetic mice, as well as the mechanism of lidocaine in affecting liver abscess formation by improving the phagocytic function of Kupffer cells. Methods C57BLKS/J db/db mice were divided into diabetes control group and diabetes+lidocaine group, and C57BLKS/J db/m mice were divided into non-diabetes control group and non-diabetes+lidocaine group, with 5 mice in each group. All mice were fed with the suspension of Klebsiella pneumoniae . Kupffer cells were collected from each group and were cultured in vitro; an electron microscope was used to measure the change in ultrastructure, and Kupffer c ells were measured in terms of the levels of inflammatory mediators, the expression level of intercellular adhesion molecule-1 (ICAM-1), the chemotactic function of neutrophils, and phagocytic function; liver abscess formation was also observed. The Kruskal-Wallis H test was used for comparison of continuous data between multiple groups, and the Mann-Whitney U test was used for further comparison between two groups; the chi-square test was used for comparison of categorical data between groups. Results Compared with the non-diabetic mice, the diabetic mice had significant reductions in mitochondria and rough endoplasmic reticulum, endoplasmic reticulum dilation, mitochondrial swelling, and an increase in lipid droplets in Kupffer cells. Compared with the non-diabetes control group, the diabetes control group had significant increases in the levels of nitric oxide (NO) (4.95±0.06 μmol/L vs 1.34±0.13 μmol/L, P 0.05). Compared with the diabetes control group, the diabetes+lidocaine group had significant reductions in the levels of NO (3.35±0.28 μmol/L vs 4.95±0.06 μmol/L, P 0.05). Conclusion Lidocaine can inhibit Kupffer cell inflammatory response and improve the phagocytic function of Kupffer cells in diabetic mice, thereby exerting a protective effect on Kupffer cells, but it had no effect on liver abscess formation.
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To explore the clinical efficacy of Herba Saxifragae cream (HS), a compound of traditional Chinese herbal medicine, on chronic eczema.
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Objective To investigate the effect of simvastatin-polylactic acid compound on critical calvarial defects in rats.Methods Twenty male SD rats(150 g?10 g),were used to establish critical cranial defect(10 mm in diameter)model.The animals were randomly divided into control and experiment groups(10 in each).In the control group,40 mg of polylactic acid were implanted into the defect area;whereas in the experiment group,simvastatin-polylactic acid compound were used(20 mg simvastatin and 40 mg polylactic acid).Four and eight weeks after the implantation,the defect area of the rats was observed by X-ray and toluidine blue staining.Results Eight weeks after the operation,X-ray examination showed high-density regions in the defect area in the experiment group,while low-density regions in the control group.The radiopacity of cranial defects were 27.33%?2.54% in the control group,and 74.63%?2.42% in the experimental group(n=5,t=-30.148,P=0.000).Toluidine blue staining showed a few new bone tissues at 4 weeks and fully filled bone defect at 8 weeks in the experiment group.Meanwhile,in the control group,only a small quantity of new bone tissue could be seen on the edge of the cranial defects.Conclusion Locally implanted simvastain-polylactic acid compound is a promising method for the treatment of bone defect owing to its high osteogenic ability.
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Objective To investigate the effect of simvastatin on the mobilization and migration of endothelial progenitor cells(EPCs).Methods EPCs were harvested from the bone marrows of two rabbits,cultured with M199,and identified by immunohistochemistry.The identified EPCs were then treated with simvastatin with different concentrations(0,0.01,0.1,1.0 ?mol/L),and their migration induced by simvastatin was determined with Transwell chamber assay.Six rabbits models of cranial bone defect were established and divided into control and experiment groups(3 in each).In order to elicit the effects of simvastatin on mobilization of EPCs,simvastatin was embedded in polylactic acid compound,and implanted into the cranial bone defect area in the experiment group.Meanwhile,polylactic acid was implanted in the control animals.After 10 days,the expression rate of CD34+/CD133+ EPCs in the rabbit peripheral blood was counted by flow cytometry to determine the motivating effect of simvastatin.Results In Transwell experiment,16 hours after adding simvastatin(0,0.01,0.1 or 1.0 ?mol/L),the cell migration ability was obviously increased showing a dose-dependent trend(OD value:0.077?0.014 in control group and 0.075?0.013 in 0.01 ?mol/L group vs 0.097?0.011 in 0.1 ?mol/L group and 0.099?0.019 in 1.0 ?mol/L group,P