Abstract

Hemin–nitrite–H 2O 2 system may play a role in liver oxidative injury in some pathological events. In this paper, the effects of the three active components of the root of Scutellaria baicalensis Georgi, i.e. baicalin, baicalein and wogonin, on hemin–nitrite–H 2O 2 induced liver injury were studied in liver homogenate, liver microsome and human hepatoblastoma cell line HepG2 cells. It was found that hemin–nitrite–H 2O 2 could induce liver homogenate protein nitration, lipid peroxidation and liver microsome protein oxidation; it also caused a decrease of HepG2 cells viability. Baicalein, baicalin and wogonin could inhibit protein nitration and lipid peroxidation in liver homogenate as well as in HepG2 cells in a dose-dependent manner, the inhibition order was baicalein > baicalin ≫ wogonin. These three flavonoids also inhibited the oxidation of protein in liver microsome, the decrease of cell viability and the content of GSH in HepG2 cells, among which baicalin represented the most inhibitory effect. Besides, hemin–H 2O 2 induced cell injury could be augmented with the existence of nitrite, indicating protein nitration involved in hemin–nitrite–H 2O 2 induced liver injury. These results demonstrated hemin–nitrite–H 2O 2 could induce liver injury through oxidizing or nitrating different biomolecules. Baicalein, baicalin and wogonin could inhibit hemin–nitrite–H 2O 2 induced liver injury in dose-dependent manners by inhibiting oxidation and nitration.

Full Text
Paper version not known

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 call

Disclaimer: 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.