CAJ | 학술논문

目的：初步探讨纳米氧化铝颗粒对 Wistar 大鼠肺部的急性炎症反应和氧化应激损伤。方法将48只雄性 Wistar 大鼠随机分为纳米氧化铝悬液低、中、高剂量组和生理盐水组4组，每组12只，制备纳米氧化铝悬液，按14、70和350 mg／kg 剂量分别进行单次气管滴注。染毒后3 d 和28 d 取肺部灌洗液（BALF）和肺部组织，检测生化指标、白细胞计数分类及氧化应激指标，并观察肺部病理变化。结果（1）染毒后3 d，中、高剂量组 BALF中的总蛋白（TP）含量明显升高（P ＜0．05），各剂量组乳酸脱氢酶（LDH）活性、碱性磷酸酶（AKP）活性、酸性磷酸酶（ACP）活性均较生理盐水组明显升高（P ＜0．05）；染毒后28 d，中、高剂量组 BALF 中的碱性磷酸酶（AKP）活性较生理盐水组明显增加（P ＜0．05）；各染毒组中，总蛋白（TP）含量、乳酸脱氢酶（LDH）活性、酸性磷酸酶（ACP）活性均较生理盐水组明显增加（P ＜0．05）。（2）染毒后3 d，中、高剂量组与生理盐水组相比，中性粒细胞的比例均有明显增加（P ＜0．05）。染毒后28 d，高剂量组中性粒细胞所占的比例仍高于生理盐水组，并且差异具有统计学意义（P ＜0．05）。（3）与生理盐水组比较，染毒后3 d，中、高剂量组中丙二醛（MDA）含量明显增加（P ＜0．05）。中、高剂量组中超氧化物歧化酶（SOD）活性明显降低（P ＜0．05）；染毒后28 d，高剂量组中丙二醛（MDA）含量明显增加（P ＜0．05）；高剂量组中超氧化物歧化酶（SOD）活性明显降低（P ＜0．05）；各剂量组过氧化氢酶（CAT）活性在染毒后3、28 d 均无差异；高剂量组中谷胱甘肽过氧化物酶（GSH-Px）活性在染毒后3、28 d 均明显降低（P ＜0．05）。（4）各染毒组中小鼠肺组织均出现明显的炎症改变，肺泡毛细血管扩张，支气管细胞周围有少量炎性细胞浸润，部分肺泡腔受压，有纤维素的渗出，间质有炎性细胞浸润，并随剂量的增加改变明显加重。结论纳米氧化铝可引起肺部急性炎症反应和氧化应激损伤。目的：初步探討納米氧化鋁顆粒對 Wistar 大鼠肺部的急性炎癥反應和氧化應激損傷。方法將48隻雄性 Wistar 大鼠隨機分為納米氧化鋁懸液低、中、高劑量組和生理鹽水組4組，每組12隻，製備納米氧化鋁懸液，按14、70和350 mg／kg 劑量分彆進行單次氣管滴註。染毒後3 d 和28 d 取肺部灌洗液（BALF）和肺部組織，檢測生化指標、白細胞計數分類及氧化應激指標，併觀察肺部病理變化。結果（1）染毒後3 d，中、高劑量組 BALF中的總蛋白（TP）含量明顯升高（P ＜0．05），各劑量組乳痠脫氫酶（LDH）活性、堿性燐痠酶（AKP）活性、痠性燐痠酶（ACP）活性均較生理鹽水組明顯升高（P ＜0．05）；染毒後28 d，中、高劑量組 BALF 中的堿性燐痠酶（AKP）活性較生理鹽水組明顯增加（P ＜0．05）；各染毒組中，總蛋白（TP）含量、乳痠脫氫酶（LDH）活性、痠性燐痠酶（ACP）活性均較生理鹽水組明顯增加（P ＜0．05）。（2）染毒後3 d，中、高劑量組與生理鹽水組相比，中性粒細胞的比例均有明顯增加（P ＜0．05）。染毒後28 d，高劑量組中性粒細胞所佔的比例仍高于生理鹽水組，併且差異具有統計學意義（P ＜0．05）。（3）與生理鹽水組比較，染毒後3 d，中、高劑量組中丙二醛（MDA）含量明顯增加（P ＜0．05）。中、高劑量組中超氧化物歧化酶（SOD）活性明顯降低（P ＜0．05）；染毒後28 d，高劑量組中丙二醛（MDA）含量明顯增加（P ＜0．05）；高劑量組中超氧化物歧化酶（SOD）活性明顯降低（P ＜0．05）；各劑量組過氧化氫酶（CAT）活性在染毒後3、28 d 均無差異；高劑量組中穀胱甘肽過氧化物酶（GSH-Px）活性在染毒後3、28 d 均明顯降低（P ＜0．05）。（4）各染毒組中小鼠肺組織均齣現明顯的炎癥改變，肺泡毛細血管擴張，支氣管細胞週圍有少量炎性細胞浸潤，部分肺泡腔受壓，有纖維素的滲齣，間質有炎性細胞浸潤，併隨劑量的增加改變明顯加重。結論納米氧化鋁可引起肺部急性炎癥反應和氧化應激損傷。
목적：초보탐토납미양화려과립대 Wistar 대서폐부적급성염증반응화양화응격손상。방법장48지웅성 Wistar 대서수궤분위납미양화려현액저、중、고제량조화생리염수조4조，매조12지，제비납미양화려현액，안14、70화350 mg／kg 제량분별진행단차기관적주。염독후3 d 화28 d 취폐부관세액（BALF）화폐부조직，검측생화지표、백세포계수분류급양화응격지표，병관찰폐부병리변화。결과（1）염독후3 d，중、고제량조 BALF중적총단백（TP）함량명현승고（P ＜0．05），각제량조유산탈경매（LDH）활성、감성린산매（AKP）활성、산성린산매（ACP）활성균교생리염수조명현승고（P ＜0．05）；염독후28 d，중、고제량조 BALF 중적감성린산매（AKP）활성교생리염수조명현증가（P ＜0．05）；각염독조중，총단백（TP）함량、유산탈경매（LDH）활성、산성린산매（ACP）활성균교생리염수조명현증가（P ＜0．05）。（2）염독후3 d，중、고제량조여생리염수조상비，중성립세포적비례균유명현증가（P ＜0．05）。염독후28 d，고제량조중성립세포소점적비례잉고우생리염수조，병차차이구유통계학의의（P ＜0．05）。（3）여생리염수조비교，염독후3 d，중、고제량조중병이철（MDA）함량명현증가（P ＜0．05）。중、고제량조중초양화물기화매（SOD）활성명현강저（P ＜0．05）；염독후28 d，고제량조중병이철（MDA）함량명현증가（P ＜0．05）；고제량조중초양화물기화매（SOD）활성명현강저（P ＜0．05）；각제량조과양화경매（CAT）활성재염독후3、28 d 균무차이；고제량조중곡광감태과양화물매（GSH-Px）활성재염독후3、28 d 균명현강저（P ＜0．05）。（4）각염독조중소서폐조직균출현명현적염증개변，폐포모세혈관확장，지기관세포주위유소량염성세포침윤，부분폐포강수압，유섬유소적삼출，간질유염성세포침윤，병수제량적증가개변명현가중。결론납미양화려가인기폐부급성염증반응화양화응격손상。
