The aim of this study is to evaluate differential expression of different isoforms of NOX in early phase of liver injury and its mechanism to develop inflammation and cellular senescence.
C57BL/6 mice were treated with carbone tetra chloride (CCl4) (0.2 and 0.5 ml/kg) thrice in a week by ip route to develop a acute liver injury models and Di phenyl indinium chloride (DPI) is injected 30 min prior to CCl4 injection. Batches of mice were sacrificed after 3rd injection to evaluate the role of isoforms of NADPH oxidase. Liver histology, immunohistochemistry, b-galactosidase activity, Western blotting, Real Time PCR were performed.
Among different isoforms of NOX in the liver NOX2 is expressed in significantly (p<0.001) high amount in response to CCl4 treatment mainly in kupffer cells resulting in inflammation and subsequently cellular senescence. Administration of a NOX inhibitor (DPI) resulted in marked reduction the NOX expression, liver injury and inflammation which ultimately reduce cellular senescence.
As mainly the expression of phagocytic NOX2 is high in early phase of liver injury resulting inflammation and senescence NOX2 may be a therapeutic target to reduce early phase of liver injury.
Impact Factor
2022: 6.012
This work is licensed under a