Hepatoprotective effects of Roxb. extract via free radical scavenger, inhibiting apoptosis and inflammation mechanisms in acetaminophen-induced liver injury.

OBJECTIVES

Acetaminophen (APAP)-mediated liver injury poses a significant public health concern. extract (CXE) has been traditionally used for its hepatoprotective properties. This research aimed to assess the hepatoprotective effects of CXE in APAP-mediated hepatotoxicity by investigating the modulatory effects of CXE on key biomarkers, including Interleukin (IL), namely, (IL-6), IL-10, IL-1β, Nitric Oxide (NO), Lactate Dehydrogenase (LDH), and the genes expression related to apoptosis-like Caspase-3 (Casp-3), Casp-9, and genes related to liver metabolic c-Jun N-terminal Kinase (JNK), in APAP-mediated HepG2 cells.

MATERIALS AND METHODS

APAP-induced HepG2 cells were treated with different concentrations of CXE. IL-6, IL-10, IL were measured using an Enzyme-linked Immunosorbent Assay (ELISA) and NO, LDH were measured using colorimetric assay. Gene expression was analyzed using quantitative Real-Time Reverse Transcription (qRT-PCR).

RESULTS

CXE significantly reduced IL-1β and IL-6 levels, enhanced IL-10 production, and attenuated NO levels in APAP-mediated hepatotoxicity. CXE also suppressed the expression of Casp-9, Casp-3, JNK, and LDH levels. The study presented a concentration-dependent response, with 125 μg/ml CXE exhibiting the most pronounced effects. CXE effectively modulated immune responses, decreased oxidative stress, and inhibited apoptotic and inflammatory pathways in APAP-mediated hepatotoxic cells.

CONCLUSION

These studies highlight the CXE potential as a therapeutic candidate for liver disorders, particularly in drug-mediated liver injury.