The inhibitory effects of selenium nanoparticles modified by fructose-enriched polysaccharide from Codonopsis pilosula on HepG2 cells

The morbidity and mortality of hepatocellular carcinoma, the most common cancer, are increasing continuously worldwide. Galangin (Ga) has been demonstrated to possess anti-cancer effect, but the efficacy of Ga was limited by its low permeability and poor solubility. To develop aqueous formulation and improve the anti-cancer activity of Ga, surface decoration of functionalized selenium nanoparticles with Ga (Se@Ga) was synthesized in the present study. The aim of this study was to evaluate the anti-cancer effect of Se@Ga and the mechanism on HepG2 cells. Se@Ga-induced HepG2 cell apoptosis was confirmed by depletion of mitochondrial membrane potential, translocation of phosphatidylserine and caspase-3 activation. Furthermore, Se@Ga enhanced the anti-cancer activity of HepG2 cells through ROS-mediated AKT and p38 signalling pathways. In summary, these results suggest that Se@Ga might be potential candidate chemotherapy for cancer.

Download Full-text

Morin Exerts Anti-Diabetic Effects in Human HepG2 Cells Via Down-Regulation of miR-29a

Experimental and Clinical Endocrinology & Diabetes ◽

10.1055/a-0650-4082 ◽

2018 ◽

Vol 127 (09) ◽

pp. 615-622 ◽

Cited By ~ 2

Author(s):

Toktam Razavi ◽

Shideh Montasser Kouhsari ◽

Khalil Abnous

Keyword(s):

Insulin Signaling ◽

High Glucose ◽

Hepg2 Cells ◽

Target Genes ◽

Expression Level ◽

Inhibitory Effects ◽

Down Regulation ◽

Insulin Mimetic ◽

Important Regulator ◽

First Time

Abstract Diabetes mellitus is a complex metabolic disease around the world that is characterized by hyperglycemia resulting from impaired insulin secretion, insulin action, or both. MicroRNA-29a is an important regulator of insulin signaling and gluconeogenesis pathways through IRS2, PI3K and PEPCK expressions which up regulates in Diabetes. Morin is a substantial bioflavonoid which has insulin mimetic effect, and interacting with nucleic acids and proteins. In this study HepG2 cells, were exposed to high glucose to induce diabetic condition. We have determined whether high glucose stimulation might promotes miR-29a expression level in HepG2 cells and subsequently evaluated the Morin treatment effects on this state. In HepG2 cells, high glucose increases miR-29a expression level and decreases its target genes, IRS2 and PI3K expression, and increases associated downstream gene in gluconeogenic pathway, PEPCK. Morin treatment down regulates miR-29a expression level and improves insulin signaling and glucose metabolism. To confirm the inhibitory effects of Morin on miR-29a, we have transfected cells with mimic and inhibitor-miR-29a. This study for the first time identifies that Morin improves diabetic condition through down regulation of the miR-29a level, and suggest that this new inhibitor of miR-29a may be a useful biomedicine to treat diabetes.

Download Full-text

Antioxidant Capacity of Proteins and Hydrolysates from the Liver of Newborn Piglets, and Their Inhibitory Effects on Steatosis in vitro

Food Technology and Biotechnology ◽

10.17113/ftb.58.04.20.6657 ◽

2020 ◽

Vol 58 (4) ◽

Author(s):

Ruilin Zhang ◽

Lasheng Yin ◽

Jian Chen ◽

Xuewu Zhang

Keyword(s):

