CAJ | 학술논문

目的：观察白细胞介素-32（IL-32）在大鼠克雷伯杆菌肺炎中的变化，并探讨其意义。方法选择72只SD大鼠，按随机数字表法分为对照组、模型组和实验组，再按实验4 h和1、3、5 d分为4个亚组，每组6只。采用经气管注入0.3 mL细菌混悬液的方法建立大鼠克雷伯杆菌肺炎模型，实验组大鼠制模前腹腔注射IL-32抑制剂蛋白酶活化受体2（PAR2）；于制模后不同时间点尾静脉取血观察各组大鼠血清IL-32、肿瘤坏死因子-α（TNF-α）、IL-6、IL-8水平的变化；取肺组织行苏木素-伊红（HE）染色，光镜下观察肺组织的病理学改变。结果与对照组比较，模型组IL-32、TNF-α、IL-8、IL-6随时间延长均逐渐升高，3 d时达峰值〔IL-32（ng/L）：84.40±28.24比18.57±3.86，t＝5.544，P＝0.002；TNF-α（ng/L）：79.27±14.64比17.82±3.86， t＝9.994，P＝0.000；IL-8（ng/L）：55.85±10.90比16.66±3.76，t＝8.544，P＝0.000；IL-6（ng/L）：56.65±2.57比28.48±2.11，t＝19.693，P＝0.000〕；PAR2预处理可使上述各指标均明显降低，3 d时与模型组比较差异有统计学意义〔IL-32（ng/L）：54.13±6.68比84.40±28.24，t＝2.560，P＝0.046；TNF-α（ng/L）：49.12±3.56比79.27±14.64，t＝4.901，P＝0.003；IL-8（ng/L）：22.95±2.52比55.85±10.90，t＝7.204，P＝0.000；IL-6（ng/L）：36.49±2.63比56.65±2.57，t＝13.443，P＝0.000〕。光镜下观察，实验组大鼠肺组织炎症改变较模型组有所减轻。结论 IL-32作为一种前炎症反应细胞因子，可诱导TNF-α、IL-6和IL-8的产生，抑制IL-32产生对克雷伯杆菌肺炎病情的进展有一定的作用。
목적：관찰백세포개소-32（IL-32）재대서극뢰백간균폐염중적변화，병탐토기의의。방법선택72지SD대서，안수궤수자표법분위대조조、모형조화실험조，재안실험4 h화1、3、5 d분위4개아조，매조6지。채용경기관주입0.3 mL세균혼현액적방법건립대서극뢰백간균폐염모형，실험조대서제모전복강주사IL-32억제제단백매활화수체2（PAR2）；우제모후불동시간점미정맥취혈관찰각조대서혈청IL-32、종류배사인자-α（TNF-α）、IL-6、IL-8수평적변화；취폐조직행소목소-이홍（HE）염색，광경하관찰폐조직적병이학개변。결과여대조조비교，모형조IL-32、TNF-α、IL-8、IL-6수시간연장균축점승고，3 d시체봉치〔IL-32（ng/L）：84.40±28.24비18.57±3.86，t＝5.544，P＝0.002；TNF-α（ng/L）：79.27±14.64비17.82±3.86， t＝9.994，P＝0.000；IL-8（ng/L）：55.85±10.90비16.66±3.76，t＝8.544，P＝0.000；IL-6（ng/L）：56.65±2.57비28.48±2.11，t＝19.693，P＝0.000〕；PAR2예처리가사상술각지표균명현강저，3 d시여모형조비교차이유통계학의의〔IL-32（ng/L）：54.13±6.68비84.40±28.24，t＝2.560，P＝0.046；TNF-α（ng/L）：49.12±3.56비79.27±14.64，t＝4.901，P＝0.003；IL-8（ng/L）：22.95±2.52비55.85±10.90，t＝7.204，P＝0.000；IL-6（ng/L）：36.49±2.63비56.65±2.57，t＝13.443，P＝0.000〕。광경하관찰，실험조대서폐조직염증개변교모형조유소감경。결론 IL-32작위일충전염증반응세포인자，가유도TNF-α、IL-6화IL-8적산생，억제IL-32산생대극뢰백간균폐염병정적진전유일정적작용。
Objective To study the changes in interleukin-32 (IL-32) in rats with Klebsiella bacillus pneumonia and approach its significance. Methods Seventy-two Sprague-Dawley(SD)rats were divide into control group,model group and experimental group by the method of random digits table,then the experimental group was subdivided into 4 hours and 1,3 and 5 days experimental subgroups(each n=6). The rat model of Klebsiella bacillus pneumonia was established by injection of 0.3 mL Klebsiella bacterial suspension into the trachea. Before the establishment of the model in the experimental group,IL-32 inhibitory agent,protease activated receptor-2(PAR2) was injected into the abdominal cavity. After model establishment,at different time points,blood was collected via tail vein to observe the changes in serum levels of IL-32,tumor necrosis factor-α(TNF-α),IL-6 and IL-8 in all the groups. The lungs were removed and stained with hematoxylin-eosin(HE)method to investigate the histopathological changes of the lung tissues under the light microscope. Results Compared to the control group, with the prolongation of time the levels of IL-32,TNF-α,IL-8 and IL-6 were increased gradually in the model group,and reached their peaks at 3 days〔IL-32(ng/L):84.40±28.24 vs. 18.57±3.86,t=5.544,P=0.002;TNF-α(ng/L):79.27±14.64 vs. 17.82±3.86, t=9.994, P=0.000;IL-8(ng/L):55.85±10.90 vs. 16.66±3.76,t=8.544, P=0.000;IL-6(ng/L):56.65±2.57 vs. 28.48±2.11,t=19.693,P=0.000〕;PAR2 could inhibit above indexes significantly,there was statistical difference at 3 days compared with the model group〔IL-32(ng/L):54.13±6.68 vs. 84.40±28.24,t=2.560,P=0.046;TNF-α(ng/L):49.12±3.56 vs. 79.27±14.64,t=4.901,P=0.003;IL-8 (ng/L):22.95±2.52 vs. 55.85±10.90,t=7.204,P=0.000;IL-6(ng/L):36.49±2.63 vs. 56.65±2.57,t=13.443, P=0.000〕. Under the light microscope,the inflammatory changes in the lung tissue in experimental group were milder than those in the model group. Conclusion As a pro-inflammatory cytokine,IL-32 can induce the production of TNF-α,IL-6 and IL-8,and the inhibition of IL-32 production may play a role in suppression of the development of Klebsiella bacillus pneumonia.