Abstract
ObjectiveAs an environmental endocrine disruptor, mono-2-ethylhexyl phthalate (MEHP) can interfere with liver metabolism and lead to liver diseases. We aimed to investigate the role of MEHP in liver fibrosis and its molecular mechanism. MethodsBRL-3A hepatocytes were exposed to MEHP (0, 10, 50, 100 and 200 μM) for 24 h. STAT5A gene was overexpressed by lentivirus transfection. The reactive oxygen species (ROS) was tested by the flow cytometer. The malondialdehyde (MDA), glutathione peroxidase (GSH-PX), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were detected by commercial kits. Real-Time PCR and Western blot were performed to test the relative mRNA and proteins levels, respectively. ResultsMEHP exposure significantly induced oxidative damage in BRL-3A cells, which inhibited the expression of STAT5A and promoted the expression of fibrosis related proteins MMP2, MMP9, TIMP2 and CTGF. After over-expression of STAT5A gene in BRL-3A cells, the elevated expression levels of CTGF, MMP2, MMP9 and TIMP2 induced by MEHP exposure were significantly reversed. ConclusionThis study demonstrated that MEHP exposure inhibited the expression of STAT5A by causing oxidative damage in BRL-3A hepatocytes, thus accelerating the expression of key molecules in fibrosis and promoting the occurrence of liver fibrosis.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
