Published online Mar 28, 2020. doi: 10.3748/wjg.v26.i12.1286
Peer-review started: November 5, 2019
First decision: December 5, 2019
Revised: January 8, 2020
Accepted: February 28, 2020
Article in press: February 28, 2020
Published online: March 28, 2020
Processing time: 144 Days and 6.1 Hours
Tamarix chinensis Lour (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.
To investigate the possible protective effects of TCL against liver injury induced by chronic ethanol intake.
Eighty C57BL/6J male mice (8-10 wk old) were purchased from Beijing HFK Bioscience Co. Ltd. (Beijing, China).
The mice were randomly assigned to the following 5 groups: Control (Ctrl) group, ethanol (EtOH) group, reduced glutathione (GSH) group as the positive Ctrl (EtOH + GSH at 86 mg/kg BW), and two TCL groups (EtOH + TCL-L at 100 mg/kg BW and EtOH+TCL-H at 200 mg/kg BW). Histological examination of the liver was done after staining sections with hematoxylin-eosin. Alanine aminotransferase and aspartate aminotransferase are commonly used as biochemical indicators of liver injury. TCL inhibits hepatic expression of NOD-like receptor family, pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein (ASC), caspase-1, and interleukin (IL)-1β at the transcriptional and protein levels by Western blotting. Hepatic expression of NLRP3, ASC, caspase-1 and IL-1β mRNA was also measured by quantitative PCR. Hepatic lymphocytes were isolated by Discontinuous Percoll Gradient Centrifugation and immunostained with fluorescent antibodies (FITC-CD3 and PE-CY7-NK1.1). Fluorescence was detected by using a BD FACS caliber flow cytometry and data were analyzed with FLOW JO 7.6.1software. Liver homogenate was prepared and hepatic tissue levels of reactive oxygen species, malondialdehyde, and superoxide dismutase were determined by using commercial assay kits (Nanjing Jiancheng Bioengineering Institute, Nanjing, China). Statistical analyses were performed with SPSS 22.0 software. Values are expressed as the mean ± standard deviation. Between-group comparisons were evaluated by one-way analysis of variance (with Dunnett's test and Bonferroni's multiple comparison test). Statistical significance was established at P < 0.05. All experiments were performed at least in triplicate.
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 vs 45.3 IU/L, P < 0.01) and aspartate aminotransferase (mean, 89.6 IU/L vs 115.7 IU/L, P < 0.01), as well as marked reduction of hepatic tissue reactive oxygen species (decreased by 27.5%, P < 0.01) and malondialdehyde (decreased by 76.6%, P < 0.01) levels, with a significant increase of superoxide dismutase (Increased by 73.2%, P < 0.01). Expression of the NLRP3 inflammasome and its downstream cytokines (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.
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.
Our findings provide information that TCL may be a potential candidate for prevention and treatment of ethanol-induced liver damage.