RESUMO
Objective To observe the protective effect of Xiaohuangdecotion against liver damage inα-naphthylisothiocyanate (ANIT)- induced cholestasis in rats and probe the potential mechanisms.Methods Male Wistar rats (40) were randomly divided into a normal group, a model group, aXiaohuangdecotion treatment group, and a UDCA control group (10 for each). Except for rats in the normal group, ANIT solution (6 ml/kg) was administered in other rats by gavages for cholestasis model. After ANIT treated 48 h, rats inXiaohuangdecotion group and UDCA group were treated withXiaohuangdecotion (1.73 g/kg) and UDCA (10 mg/kg) respectively for 1 week. And, rats in the normal group and the model group were given an equal volume of saline. At the end of the experiment, liver function rats were examined. Liver histology was examined by HE staining, and CD68 factor was tested by immunohistochemistry and Western blot.Results Compared with the model group, the content of ALT (164.6 ± 53.4 U/Lvs. 208.4 ± 28.5 U/L), AST (247.6 ± 76.1 U/Lvs. 341.8 ± 32.8 U/L), ALP (601.0 ± 101.1 U/Lvs. 720.6 ± 123.3 U/L), TBiL (96.5 ± 18.1μmol/Lvs. 149.6 ± 30.2μmol/L), DBiL (73.7 ± 16.6μmol/Lvs. 140.3 ± 28.6μmol/L) and TBA (93.4 ± 13.0μmol/Lvs. 146.5 ± 38.9μmol/L) were significantly reduced in the treatment group (P<0.01 orP<0.05). Compared with the model group, CD68 level (7.08 ± 0.19 vs. 17.42 ± 0.48)were significantly reduced by intervention ofXiaohuangdecotion (P<0.01).ConclusionsXiaohuangdecotion could improve liver functions and reduce CD68 expression, leading to a good hepatoprotective and jaundice-relieving effects.
RESUMO
ObjectiveTo investigate the protective effects and mechanism of ursodeoxycholic acid (UDCA) on α-naphthylisothi (ANIT)-induced cholestatic liver injury in rats.MethodsA total of 48 Sprague-Dawley (SD) rats were selected.Fouty-two rats were gavaged with ANIT (100 mg/kg) to induce acute liver injury,six rats were sacrificed 24 hours after the liver injury and the rats left were evenly divided into control group which were gavaged with saline and UDCA group which were gavaged with UDCA (20 mg/kg).Six rats were sacrificed at 48 hours,72 hours and 96 hours after modeling.The six untreated rats were set as blank control group.Serum and liver tissues of all rats were kept after sacrificed.Serum levels of alanine transaminase (ALT),aspartate transaminase (AST),total bilirubin (TBil) and total bile acid (TBA) were tested,interleukin-10 (IL-10),interleukin-6 (IL-6),and tumor necrosis factor-α (TNF-α) were detected by enzyme linked immunosorbent assay (ELISA).The expression of multidrug resistance associated protein2 (Mrp2) at mRNA level in liver tissue was measured by quantitative real-time polymerase chain reaction (qRT-PCR) and the inflammatory reaction activity of liver tissues was inspected with Haematoidin-Eosin (HE)staining under microscope.ResultsAt 48 hours after liver injury modeling,serum TBil (143.80± 12.08) μmol/L vs.(178.50±15.19) μmol/L,TBA (13.15±3.81) μmol/L vs.(21.68±7.93)mol/L,IL-10 (44.13±3.68,37.15±6.25 ng/L),IL-6(50.80±2.09,57.32±4.63 ng/L) and TNF-α (17.53±0.84) ng/L vs,(19.10±1.64) ng/L of UDCA group and control group were compared,and the differences were statistically significant (P ＜ 0.01 or P＜ 0.05).At 72 hours after liver injury modeling,serum ALT (721.67±97.54) U/L vs.(929.50±148.29) U/L and IL-10 (54.68±6.79)ng/L vs.(43.85±4.08) ng/L of UDCA group and control group were compared,and the differences were statistically significant (P＜0.01 or P＜0.05).At 96 hours after liver injury modeling,serum ALT (156.83±14.99) U/L vs.(250.67±42.29) U/L,AST (143.67±27.45) U/L vs.(206.00±63.94) U/L and TBil (23.53±5.08) μmol/L vs.(34.02±9.98) μmol/L of UDCA group and control group were compared,and the differences were statistically significant (P＜0.01 or P＜0.05).The differences of Mrp2 expression at mRNA level in liver tissues between UDCA group and control group at 48 hours (0.77 ± 0.21,0.46 ± 0.25),72 hours (2.27 ±0.84,1.10 ±0.38) and 96 hours (3.64±0.54,2.75±0.69) after liver injury modeling were statistically significant (P＜0.01 or P＜0.05).ConclusionThe mechanism of the protective effects of UDCA on ANIT-induced liver injury may be related with the regulation of serum cytokines and liver Mrp2 expression.