Objective To study the effect on expression of high mobility group box-1 （HMGB1） mRNA for the expression of zonula occludens-1 （ZO-1） in ileum tissues， and to explore the possible mechanism of intestinal mucosal barrier injury in rats with acute necrotizing pancreatitis （ANP）. Methods Ninety-six male Wistar rats were divided randomly （random number method） into ANP group， ethyl pyruvate （EP）group， and sham operation group. Eight rats of 3 groups were killed to get abdominal aortic blood and ileal tissues at 6， 12， 24， and 48h after operation， respectively.The levels of plasma amylase （AMY） ， D-lactate acid， and the activity of malonyl dialdehyde （MDA） in the ileum tissues were determined by using automatic biochemical analyzer， improved enzymatic spectrophotometry， and thiobarbituric acid （TAB） colorimetry respectively. The pathological changes of ileum tissues were observed under microscopy by HE staining， the expression of ZO-1 protein in ileum tissues was observed by immunohistochemistry （SP method）， and the expressions of HMGB1 mRNA and ZO-1 mRNA in ileum tissues were detected by reverse transcription-polymerase chain reaction （RT-PCR）. Results Compared with ANP group at the same time， levels of AMY， D-lactate acid， and MDA in ileum tissues of EP group were all significantly lower （P＜0.05）. The expression level of HMGB1 mRNA increased at 6 h while ZO-1 mRNA decreased in ANP group. Compared with ANP group at the same time， the expression level of HMGB1 mRNA of EP group was significantly lower while ZO-1 mRNA was higher （P＜0.05）， and the pathological damage in ileum tissues was lighter. Conclusions The decreased expression of ZO-1 in ileum tissues is one of the vitalcauses for intestinal mucosal barrier injury in ANP， and it probably occurs in case of the excessive expression of HMGB1.
ObjectiveTo explore the effect of the serum high mobility group box-1 (HMGB1) on oncosis of pancreatic acinar cells in the rat with severe acute pancreatitis (SAP). MethodsThirty-two healthy SD rats were randomly divided into 2 groups:sham operation group (SO group, n=8) and SAP group (n=24). Rats of SO group were only flipped the intestinal canal after laparotomy, but rats of SAP group were induced by retrograde injection of 3% sodium taurocholate into bilio-pancreatic duct in addition. Rats of SO group were sacrificed at 6 hours after operation, and rats of SAP group were sacrificed at 6 (SAP-6 hour group, n=8), 12 (SAP-12 hour group, n=8), and 24 hours (SAP-24 hour group, n=8) after operation respectively. Pancreatic tissues were stained by HE to observe pathological changes. Serum HMGB1 was measured by ELISA, and the oncosis percentage of pancreatic acinar cells was examined by flowcytometry. ResultsPathological results showed that structural integrity was observed in pancreatic acinar, and occasionally a single inflammatory cell infiltration was observed in rats of SO group. Swelling, interstitial edema, and inflammatory cell infiltration were observed in rats of SAP-6 hour group. Some necrosis of pancreatic acinar cell, stromal vascular congestion, and focal necrosis were observed in rats of SAP-12 hour group and SAP-24 hour group, which the pathological damage were worse over time. Levels of serum HMGB1 and oncosis percentages of pancreatic acinar cells in rats of 3 SAP subgroups were all higher than those of SO group (P < 0.01), and the 2 kinds of indexes both increased over time (P < 0.05). There was positive correlation between concentration of serum HMGB1 and oncosis percentages of pancreatic acinar cells in SAP rat during 24 hours after operation (r=0.846, P < 0.01). ConclusionsHMGB1 seems to play an important role in SAP by inducing oncosis of pancreatic acinar cells when inducing inflammatory reaction in rat with SAP.
ObjectiveTo investigate the effect and mechanism of ulinastatin to ventilator induced lung injury (VILI). MethodsTotal 24 SD rats were randomly divided into a control group, a VILI group, and a VILI+ ulinastatin group. High mobility group box-1 (HMGB-1), tumor necrosis factor (TNF)-α and interleukin (IL)-6 in bronchoalveolar lavage fluid, toll like receptor-4, dry/wet ratio and pathological scores of lung tissue were detected in the three groups. ResultsHMGB-1, TNF-α, and IL-6 in bronchoalveolar lavage fluid, toll like receptor-4, dry/wet ratio and pathological scores of lung tissue were significantly higher in the VILI group than those in the control group with statistical differences (P<0.05). While HMGB-1, TNF-α, and IL-6 in bronchoalveolar lavage fluid, toll like receptor-4, dry/wet ratio and pathological scores of lung tissue were reduced in the VILI+ ulinastatin group compared with those in the VILI group. ConclusionUlinastatin may protect ventilator induced lung injury by reducing inflammation level in lung through HMGB-1-TLR4 pathway.