CAJ | 학술논문

目的：本研究观察乌司他丁对中度烧冲复合伤大鼠肺组织炎症介质、肺微血管通透性和肺组织含水率的影响。方法将80只 SD 雄性大鼠随机分为对照组（n ＝40）和乌司他丁组（n ＝40），两组均造成25％总体表面积深Ⅱ度烧伤＋中度冲击伤的中度烧冲复合伤模型。于伤后即刻分别静脉注射0．9％氯化钠溶液和乌司他丁40000 U ／kg 1 mL。分别于伤后6、24 h 采用酶联免疫吸附试验（ELISA）检测2组大鼠肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和白细胞介素-8（IL-8）的含量，伊文斯蓝法（EB）测定肺微血管通透性，干／湿重法测定肺组织含水率，组间计量数据行 t 检验。结果伤后6 h 与对照组 TNF-α（2912±184）pg／mL、IL-6（2793±223）pg／mL 和 IL-8（2178±145）pg／mL 水平比较，乌司他丁组肺组织 TNF-α（2103±168）pg／mL、IL-6（2315±185）pg／mL和 IL-8（1827±134）pg／mL 水平明显降低，差异有统计学意义（t ＝6．114、8．123、7．347，P ＜0．05）；伤后24 h与肺组织 TNF-α（1853±166）pg／mL、IL-6（2152±172）pg／mL 和 IL-8（1807±126）pg／mL 水平比较，乌司他丁组 TNF-α（1235±86）pg／mL、IL-6（1093±98）pg／mL 和 IL-8（973±77）pg／mL 水平明显降低（t ＝5．176、7．043、5．732，P ＜0．05）；乌司他丁组大鼠肺组织 EB 含量在伤后6、24 h[（63．9±3．3）、（59．8±3．2）μg／g]，均明显低于对照组（78．2±3．7）、（76．3±3．5）μg／g，差异有统计学意义（t ＝7．023、7．382，P ＜0．05）。乌司他丁组大鼠肺组织含水率在伤后6、24 h [（76．3±1．45）％、（73．8±1．35）％]明显低于对照组（79．8±1．52）％、（78．3±1．47）％，差异有统计学意义（t ＝2．041、2．758， P ＜0．05）。结论乌司他丁能降低中度烧冲复合伤大鼠血清 TNF-α、IL-6、IL-8炎症介质水平，抑制血管内皮细胞活化和通透性增加，对血管内皮细胞有保护作用。目的：本研究觀察烏司他丁對中度燒遲複閤傷大鼠肺組織炎癥介質、肺微血管通透性和肺組織含水率的影響。方法將80隻 SD 雄性大鼠隨機分為對照組（n ＝40）和烏司他丁組（n ＝40），兩組均造成25％總體錶麵積深Ⅱ度燒傷＋中度遲擊傷的中度燒遲複閤傷模型。于傷後即刻分彆靜脈註射0．9％氯化鈉溶液和烏司他丁40000 U ／kg 1 mL。分彆于傷後6、24 h 採用酶聯免疫吸附試驗（ELISA）檢測2組大鼠腫瘤壞死因子-α（TNF-α）、白細胞介素-6（IL-6）和白細胞介素-8（IL-8）的含量，伊文斯藍法（EB）測定肺微血管通透性，榦／濕重法測定肺組織含水率，組間計量數據行 t 檢驗。結果傷後6 h 與對照組 TNF-α（2912±184）pg／mL、IL-6（2793±223）pg／mL 和 IL-8（2178±145）pg／mL 水平比較，烏司他丁組肺組織 TNF-α（2103±168）pg／mL、IL-6（2315±185）pg／mL和 IL-8（1827±134）pg／mL 水平明顯降低，差異有統計學意義（t ＝6．114、8．123、7．347，P ＜0．05）；傷後24 h與肺組織 TNF-α（1853±166）pg／mL、IL-6（2152±172）pg／mL 和 IL-8（1807±126）pg／mL 水平比較，烏司他丁組 TNF-α（1235±86）pg／mL、IL-6（1093±98）pg／mL 和 IL-8（973±77）pg／mL 水平明顯降低（t ＝5．176、7．043、5．732，P ＜0．05）；烏司他丁組大鼠肺組織 EB 含量在傷後6、24 h[（63．9±3．3）、（59．8±3．2）μg／g]，均明顯低于對照組（78．2±3．7）、（76．3±3．5）μg／g，差異有統計學意義（t ＝7．023、7．382，P ＜0．05）。烏司他丁組大鼠肺組織含水率在傷後6、24 h [（76．3±1．45）％、（73．8±1．35）％]明顯低于對照組（79．8±1．52）％、（78．3±1．47）％，差異有統計學意義（t ＝2．041、2．758， P ＜0．05）。結論烏司他丁能降低中度燒遲複閤傷大鼠血清 TNF-α、IL-6、IL-8炎癥介質水平，抑製血管內皮細胞活化和通透性增加，對血管內皮細胞有保護作用。
목적：본연구관찰오사타정대중도소충복합상대서폐조직염증개질、폐미혈관통투성화폐조직함수솔적영향。방법장80지 SD 웅성대서수궤분위대조조（n ＝40）화오사타정조（n ＝40），량조균조성25％총체표면적심Ⅱ도소상＋중도충격상적중도소충복합상모형。우상후즉각분별정맥주사0．9％록화납용액화오사타정40000 U ／kg 1 mL。분별우상후6、24 h 채용매련면역흡부시험（ELISA）검측2조대서종류배사인자-α（TNF-α）、백세포개소-6（IL-6）화백세포개소-8（IL-8）적함량，이문사람법（EB）측정폐미혈관통투성，간／습중법측정폐조직함수솔，조간계량수거행 t 검험。결과상후6 h 여대조조 TNF-α（2912±184）pg／mL、IL-6（2793±223）pg／mL 화 IL-8（2178±145）pg／mL 수평비교，오사타정조폐조직 TNF-α（2103±168）pg／mL、IL-6（2315±185）pg／mL화 IL-8（1827±134）pg／mL 수평명현강저，차이유통계학의의（t ＝6．114、8．123、7．347，P ＜0．05）；상후24 h여폐조직 TNF-α（1853±166）pg／mL、IL-6（2152±172）pg／mL 화 IL-8（1807±126）pg／mL 수평비교，오사타정조 TNF-α（1235±86）pg／mL、IL-6（1093±98）pg／mL 화 IL-8（973±77）pg／mL 수평명현강저（t ＝5．176、7．043、5．732，P ＜0．05）；오사타정조대서폐조직 EB 함량재상후6、24 h[（63．9±3．3）、（59．8±3．2）μg／g]，균명현저우대조조（78．2±3．7）、（76．3±3．5）μg／g，차이유통계학의의（t ＝7．023、7．382，P ＜0．05）。오사타정조대서폐조직함수솔재상후6、24 h [（76．3±1．45）％、（73．8±1．35）％]명현저우대조조（79．8±1．52）％、（78．3±1．47）％，차이유통계학의의（t ＝2．041、2．758， P ＜0．05）。결론오사타정능강저중도소충복합상대서혈청 TNF-α、IL-6、IL-8염증개질수평，억제혈관내피세포활화화통투성증가，대혈관내피세포유보호작용。