Oleic Acid ◽

Hepg2 Cells ◽

Early Stage ◽

Lipid Lowering ◽

Inhibitory Effects ◽

Hepatic Disorder ◽

Newborn Piglets ◽

End Stage ◽

Lipid Lowering Effect

Research background. Non-alcoholic steatohepatitis is a potentially progressive hepatic disorder that can lead to end-stage liver disease and hepatocellular carcinoma. The inhibitory effects of proteins and hydrolysates from the liver of newborn piglets on hepatic steatosis in oleic-acid-induced HepG2 cells were investigated in vitro. Experimental approach. The extracted proteins from the liver of newborn piglets (NPLP) were hydrolysed with papain, pepsin, trypsin and Alcalase. Based on comparison of different enzyme digestion condition, a protein hydrolysis protocol was established to obtain hydrolysates with lipid-lowering effect. Results and conclusions. NPLH-trypsin (trypsin-digested NPLP hydrolysate) exhibited strong antioxidant activity and possessed good inhibitory effects on lipogenesis and cholesterol accumulation in HepG2 cells at 150 μg/mL, with a triglyceride decrease of (43±3) % and cholesterol decrease of (31±5) %, comparing with 0.75 mM oleic acid induced model. The addition of NPLH-trypsin (300 μg/mL) decreased alanine aminotransferase and aspartate aminotransferase activities and increased superoxide dismutase activity. Novelty and scientific contribution. This study demonstrated that NPLH-trypsin have a potential preventive effect on NAFLD in its early stage, and NPLH-trypsin has potential use as the modulator of lipid overaccumulation disease in food supplements.

Download Full-text

Inhibitory effects and molecular mechanisms of pentagalloyl glucose in combination with 5-FU on aggressive phenotypes of HepG2 cells

Natural Product Research ◽

10.1080/14786419.2019.1598991 ◽

2019 ◽

pp. 1-4

Author(s):

Xiao-Qing Ding ◽

Shuang Zhao ◽

Jian-Ye Wang ◽

Hua-chuan Zheng ◽

Chao-Mei Ma

Keyword(s):

Hepg2 Cells ◽

Molecular Mechanisms ◽

Inhibitory Effects ◽

Pentagalloyl Glucose

Download Full-text

A New Cytotoxic Cyclolanostane Triterpenoid Xyloside from Souliea vaginata

Natural Product Communications ◽

10.1177/1934578x1701200222 ◽

2017 ◽

Vol 12 (2) ◽

pp. 1934578X1701200 ◽

Cited By ~ 1

Author(s):

Haifeng Wu ◽

Zhixin Yang ◽

Qiru Wang ◽

Nailiang Zhu ◽

Xudong Xu ◽

...

Keyword(s):

Cell Lines ◽

Cancer Cell ◽

Hepg2 Cells ◽

Human Cancer ◽

Cancer Cell Lines ◽

Hepatoprotective Effect ◽

Human Cancer Cell ◽

Inhibitory Effects ◽

Chemical Methods ◽

Human Cancer Cell Lines

A new cyclolanostane triterpenoid xyloside, soulieoside P (1), and a known oleanane-type saponin, hederasaponin B (2), were isolated from the rhizomes of Souliea vaginata. Their structures were established by extensive spectroscopic and HRESIMS analysis, as well as chemical methods. Compound 1 showed significant inhibitory effects with IC50 values of 7.6–11.2 μM against three human cancer cell lines, while compound 2 exhibited no hepatoprotective effect on CCl4-induced injury of human HepG2 cells, in the tested range of 0.1–100 μM.

Download Full-text

Inhibition of Liver Tumor Cell Metastasis by Partially Acetylated Chitosan Oligosaccharide on A Tumor-Vessel Microsystem

Marine Drugs ◽

10.3390/md17070415 ◽

2019 ◽

Vol 17 (7) ◽

pp. 415 ◽

Cited By ~ 2

Author(s):

Bolin Jing ◽

Gong Cheng ◽

Jianjun Li ◽

Zhuo A. Wang ◽

Yuguang Du

Keyword(s):

