Quantum dots enhance Cu^(2+)-induced hepatic L02 cells toxicity

As a new class of xenogenous nanoparticle, quantum dots （QDs） possess the potential to co-exist with Cu^2＋ in human liver. The combined toxicity is thus concerned. Considering QDs and Cu^2＋ are known ROS （reactive oxygen species） inducer, we investigated the combined oxidative stress and corresponding protective strategy using human hepatic L02 cells. The results demonstrated that the presence of a small amount of MPA-CdTe QDs （2 μg/mL） in a Cu^2＋ solution （2.5-20 μg/mL） resulted in a higher toxicity with up to 8-fold cell viability decrease, which was accompanied by cell morphology changes. The combined toxicity was then confirmed as ROS associated oxidative stress with up to 300% and 35% increase of the intracellular ROS level and glutathione S-transferase （GST） activity, respectively. N-acetylcysteine （NAC） can also provide almost complete protection against the induced toxicity. Therefore, the ROS associated oxidant injury might be responsible for the QDs-Cu^2＋/Cu^2＋ induced toxicity and could be balanced through cytoprotective antioxidant enzyme GST.

Protective effects of docosahexaenoic acid against non-alcoholic hepatic steatosis through activating of JAK2/STAT3 signaling pathway

Non-alcoholic fatty liver disease is the most common cause of hepatic dysfunction.In the present study,human normal hepatocyte L02 cells were treated with 50%fetal bovine serum to induce the formation of hepatic steatosis in vitro,and then the cells were treated with docosahexaenoic acid to investigate its protective effect on Non-alcoholic fatty liver disease.Our results showed that 50%of fetal bovine serum significantly induced intracellular lipid accumulation and hepatocyte fatty degeneration within 48 h.The expression level of adipose formation-related genes was significantly up-regulated,such as PPARγ,C/EBPαand SREBP-1;meanwhile,the content of cellular total lipid,total cholesterol and triglycerides were significantly increased after 50%fetal bovine serum treatment.Interestingly,docosahexaenoic acid treatment could inhibit FBS-induced intracellular lipid accumulation in L02 cells and the expression of lipogenic genes.Moreover,docosahexaenoic acid treatment could reduce hepatic steatosis-induced oxidative stress and endoplasmic reticulum stress response,and these responses were shown by the modification of antioxidant enzyme activities and GRP78,CHOP expression.In addition,the results showed that docosahexaenoic acid can activate the JAK2/STAT3 signaling pathway in fatty liver L02 cell;inhibition of JAK2/STAT3 signaling pathway by WP1066 abolished the beneficial effects of docosahexaenoic acid on hepatic steatosis accompanied with the increased expression of lipogenic genes and endoplasmic reticulum stress response.Above all,the present study showed that docosahexaenoic acid can alleviate non-alcoholic hepatic steatosis by activating JAK2/STAT3 signaling pathway.

Differential Proteomics in Malignant and Normal Liver Cell Lines

Objective： To detect differential protein expression in malignant and normal liver cell lines in vitro using the SELDI ProteinChip platform, for investigating the pathogenesis of liver cancer. Methods： Two cell lines, human normal liver cell line L02 and hepatoma cell line SMMC-7721 were cultured routinely, harvested in good condition and lysed. After quantification, the supernatant of the lysate was tested by IMAC3 （Immobilized Mental Affinity Capture） and WCX2 （Weak Cation Exchange） chips on the SELDI-TOF-MS ProteinChip reader. Results： Protein expression differed between the malignant and normal liver cell lines. A total of 20 differentially expressed proteins were found, among which, 7 were captured by the IMAC3 chip and 14 by the WCX2 chip. Peaks at 5,419, 7,979 and 11,265 Da were higher and at 8,103, 8,492, 10,160 and 11,304 Da lower in SMMC-7721 cells by the IMAC3 chip; peaks at 7,517, 7,945 and 7,979 Da were higher and at 5,061, 5,551, 5,818, 7,439, 9,401,10,100, 10,312, 11,621, 11,662, 11,830 and 12,772 Da lower in SMMC-7721 cells by the WCX2 chip. Interestingly, both chips captured the 7,979 Da peak. In addition, the 11,081 Da peak corresponded precisely with the molecular mass of the calcium binding protein S100A10, which may participate in the formation of liver cancer in association with p36. Conclusion： Detecting differential protein expression in malignant and normal liver cell lines using the SELDI ProteinChip platform was simple, sensitive and repeatable. The results we obtained can serve as a basis for investigating the pathogenesis of liver cancer and aid the discovery of new therapeutic targets.