Objective To investigate the effects of different doses Alpha-Linolenic acid ( ALA ) on the expressions of fatty acid synthesis-related genes in HepG2 cells.Methods HepG2 cells were divided into two groups, normal control group (NC) and high fat group (HF) in which cells were firstly cultured for 36h in the medium contained 0.5mmol/L stearic acid.Real-time quantitative PCR was taken to detect mRNA expression of genes SREBP1C, FAS and ACC which are related to fatty synthesis.While there are significant differences in fatty synthesis, 10%, 20%, 50%, 70% and 100%ALA took the place of stearic acid, 36h later, real-time quantitative PCR and Western blotting were taken to detect mRNA and protein expression of genes related to fatty synthesis.Results SREBP1C mRNA expression of ALA substitution groups were significantly lower than the high-fat group ( P <0.001) .The FAS of 0.5 mmol/L ALA group and 0.35 mmol/L ALA group were significantly lower than the high-fat group (P <0.001).ACC genes mRNA level was not significantly different from high-fat group.SREBP1C and FAS protein expression were significantly lower than the high-fat group, but ACC showed no significant difference.Conclusions Saturated fatty acids promote hepatocyte fatty acid synthesis, ALA abates fatty acid synthesis by inhibiting FAS and SREBP1C gene expression.

OBJECTIVE: To study the effects of adenovirus-mediated tissue factor pathway inhibitor-2 gene on the invasion of laryngeal squamous cancer. METHOD: Ad-TFPI-2 was transfected into laryngeal squamous cancer (Hep-2) cell. Western-blot was used to test the TFPI-2 protein expression and Boyden Chamber experiment was used to examine the invasive ability of Hep-2 cells. Furthermore, the Ad-TFPI-2 infected Hep-2 cells were subcutaneously inoculated in nude mice and the tumor formation capability were observed. RESULT: Ad-TFPI-2 was identified correctly by endonuclease and sequencing and the virus titer was 2.8 x 10(13) PFU/L. In the Hep-2 cells of treated group, the TFPI-2 protein expression was increased while the invasive capability was descent. The tumor formation capability was also decreased in the treated group nude mouse model. CONCLUSION TFPI-2 recombinant adenovirus can effectively inhibit the invasive capability of laryngeal squamous cancer.
Adenoviridae ; genetics ; Animals ; Carcinoma, Squamous Cell ; pathology ; Cell Line, Tumor ; Genetic Therapy ; Genetic Vectors ; Glycoproteins ; genetics ; Humans ; Laryngeal Neoplasms ; pathology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Transfection

In the context of non-alcoholic fatty liver disease (NAFLD), characterized by dysregulated lipid metabolism in hepatocytes, the quest for safe and effective therapeutics targeting lipid metabolism has gained paramount importance. Sanhuang Xiexin Tang (SXT) and Baihu Tang (BHT) have emerged as prominent candidates for treating metabolic disorders. SXT combined with BHT plus Cangzhu (SBC) has been used clinically for Weihuochisheng obese patients. This retrospective analysis focused on assessing the anti-obesity effects of SBC in Weihuochisheng obese patients. We observed significant reductions in body weight and hepatic lipid content among obese patients following SBC treatment. To gain further insights, we investigated the effects and underlying mechanisms of SBC in HFD-fed mice. The results demonstrated that SBC treatment mitigated body weight gain and hepatic lipid accumulation in HFD-fed mice. Pharmacological network analysis suggested that SBC may affect lipid metabolism, mitochondria, inflammation, and apoptosis-a hypothesis supported by the hepatic transcriptomic analysis in HFD-fed mice treated with SBC. Notably, SBC treatment was associated with enhanced hepatic mitochondrial biogenesis and the inhibition of the c-Jun N-terminal kinase (JNK)/nuclear factor-kappa B (NF-κB) and extracellular signal-regulated kinase (ERK)/NF-κB pathways. In conclusion, SBC treatment alleviates NAFLD in both obese patients and mouse models by improving lipid metabolism, potentially through enhancing mitochondrial biogenesis. These effects, in turn, ameliorate inflammation in hepatocytes.
Humans ; Mice ; Animals ; Non-alcoholic Fatty Liver Disease/metabolism* ; NF-kappa B/metabolism* ; Organelle Biogenesis ; Retrospective Studies ; Mice, Inbred C57BL ; Obesity/metabolism* ; Liver ; Inflammation/metabolism* ; Body Weight ; Lipid Metabolism ; Lipids ; Diet, High-Fat/adverse effects*