Tumor Cells ◽

Liver Tumor ◽

Hepg2 Cells ◽

Tumor Metastasis ◽

Inhibitory Effect ◽

Chitosan Oligosaccharide ◽

Inhibitory Effects ◽

Tumor Vessel ◽

Destructive Effect ◽

Cell Metastasis

Chitooligosaccharides (COS), the only cationic oligosaccharide in nature, have been demonstrated to have anti-tumor activity. However, the inhibitory effects of COS on different stages of tumor metastasis are still unknown, and it is not clear what stage(s) of tumor metastasis COS targeted. To study the inhibitory effects of a new partially acetylated chitooligosaccharide (paCOS) with fraction of acetylation (FA) 0.46 on each phase of liver cancer cell metastasis, a dynamic tumor-vessel microsystem undergoing physiological flow was leveraged. paCOS (FA = 0.46) significantly inhibited proliferation of HepG2 cells through vascular absorption on the chip, and inhibited migration of HepG2 cells by inhibiting the formation of pseudopod in liver tumor cells. It was also found that paCOS at 10 μg/mL had a stronger inhibitory effect on liver tumor cells invading blood vessels than that of paCOS at 100 μg/mL, and paCOS at 100 μg/mL, which had a significant destructive effect on tumor vascular growth and barrier function. Moreover, paCOS reduced the number of liver tumor cells adhering onto the surface of HUVECs layer after 3 h of treatment. Therefore, the results revealed that paCOS had considerable potential as drugs for anti-tumor metastasis.

Download Full-text

PEG-nanolized ultrasmall selenium nanoparticles overcome drug resistance in hepatocellular carcinoma HepG2 cells through induction of mitochondria dysfunction

International Journal of Nanomedicine ◽

10.2147/ijn.s30940 ◽

2012 ◽

pp. 3939 ◽

Cited By ~ 9

Author(s):

Tianfeng Chen ◽

Zheng ◽

Li ◽

Zhang ◽

Zheng ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Drug Resistance ◽

Hepg2 Cells ◽

Selenium Nanoparticles ◽

Mitochondria Dysfunction

Download Full-text

Dihydromyricetin Attenuates Palmitate Acid-Induced Oxidative Stress by promoting Autophagy via SIRT3-ATG4B Signaling in Hepatocytes

10.21203/rs.3.rs-295541/v1 ◽

2021 ◽

Author(s):

Mantian Mi ◽

Li Huang ◽

Xianglong Zeng ◽

Bo Li ◽

Cong Wang ◽

...

Keyword(s):

Oxidative Stress ◽

Hepg2 Cells ◽

Underlying Mechanism ◽

Protective Effects ◽

Inhibitory Effects ◽

Potential Therapeutic Target ◽

Mitochondrial Ros ◽

Intracellular Ros ◽

Protein Expressions ◽

And Oxidative Stress

Abstract Background Oxidative stress in hepatocytes was an important pathogenesis of nonalcoholic steatohepatitis (NASH). Autophagy was a cellular process that can remove damaged organelles under oxidative stress, and thus presented a potential therapeutic target against NASH. The aim of this work was to investigate whether autophagy participated the protective effects of dihydromyricetin (DHM) on palmitic acid (PA)-induced oxidative stress in hepatocytes and the underlying mechanism. Methods HepG2 cells were pretreated with DHM (20 µM) for 2 h, followed by PA (0.2 mM) treatment for 16 h. The oxidative stress was assessed by the quantification of intracellular reactive oxygen species (ROS), mitochondrial ROS (mtROS), mitochondrial membrane potential (MMP) and mitochondrial ultrastructural analyses. The protein expressions of SIRT3, LC3I/II, P62 and ATG4B, as well as the acetylation of AGT4B were determined by western blotting using HepG2 and HepG2/ ATG4B+/− cells with heterozygous knockout of ATG4B. Results Exposure to PA resulted in increased intracellular ROS and mtROS, decreased MMP and aggravated mitochondrial injury in HepG2 cells, which were notably attenuated by DHM treatment. DHM-induced inhibition of oxidative stress was associated with the induction of autophagy, characterized by upregulated ATG4B and LC3 II as well as downregulated P62 levels. Furthermore, the inhibitory effects of DHM on PA-induced autophagy arrest and oxidative stress were eliminated when pretreated with a SIRT3 inhibitor 3-TYP or conducted in HepG2/ATG4B+/− cells, suggesting that SIRT3 and ATG4B were involved in DHM-induced benefits. Moreover, DHM treatment increased the protein expression of SIRT3 and SIRT3-dependent deacetylation of ATG4B in HepG2 cells. Conclusion Our results demonstrated that DHM attenuated PA-induced oxidative stress in hepatocytes through induction of autophagy, which was mediated through the increased expression of SIRT3 and SIRT3-mediated ATG4B deacetylation following DHM treatment.

Download Full-text