Objective To investigate the effet of ulinastatin on pulmonary tissue inflammatory mediators,vistal vasopermeability and tissue water content after moderate burn-blast combined injury in rats. Methods Eighty male Sprague-Dawley rats were randomly divided into the control group and ulinastatin group.A model with moderate burn-blast combined injury,was produced in both groups.Immediately after injury rats were intravenously given either 1 mL sodium chloride solution in control group or 1 mL sodium chloride solution containing ulinastatin in ulinastatin group (40 000 U /kg).The content of tumor necrosis factor-α,interleukin (IL)-6 and interleukin (IL)-8 were detected by enzyme linked immuno sorbent assay (ELISA)at 6 hours and 24 hours after injury.The vasopermeability was detected by the method of evans blue and the rates of tissue water content in lung were detected by the dry /wet weight.Measurement data between groups was analyzed by t test.Results Compared with control group after 6 h,the inflammatory mediators of TNF-α、IL-6 and IL-8 in ulinastatin group were (21 03 ±1 68)pg/mL,(231 5 ±1 85)pg/mL and(1 827 ±1 34)pg/mL,significantly lower than those (291 2 ±1 84)pg/mL,(2793 ±223)pg/mL and (21 78 ±1 45)pg/mL in control group,the difference was statistically significant(t =6.1 1 4,8.1 23,7.347, P <0.05).Compared with 24 hours,the inflammatory mediators of TNF-α、IL -6 and IL -8 in ulinastatin group were (1 235 ±86)pg/mL,(1 093 ±98)pg/mL and(973 ±77)pg/mL,even more significantly lower than those(1 853 ±1 66 )pg/mL,(21 52 ±1 72 )pg/mL and (1 807 ±1 26 )pg/mL in control group,the difference was statistically significant(t =5.1 76,7.043,5.732,P <0.05).Compared with control group after 6 hours and 24 hours,the visceral content of evans blue in ulinastatin group were (63.9 ±3.3), (59.8 ±3.2)μg/g,significantly lower than those(78.2 ±3.7),(76.3 ±3.5)μg/g in control group,the difference was statistically significant(t =7.023,7.382,P <0.05 ).Compared with control group after 6 hours and 24 hours,the rate of tissue water content in lung in ulinastatin group were (76.3 ±1 .45)%、(73.8 ±1 .35)%,obviously lower than those (79.8 ±1 .52)%、(78.3 ±1 .47 )% in enzyme linked immuno sorbent assay,the difference was statistically significant(t =2.041 ,2.758,P <0.05).Conclusions The results indicate that ulinastatin significantly alleviate systemic inflammation,inhibit visceral vasopermeability and tissue edema,and it can be used to be early period therapy of burn shock and improve the survival rate.