Objective To compare the different doses of low-temperature plasma (LTP) on wound healing in BALB/c mice so as to discuss the effects of the optimal dose of low-temperature plasma dealing with wound in mice and the acting mechanism of wound healing.Methods Adoptatmospheric pressure plasma jet discharged by the dielectric barrier was used to treat mouse skin wound.According to the processing time, the wounds were divided into 10s, 20s, 30s, 40s and 50s experimental groups, while naturally healing wounds served as negative controls and the wounds dealt with recombinant human epidermal growth factor served as positive controls.We recorded the wound size every day, observed the histopathological changes, the expression level of type Ⅰ collagen by immunofluorescence, and analyzed the composition of low-temperature plasma jet.Results The wounds with plasma treatment time of 10s, 20s, 30s, and 40s showed significant daily improvement and almost complete closure at days 12, 10, 7, 13, respectively.However, the wounds with plasma treatment time of 50s remained unhealed atday 14.The wounds in positive control group all healed, and the wound healing effect in positive control group could be achieved in 30s group.HE staining and immunofluorescence staining assays showed the optimal result of epidermal cell regeneration, granulation tissue hyperplasia, and collagen deposition in histological aspect at day 7 in 30 s group.The low-temperature plasma jet contained highly reactive free radicals of nitrogen and oxygen, which play an important role in wound healing process.Conclusion Appropriate doses of cold plasma can accelerate wound healing whereas over-doses of plasma can suppress wound healing.The process of wound healing may be related to reactive oxygen and nitrogen species in LTP.

Objective To study the effect of homocysteine(Hcy)on the formation of atherosclerotic and acceleration of ApoE-/-mice liver lipid metabolism disorder .Methods 12 normal 5 weeks old C57BL/6J mice served as control group ,and 36 5 weeks old C57BL/6J A poE-/- mice were randomly divided into 3 groups(n=12 for each group) ,the model control group ,the hyperhomocys-teinemia(HHcy)group and the intervention group(intervened by folate and vitamin B12 ) .18 weeks later ,the blood of the mice was gotten using a Unilateral enucleation method ,and the Serum Hcy and lipid changes were detected by Biochemical analyzer .And the changes of plaque size were measured by HE staining .The liver tissues of the 4 groups mice were taken and the changes in hepato-cyte lipid were detected by oil red O staining ,and the hepatic lipid levels were measured by enzymatic determination(by Semi-quan-titative image analysis) .Results The results showed that ,when compared with the control group ,the serum Hcy ,LDL ,TG and CHOL levels of the HHcy group significantly increased by 2 .3 ,2 .8 ,5 .0 ,10 .7 fold(P<0 .01)and the content of HDL decreased by 64% (P<0 .01) ,and the result showed that ,conpared with the HHcy group ,the seram Hcy ,LDL and CHOL levels of the interven-tion group were significantly decreased by 43% ,34% ,21% (P<0 .05) .Atherosclerotic fatty plaque could be seen in the hyperlipi-demic ,model and intervention group .Meanwhile ,there was a large number of scattered fat in A poE-/-mice liver by oil red O staining in the HHcy group ,and the CHOL and TG levels were 2 .2 fold and 2 .8 fold higher in the HHcy than that in the normal control group respectively(P<0 .01) .And compared with the HHcy group ,the serum CHOL and TG levels of the intervention group sig-nificantly decreased by 34% ,33% (P<0 .01) .Conclusion It is found that Hcy can induce the formation of As and accelerate liver lipid metabolism disorder .

ObjectiveTo explore the expression of transcription factor KLF16 in nonalcoholic fatty liver disease （NAFLD） and its effect on lipid metabolism. MethodsAn animal model of NAFLD was constructed in mice induced by a high-fat diet. The mice were divided into normal diet group （ND） and high fat diet group （HFD）. NAFLD cell model was constructed by primary mouse liver cells induced by oleic acid. The cells were divided into control group （Control group） and oleic acid induction group （OA group）. Real-time fluorescence quantitative PCR （RT-qPCR） and Western blot were used to detect KLF16 expression in NAFLD animal and cell models. In vitro and in vivo models of KLF16 knockdown were constructed by injection of adeno-associated virus （AAV） into mouse tail veins and transient transfection of cell siRNA. Hematoxylin-eosin staining （HE） and other methods were used to detect changes in lipid deposition in NAFLD models before and after KLF16 knockout. RT-qPCR was used to detect the expression of key genes of lipid metabolism in both cellular and animal NAFLD models before and after KLF16 knockdown. Western blot assay was used to detect the expression of endoplasmic reticulum stress protein in NAFLD model before and after KLF16 knockdown. ResultsThe expression level of KLF16 was up-regulated in HFD group and OA group， and lipid deposition was increased in OA group after KLF16 was depressed. There was no change in TC level in hepatocytes between groups （P>0.05）， and TG level was increased in different degrees （P<0.05， P<0.001）. At the same time， the change of KLF16 expression also caused the change of ER stress protein expression in OA group. ConclusionThe transcription factor KLF16 may alleviate lipid deposition in nonalcoholic fatty liver disease by endoplasmic reticulum stress.