Objective To make a preliminary assessment on lung inflammation and oxidative stress caused by nano-alumina particles in Wistar rats.Methods 48 healthy male Wistar rats were randomly divided into four groups according to the body weight.14,70 and 350 mg/kg of nano-alumina suspension were instilled into lung single intratracheally as test groups and NS was instilled as negative group.Lung lavage fluid (BALF)and lung tissues were collected for analysis on the 3 rd and the 28 th day after treatment;lung patho-logical changes were observed.Results (1)BALF biochemical examinations showed:on the 3 rd day after treatment,the total protein (TP)levels in MG and HG were significantly higher (P <0.05).Lactate de-hydrogenase (LDH)activity,alkaline phosphatase (AKP)activity and acid phosphatase (ACP)activity in each dose group were significantly higher (P <0.05)than those in saline group;on the 28 th day after treat-ment,in MG and HG,the alkaline phosphatase (AKP)activity was higher than that in the saline group (P <0.05);in 3 test groups,the total protein (TP)content,lactate dehydrogenase (LDH)activity and acid phosphatase (ACP)activity were higher than those in the saline group (P <0.05).(2)BALF leuko-cyte count showed:on the 3 rd day after treatment,the proportion of neutrophils were increased obviously in the MG and HG (P <0.05);on the 28 th day after treatment,the percentage of neutrophils was still higher than that in saline group (P <0.05).(3)Oxidative stress test in lung tissue showed:Compared with the saline group,on the 3 rd day after treatment,MDA content in MG and HG were increased (P <0.05).The superoxide dismutase (SOD)activity in MG and HG was lower than that in saline group (P <0.05);on the 28th day after treatment,malondialdehyde (MDA)content in HG was increased (P <0.05);superoxide dismutase (SOD)activity in HG was lower than that in saline group (P < 0.05);catalase (CAT)in each dose group showed no significant difference in activity after the exposure of 3 days and 28 days;glutathione peroxidase enzymes (GSH-Px)activity in HG were significantly lower on the 3rd day and 28th day than that in saline group (P <0.05).(4)Lung histopathology showed alveolar capillary dila-tion,inflammatory cell infiltration in bronchial cells,alveolar partial pressure,cellulose exudation,inter-stitial inflammatory cell infiltration in cats in 3 dose groups.Changes became worse with the dose increased significantly.Conclusion Nano-alumina can cause inflammation and oxidative stress in lung.