| Marshall [1] formally proposed the concept of gut-liver axis in 1998.The gut-liver axis have a common embryonic origin: foregut, intestinal lymphocytes are derived from the the developed liver. A large number of studies show that liver and intestine have a close relationship in the anatomical and biological functions. On the anatomical position, portal bridge links the liver and intestines,80% blood of the liver originate from the portal vein which includes nutrients from the gut, food antigens, bacterial products and environmental toxins.Acute liver injury can be caused by various reasons.acute liver injury will occur after a series of complications, severe acute liver failure will occur. When liver damage, liver Kupffer cell function will be suppressed, on the one hand the gut bacteria and endotoxin would lead to the invasion of the blood circulatory system intestinal infections; hand-invasive liver endotoxin activates Kupffer s cells, a variety of inflammatory cytokines are released, these interactions further aggravate inflammatory cytokines damage the intestinal mucosal barrier.Defensin play an important protective role in the intestinal epithelial cells. β- defensin 2(β- defensin-2, HBD-2) is a hot topic of research. β- defensin 2 as an inducible expression of defensin is mainly expressed in the skin, respiratory, gastrointestinal, it has broad antimicrobial activity, which composes of the important elements of the innate immune system and acquired immunity. How to liver injury gut β- defensin 2 expression? This experiment established different models of acute liver injury, acute liver injury was to explore different gut β- defensin 2 expression.Objective: To establish the different liver injury models, observe the expression of β- defensin 2 in intestinal.Methods: ① healthy SD rats were randomly divided into three groups:CCL4-treated group, 2-AAF / PH group and control group. The animals were killed and take out the liver tissue and small intestine at the first day, 7th day, 14 th day and 21 st dayand. ②using hematoxylin & eosin staining(H & E staining) were observed in rat liver and small intestine tissue histopathologic performance. ③Western Blotting Detection Technology observe β- defensin-2 expression in the intestine. ④RT-PCR observe β- defensin 2 gene expression in the intestine.Results: ①Compared with the control group, the 2-AAF / PH group, liver color is light red, crisp at the first day,it got back to normal about at 21 th days. CCL4-treated group with which to compare, rat liver dark red, crisp, it got back to normal about at 14 th days; ②liver tissue H & E showed that compared with the control group, the CCL4-treated group, 2-AAF / PH group showed liver cell swelling, disorder, inflammatory cell infiltration. 2-AAF / PH group, inflammatory cell infiltration than CCL4-treated group, cell swelling most serious. ③intestinal pathology results show, 2-AAF / PH group of intestinal mucosal injury is more serious intestinal mucosal shedding, intestinal villi disorder, inflammatory cell infiltration, with the restoration of liver injury, returned to normal intestinal injury; CCL4-treated group of intestinal mucosal injury compared 2AAF / PH group light, mild intestinal mucosal shedding a little inflammatory cell infiltration, but also with the repair of liver injury, returned to normal intestinal mucosa. ④Liver function tests: there is no significant difference in control group; ALT,AST and ALP were significantly increased in CCL4-treated group, 2-AAF/PH group compared with the control group(ALT: 47.01 ± 9.36 U / L vs 41.98 ± 6.65 U / L, P <0.05; 249.1 ± 19.72 U / L vs 41.98 ± 6.65 U / L, P <0.05; AST: 133.96 ± 14.36 U / L vs 82.48 ± 21.87 U / L, P <0.05; 557.97 ± 12.86 U / L vs 82.48 ± 21.87 U / L, P <0.05; ALP: 270.32 ± 36.08 U vs 53.27 ± 8.51 U, P <0.05; 520.67 ± 33.01 U vs 53.27 ± 8.51 U, P <0.05;), albumin(albumin, ALB) levels were significantly decreased(23.36 ± 2.22 g / L vs 32.14 ± 3.73 g / L, P <0.05; 23.9 ± 1.05 g / L vs 32.14 ± 3.73 g / L, P <0.05). The liver function change of 2- AAF/PH group is large compared with CCL4-treated group.⑤β- defensin 2 changes: RT-PCR results showed that the control group 1 days, 7 days, 14 days, 21 days no significant difference at all time points(1.090 ± 0.004 1.092 ± 0.003 1.089 ± 0.002 1.087 ± 0.002 P> 0.05); CCL4-treated group and 2-AAF / PH group amount β- defensin 2 m RNA, and one day, 7 days, 14 days three time points with the blank control group, have increased, with statistical significance(P <0.05), the first 21 days with no control group significant difference was not statistically significant(P> 0.05), 2-AAF / PH group and CCL4-treated group 1 days, 7 days, 14 days compared to significantly increased, with statistical significance(P <0.05), 21 Compared with that of carbon tetrachloride group, no significant changes were not statistically significant(P> 0.05), no significant change(p in the control group at each time point> 0.05); Western Blot results are consistent with the results of PCR, 2-AAF / PHβ- defensin-2 protein expression levels of group 1 days, 7 days, 14 days(1.90 ± 0.07 1.60 ± 0.02 1.41 ± 0.01) than the control group( 1.04 ± 0.03 1.04 ± 0.03 1.03 ± 0.01) was significantly increased, the difference was statistically significant P <0.05, 21 days(1.06 ± 0.06) and the control group(1.04 ± 0.03) showed no significant change was not statistically significant(P > 0.05), 2-AAF / PH trend for the first 1-21 days of decline, the first 21 days and the control group is consistent; CCL4-treated group 1 days, 7 days, 14 days and the control group over time a downward trend, with statistical significance P <0.05,21 day was no significant difference(P> 0.05); and 2-AAF / PH group than CCL4-treated group decreased more significantly among the three groups one day, seven days 14 days the difference was statistically significant P <0.05,21 days no significant difference(P> 0.05).Conclusions: β- defensin 2 in acute liver injury in rats increased expression of the small intestinal tract, and with the severity of mucosal damage rises. |
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