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Objective To investigate the effect of deletion of Sirtuin type 1(Sirt1) gene on liver inflammation of mice and its mechanism. Methods The body weight of C57BL/6J male mice and liver specific Sirt1 deficiency (Sirt1-LKO) male mice were recorded weekly. The sensitivity of inflammatory response was tested by intraperitoneal injection of 20 mg/kg LPS. The survival curve was used to reflect the sensitivity of mice to inflammatory response.The expression of inflammatory factors was detected by Western blot and q-PCR. Results Compared with control wild type mice, Sirt1-LKO mice showed significantly reduced body weight (P＜0.05). In addition, The survival curve was shown by kaplane Meier diagram,Sirt1-LKO mice showed lower sensitivity to LPS (P＜0.05).The protein level of NF-κB in primary liver cells of Sirt1-LKO mice was increased (P＜0.05),Tnfα and IL6 of NF-κB downstream target genes were up-regulated(P＜0.05). Conclusions Hepatocyte-specific Sirt1 deletion aggravates liver inflammation response in mouse model.

Objective To explore the effect of barley plus butter dietary on the symptoms of dextran sodium sulfate induced chronic ulcerative colitis and intestinal microbial distribution in mice. Methods In customized feed(C feed), soybean oil and corn meal in standard mice breeding feed (N feed) were replaced with equal proportion of ghee and raw barley powder.28 male mice were randomly divided into 4 groups(n=7,each group):NW group fed with N feed and water; ND group fed with N feed and 1.8% DSS; CW group fed with C feed and water; CD group fed with C feed and 1.8% DSS. Colitis model was established by three cycles of 10 days supply of distilled water after 7 days supply of 1.8% DSS solution. Finally, the effects were evaluated by DAI score, colon HE staining and 16S rRNA high-throughput sequencing of gut microbes. Results The abundance of bacteria was increased and the diversity of intestinal flora, such as allobaculum, was improved in wild type mice fed on the barley and butter dietary. However, when the mice were treated with DSS, the barley plus butter dietary group had high DAI score(P＜0.05), showed obvious intestinal ulcers and disorganized intestinal glands by histopathological microscopy, and decreased intestinal flora abundance and diversity(P＜0.05). But the quantity of Clostridium and Sartreella was increased in barley and butter dietary group(P＜0.05). Conclusions The barley plus butter dietary increases intestinal flora Allobaculum of wild type mice and improves the composition of intestinal flora, but the dietary intervention fails to show any significant impact on the chronic ulcerative colitis symptoms induced by DSS.

Objective To observe the changes of insulin sensitivity of flavonoids 4, 4'-dimethoxy chalcone (DMC) in mice fed on high-fat diet (HFD) and to investigate its effect. Methods Wild-type C57/BL 6 mice fed on HFD were divided into control group and experimental group. DMC and solvent DMSO were injected intraperitoneally at 3 μg/kg every other day. Food intake and body weight of the two groups were recorded weekly, glucose tolerance test (GTT), insulin tolerance test (ITT) and sodium pyruvate tolerance test(PTT) were measured at week 6. The adipose tissues were examined by immunohistochemistry and HE staining. Results Compared with the control mice, the mice treated with DMC drug was no different in body weight and food intake. ITT indicated that DMC administration increased insulin sensitivity (P＜0.05), but GTT and PTT showed no significant difference. HE staining microscopy showed that adipose tissue contained less mononuclear cells in mice treated with DMC than control mice. There was weak staining for F4/80 in the adipose tissue of mice treated with DMC, defined as F4/80-positive cells. Conclusions DMC can improve the insulin sensitivity of mice in high-fat diet by decreasing the infiltration of macrophages in adipose tissue.

Objective To investigate the role of mammalian sterile line 20-like kinas 1(MST1) and its regulatory mechanism in hepatic gluconeogenesis of mouse. Methods The mRNA expression of MST1 in the liver of db/db mice and db/m mice was detected by RT-qPCR. MST1 was overexpressed with adenovirus to detect glucose output capacity in mouse primary hepatocytes. Luciferase reporter assay was adopted to detect the effect of MST1 on phosphoenolpyruvate carboxykinase (PEPCK) promoter activity in HepG2 cells. Forkhead transcription factor O1 (FOXO1) was knocked down by interfering adenovirus in primary mouse liver cells to detect the effect of MST1 overexpression on the mRNA levels of PEPCK. Results The mRNA level of MST1 was significantly upregulated in the liver of db/db mice (P＜0.001). MST1 overexpression enhanced glucose output in mouse primary hepatocytes (P＜0.05). In HepG2 cells, MST1 overexpression increased the mRNA of PEPCK (P＜0.001) and the activity of PEPCK promoter (P＜0.01). Furthermore, MST1-induced increase in PEPCK mRNA was abolished when FOXO1 was knocked down by interfering adenovirus. Conclusions MST1 promotes hepatic gluconeogenesis by regulating the mRNA expression of PEPCK dependent on FOXO1.

The effects of hot pressing and hot extrusion temperatures on the properties of 12%SiCp/6066Al (volume fraction) composites fabricated by powder metallurgy have been studied. The experimental results indicate that the hot extrusion, an essential stage of powder metallurgy to produce this sort of particle reinforced metal matrix composites, can redistribute SiC particles in metal matrix and refine the matrix grain size, and that the hot pressing can improve the interfacial cohesion strength between SiC particles and metal matrix. When hot-pressed at temperatures slightly higher than the solidus temperature of the composite and hot-extruded at lower temperatures, the composites are stronger due to the high metal matrix strength and interfacial cohesion. The optimum parameters of hot pressing and hot extrusion in the composites are 560 and 430 °C, respectively.