inhibits chronic ethanol-induced liver injury in mice.

BACKGROUND

(TCL) is a shrub that usually grows in arid or semiarid desert areas and saline-alkali fields. It is a traditional Chinese herbal medicine with hepatoprotective, antioxidant, antibacterial, and antitumor activities.

AIM

To investigate the possible protective effects of TCL against liver injury induced by chronic ethanol intake.

METHODS

C57BL/6J male mice were fed a Lieber-DeCarli lipid diet containing alcohol and received (by gavage) a water-alcohol extract (80%) of TCL (100 and 200 mg/kg BW) or distilled water for 4 wk. After euthanasia, liver tissues were observed histologically with hematoxylin and eosin staining and Oil red O staining, and the levels of alanine aminotransferase, aspartate transaminase, hepatic lipids, reactive oxygen species, malondialdehyde, and superoxide dismutase were measured. In addition, expression of the NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome and downstream proinflammatory cytokines were determined.

RESULTS

Compared with the ethanol group, mice in the TCL-treated group (200 mg/kg) had significantly lower serum levels of alanine aminotransferase (mean, 34.1 IU/L 45.3 IU/L, < 0.01) and aspartate transaminase (mean, 89.6 IU/L 115.7 IU/L, < 0.01), as well as marked reduction of hepatic tissue reactive oxygen species (decreased by 27.5%, < 0.01) and malondialdehyde (decreased by 76.6%, < 0.01) levels, with a significant increase of superoxide dismutase (Increased by 73.2%, < 0.01). Expression of the NLRP3 inflammasome and its downstream cytokines [interleukin (IL)-1β, tumor necrosis factor-α, and IL-6], and recruitment of natural killer T cells to the liver, were reduced in the TCL-treated incubation with a Lieber-DeCaril ethanol lipid diet group.

CONCLUSION

These findings suggest that a TCL extract (200 mg/kg) protects against chronic ethanol-induced liver injury, probably by inhibiting the NLRP3-caspase-1-IL-1β signaling pathway and suppressing oxidative stress.