Objective : To investigate the expression level of LONP1 in hepatocellular carcinoma(HCC) and its impact on the occurrence and progression of HCC. Methods : The expression of LONP1 in human liver cancer tissues was verified by real-time quantitative PCR(qPCR) and Western blot.LONP1stable knockdown Hep3B and HCCLM3 cell lines were established, and the effects of LONP1 on cell proliferation were explored through CCK-8, EdU incorporation assays, and colony formation assays. The effects of LONP1 on cell migration were assessed using scratch and Transwell migration assays. A Cre-Loxp system was employed to generateLONP1conditional knockout mice, and transcriptomic sequencing of liver tissues was performed to explore the impact ofLONP1deficiency on liver cells. The effects ofLONP1on apoptosis in hepatocellular carcinoma cell lines were explored using Tunel staining and flow cytometry with Annexin V-FITC/PI. Results : Western blot and qPCR experiments confirmed the high expression of LONP1 in human liver cancer tissues. Colony formation assays revealed that the number of cell clones inLONP1knockdown groups was significantly reduced compared to the control(P<0.01). CCK-8 and EdU assays demonstrated thatLONP1knockdown cells had a significantly lower proliferation rate than control cells(P<0.01). Scratch and migration assays showed thatLONP1knockdown liver cancer cells exhibited impaired migration compared to controls(P<0.01). Transcriptomic analysis of liver tissues fromLONP1conditional knockout mice indicated that LONP1 might affect apoptosis pathways in liver cells. Tunel staining and Annexin V-FITC/PI flow cytometry showed thatLONP1knockdown increased apoptosis in hepatocellular carcinoma cells. Conclusion LONP1 is highly expressed in liver cancer tissues. The knockdown ofLONP1in liver cancer cell lines promotes cell apoptosis and inhibits cell proliferation and migration.

Duchene muscular dystrophy (DMD) is a serious progressive muscular dystrophy.Reports in recent years about abnormal lipid in DMD patients have increased, yet little attention has been paid to liver lipid.This study aimed to explore the effect of dystrophin gene defect on liver lipid synthesis.7-week-old mdx male mice were used as DMD model.The conditions of liver function, liver lipid accumulation and liver lipid synthesis were determined through liver tissue morphological examination, blood biochemical examination, and detection of hepatic gene and protein expression.The results showed that lipid droplets in liver of mdx mice increased significantly.The contents of total cholesterol and triglyceride in liver, aspartate aminotransferase and alanine aminotransferase in serum increased.The gene and protein expression of hepatic lipid synthesis-related enzymes such as fatty acid synthase, acetyl CoA carboxylase, and sterol regulatory element binding protein 1-c were up-regulated.These results showed accumulation of liver lipid in 7-week-old mdx male mice.

Aim To investigate the hypoglycemic pathway of terpenes from Cornus officinalis(TCF) from three aspects of insulin dependence, α-glucosidase inhibition, insulin sensitizing.Methods Insulin-deficient diabetes mellitus(DM) model was induced by tail vein injection of streptozotocin(STZ) into SD rats at the dose of 50mg·kg-1 body weight.Rats were randomly divided into seven groups: control group(CON), model group(Model), metformin group(Met) 0.1g·kg-1, shenqi jiangtang granules(Shenqi) group 1.0 g·kg-1, three dose groups of TCF: 0.10, 0.05, 0.025 g·kg-1.Body weight and blood glucose were measured every week.After four weeks, glycosylated hemoglobin (HbA1c), glycosylated serum protein (GSP) were determined.Normal ICR mice were divided into seven groups: CON, Model, Met group 0.2g·kg-1, acarbose group(Acar) 0.1 g·kg-1, Shenqi group 1.5g·kg-1, three dose groups of TCF: 0.20g·kg-1;0.10g·kg-1;0.05 g·kg-1.After 10 days of administration, intraperitoneal injections of glucose and gavage starch tolerance tests were employed.Normal SD rats were divided into six groups: CON, rosiglitazone group 0.02 g·kg-1, glipizide group 0.02 g·kg-1, three dose groups of TCF: 0.10, 0.05, 0.025 g·kg-1.After seven days of administration, intraperitoneal glucose tolerance test(IPGTT) was employed and levels of insulin was determined.Results (1)High dose of TCF significantly reduced the level of HbA1c(P<0.05), GSP(P<0.05) on STZ model rats;(2)TCF significantly improved the glucose tolerance and gavage starch tolerance in ICR mice(P<0.05);(3) High dose of TCF significantly reduced the blood glucose and serum insulin level.Conclusions TCF has obvious effects on inhibiting glucose absorb and promoting the use of glucose.It is able to exert hypoglycemic effect through non-insulin dependent pathway, whereas, whether it has the effects of α-glucosidase inhibition and insulin sensitization should be further validated.