Effect ofHelicobacter pyloriinfection on growth of normal human liver cells (L-02)

2014 ◽  
Vol 22 (7) ◽  
pp. 956
Author(s):  
Li Liu
2020 ◽  
Vol 40 (12) ◽  
pp. 1661-1672
Author(s):  
An‐liu Zhang ◽  
Shun‐fang Tang ◽  
Yue Yang ◽  
Chang‐zhe Li ◽  
Xue‐jiao Ding ◽  
...  

2021 ◽  
Vol 41 (4) ◽  
pp. 650-650
Author(s):  
An‐liu Zhang ◽  
Shun‐fang Tang ◽  
Yue Yang ◽  
Chang‐zhe Li ◽  
Xue‐jiao Ding ◽  
...  

2013 ◽  
Vol 7 (6) ◽  
pp. 1970-1976 ◽  
Author(s):  
SHAO-KANG WANG ◽  
SHA LIU ◽  
LI-GANG YANG ◽  
RUO-FU SHI ◽  
GUI-JU SUN

Chemosphere ◽  
2020 ◽  
Vol 239 ◽  
pp. 124747 ◽  
Author(s):  
Ningning Chen ◽  
Qiuli Shan ◽  
Yu Qi ◽  
Wei Liu ◽  
Xiaojun Tan ◽  
...  

Toxins ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 164 ◽  
Author(s):  
Lv Chen ◽  
Shu Yang ◽  
Cong Wen ◽  
Shuilin Zheng ◽  
Yue Yang ◽  
...  

Microcystin-LR is a cyclic heptapeptide hepatotoxin produced by harmful cyanobacteria. A panel of microRNAs containing miR-451a were found to be significantly changed in normal human liver cells HL7702 after exposure to microcystin-LR (MC-LR) in our previous study. However, the functions of miR-451a in hepatotoxicity induced by MC-LR remained unclear. The study aimed to investigate the impacts of miR-451a in HL7702 cells following treatment with 5 or 10 μM MC-LR. The comet assay indicated that MC-LR can influence Olive tail moment (OTM) in HL7702 cells. Furthermore, increase of miR-451a significantly repressed DNA damage and the protein expression level of γ-H2AX induced by MC-LR. Moreover, over-expression of miR-451a inhibited the expression level of p-AKT1 protein in cells following treatment by MC-LR. These results showed that miR-451a may protect from MC-LR-induced DNA damage by down-regulating the expression of p-AKT1, which provides new clues for the diagnosis and therapy policies for liver damage induced by MC-LR.


Author(s):  
Reza Afrisham ◽  
Sahar Sadegh-Nejadi ◽  
Reza Meshkani ◽  
Solaleh Emamgholipour ◽  
Molood Bagherieh ◽  
...  

Introduction: Obesity is a disorder with low-grade chronic inflammation that plays a key role in the hepatic inflammation and steatosis. Moreover, there are studies to support the role of exosomes in the cellular communications, the regulation of metabolic homeostasis and immunomodulatory activity. Accordingly, we aimed to evaluate the influence of plasma circulating exosomes derived from females with normal-weight and obesity on the secretion of inflammatory cytokines in human liver cells. Methods: Plasma circulating exosomes were isolated from four normal (N-Exo) and four obese (O-Exo) women. The exosomes were characterized and approved for CD63 expression (common exosomal protein marker) and morphology/size using the western blot and TEM methods, respectively. The exosomes were used for stimulation of HepG2 cells in vitro. After 24 h incubation, the protein levels of TNF-α,IL-6, and IL-1β were measured in the culture supernatant of HepG2 cells using the ELISA kit. Results: The protein levels of IL-6 and TNF-α in the cells treated with O-Exo and N-Exo reduced significantly in comparison with control group (P=0.039 and P<0.001 respectively), while significance differences were not found between normal and obese groups (P=0.808, and P=0.978 respectively). However, no significant differences were found between three groups in term of IL-1β levels (P=0.069). Based on the correlation analysis, the protein levels of IL-6 were positively correlated with TNF-α (r 0.978, P<0.001). Conclusion: These findings suggest that plasma circulating exosomes have probably anti-inflammatory properties independently from body mass index and may decrease the secretion of inflammatory cytokines in liver. However, further investigations in vitro and in vivo are needed to address the anti-inflammatory function of N-Exo and O-Exo in human liver cells and/or other cells.


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