【摘要】：目的探討HMGB1、TLR4在重癥急性胰腺炎大鼠胰腺組織中的作用機(jī)制以及烏司他丁的干預(yù)效應(yīng)。方法將54只SD大鼠分為對照組、SAP組和烏司他丁治療組,3組又分為6、12h和24h3個小組(每小組n=6)。對照組開腹后僅翻動胰腺組織,SAP組用5%的�；悄懰徕c制備SAP模型,治療組在SAP造模成功后經(jīng)尾靜脈注射烏司他丁。觀察3組大鼠胰腺組織的病理學(xué)改變;EPS-G7法檢測血清中的淀粉酶;ELISA法檢測血清及胰腺組織中的HMGB1;Envision兩步免疫法檢測胰腺組織中的HMGB1、TLR4的表達(dá)水平。結(jié)果 SAP組、治療組各時間點(diǎn)的淀粉酶與對照組比較明顯升高,病理學(xué)改變明顯,差異均有統(tǒng)計學(xué)意義(P0.05),示SAP造模成功;SAP組在胰腺組織及血清中的HMGB1表達(dá)在6h開始升高,于12h快速上升,至24h保持上升趨勢,與對照組大鼠相同時間點(diǎn)比較明顯升高,差異有統(tǒng)計學(xué)意義(P0.05),治療組與SAP組相同時間點(diǎn)的HMGB1比較明顯降低,差異有統(tǒng)計學(xué)意義(P0.05);SAP組胰腺組織中的TLR4表達(dá)在6h開始升高,12h達(dá)高峰,24h開始下降,與對照組大鼠相同時間點(diǎn)比較明顯升高,差異有統(tǒng)計學(xué)意義(P0.05)。治療組與SAP組相同時間點(diǎn)的TLR4比較明顯降低,差異有統(tǒng)計學(xué)意義(P0.05)。結(jié)論 HMGB1在SAP大鼠胰腺中的致炎作用可能是部分結(jié)合其受體TLR4并通過MyD88依賴性途徑而實(shí)現(xiàn)的,而烏司他丁可能是通過中斷SAP大鼠胰腺組織中的HMGB1、TLR4信號通路發(fā)揮保護(hù)作用。
[Abstract]:Objective to investigate the mechanism of HMGB1,TLR4 in pancreatic tissue of rats with severe acute pancreatitis and the intervention effect of ulinastatin. Methods 54 SD rats were divided into three groups: control group, SAP group and ulinastatin treatment group. The 3 groups were divided into 6 groups (n = 12) and 24h3 group (n = 6). SAP group was treated with 5% sodium taurocholate to make SAP model, and the treatment group was injected with ulinastatin via tail vein after successful SAP. The histopathological changes of pancreatic tissue in the three groups were observed; the amylase in serum was detected by EPS-G7 method; and the expression of HMGB1,TLR4 in pancreatic tissue was detected by two-step immunoassay of HMGB1;Envision in serum and pancreatic tissue by ELISA method. Results in the SAP group, the amylase in each time point in the treatment group was significantly higher than that in the control group, and the pathological changes were significant (P0.05). The results showed that the SAP model was successful. The expression of HMGB1 in pancreatic tissue and serum of SAP group began to increase at 6 h, increased rapidly at 12 h, and maintained an increasing trend at 24 h. The expression of HMGB1 in SAP group was significantly higher than that in control group at the same time point (P0.05). The HMGB1 of the treatment group and the SAP group at the same time point was significantly lower than that of the control group (P0.05). The expression of TLR4 in pancreatic tissue of SAP group began to increase at 6 h, reached the peak at 12 h, and began to decrease at 24 h, which was significantly higher than that in control group at the same time point (P0.05). The TLR4 of the treatment group and the SAP group at the same time point was significantly lower than that of the control group (P0.05). Conclusion the inflammatory effect of HMGB1 in the pancreas of SAP rats may be partly combined with its receptor TLR4 and may be mediated by MyD88 dependent pathway, while ulinastatin may play a protective role by interrupting the HMGB1,TLR4 signaling pathway in the pancreatic tissue of SAP rats.
【作者單位】： 四川省自貢市第一人民醫(yī)院消化內(nèi)科;瀘州醫(yī)學(xué)院附屬醫(yī)院消化內(nèi)科;
【分類號】：R576

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