中华围产医学杂志
中華圍產醫學雜誌
중화위산의학잡지
CHINESE JOURNAL OF PERINATAL MEDICINE
2015年
3期
222-226
,共5页
金圣娟%林土连%龙文君%刘艳%廖立红%罗小平
金聖娟%林土連%龍文君%劉豔%廖立紅%囉小平
금골연%림토련%룡문군%류염%료립홍%라소평
妊娠并发症,感染性%发热%低温%胎盘%细胞因子类%妊娠末期%脂多糖类%疾病模型,动物
妊娠併髮癥,感染性%髮熱%低溫%胎盤%細胞因子類%妊娠末期%脂多糖類%疾病模型,動物
임신병발증,감염성%발열%저온%태반%세포인자류%임신말기%지다당류%질병모형,동물
Pregnancy complications,infectious%Fever%Hypothermia%Placenta%Cytokines%Pregnancy trimester,third%Lipopolysaccharides%Disease models,animal
目的 探讨妊娠晚期细菌脂多糖暴露所致宫内感染大鼠发热反应和胎盘病理的变化.方法 选用妊娠第18天Sprague-Dawley大鼠,随机分为对照组和宫内感染组(每组各6只),宫内感染组大鼠腹腔注射脂多糖350μg/kg建立宫内感染模型,对照组给予等体积灭菌生理盐水.腹腔注射脂多糖或生理盐水后每隔1h测定孕鼠体温,连续监测8h.于妊娠第19天麻醉后剖腹取胎盘,采用HE染色法观察胎盘组织炎症反应,酶联免疫吸附法测定胎盘组织肿瘤坏死因子-α、白细胞介素-6和白细胞介素-1β的表达水平.组间比较采用Student t检验. 结果 (1)实验前2组孕鼠体温差异无统计学意义(P＞0.05);宫内感染组孕鼠在腹腔注射脂多糖1h后体温上升,达到(37.67±0.08)℃,与对照组[(37.13±0.08)℃]比较差异有统计学意义(t=10.178,P＜ 0.01);2h后发热反应逐渐消退,体温下降至37 ℃以下,持续呈现低体温反应,2～6 h的体温分别为(37.70±0.10)、(37.23±0.05)、(36.57±0.06)、(36.60±0.10)和(36.57±0.08)℃,与对照组比较[分别为(36.83±0.12)、(36.63±0.12)、(36.71±0.07)、(36.87±0.12)和(36.77±0.08)℃]差异均有统计学意义(t值分别为11.402、11.163、-4.025、-4.000和-4.243,P值均＜ 0.01).(2)宫内感染组胎盘组织HE染色显示大量中性粒细胞浸润和血管腔扩大、充血等急性炎症表现,对照组胎盘组织未见大量炎性细胞浸润.(3)宫内感染组胎盘组织肿瘤坏死因子-α[(0.62±0.02)ng/g]、白细胞介素-6[(66.12±5.11) ng/g]和白细胞介素-1β[(7.09±1.23) ng/g]表达水平均明显高于对照组[分别为(0.27±0.01)、(16.71±1.55)和(2.86±0.38) ng/g],差异均有统计学意义(t值分别为-26.608、-18.749和-5.714,P值均＜0.01).结论 孕鼠在妊娠晚期暴露于脂多糖后,胎盘存在明显的炎症反应,但其发热反应被抑制并出现低体温反应.
目的 探討妊娠晚期細菌脂多糖暴露所緻宮內感染大鼠髮熱反應和胎盤病理的變化.方法 選用妊娠第18天Sprague-Dawley大鼠,隨機分為對照組和宮內感染組(每組各6隻),宮內感染組大鼠腹腔註射脂多糖350μg/kg建立宮內感染模型,對照組給予等體積滅菌生理鹽水.腹腔註射脂多糖或生理鹽水後每隔1h測定孕鼠體溫,連續鑑測8h.于妊娠第19天痳醉後剖腹取胎盤,採用HE染色法觀察胎盤組織炎癥反應,酶聯免疫吸附法測定胎盤組織腫瘤壞死因子-α、白細胞介素-6和白細胞介素-1β的錶達水平.組間比較採用Student t檢驗. 結果 (1)實驗前2組孕鼠體溫差異無統計學意義(P＞0.05);宮內感染組孕鼠在腹腔註射脂多糖1h後體溫上升,達到(37.67±0.08)℃,與對照組[(37.13±0.08)℃]比較差異有統計學意義(t=10.178,P＜ 0.01);2h後髮熱反應逐漸消退,體溫下降至37 ℃以下,持續呈現低體溫反應,2～6 h的體溫分彆為(37.70±0.10)、(37.23±0.05)、(36.57±0.06)、(36.60±0.10)和(36.57±0.08)℃,與對照組比較[分彆為(36.83±0.12)、(36.63±0.12)、(36.71±0.07)、(36.87±0.12)和(36.77±0.08)℃]差異均有統計學意義(t值分彆為11.402、11.163、-4.025、-4.000和-4.243,P值均＜ 0.01).(2)宮內感染組胎盤組織HE染色顯示大量中性粒細胞浸潤和血管腔擴大、充血等急性炎癥錶現,對照組胎盤組織未見大量炎性細胞浸潤.(3)宮內感染組胎盤組織腫瘤壞死因子-α[(0.62±0.02)ng/g]、白細胞介素-6[(66.12±5.11) ng/g]和白細胞介素-1β[(7.09±1.23) ng/g]錶達水平均明顯高于對照組[分彆為(0.27±0.01)、(16.71±1.55)和(2.86±0.38) ng/g],差異均有統計學意義(t值分彆為-26.608、-18.749和-5.714,P值均＜0.01).結論 孕鼠在妊娠晚期暴露于脂多糖後,胎盤存在明顯的炎癥反應,但其髮熱反應被抑製併齣現低體溫反應.
목적 탐토임신만기세균지다당폭로소치궁내감염대서발열반응화태반병리적변화.방법 선용임신제18천Sprague-Dawley대서,수궤분위대조조화궁내감염조(매조각6지),궁내감염조대서복강주사지다당350μg/kg건립궁내감염모형,대조조급여등체적멸균생리염수.복강주사지다당혹생리염수후매격1h측정잉서체온,련속감측8h.우임신제19천마취후부복취태반,채용HE염색법관찰태반조직염증반응,매련면역흡부법측정태반조직종류배사인자-α、백세포개소-6화백세포개소-1β적표체수평.조간비교채용Student t검험. 결과 (1)실험전2조잉서체온차이무통계학의의(P＞0.05);궁내감염조잉서재복강주사지다당1h후체온상승,체도(37.67±0.08)℃,여대조조[(37.13±0.08)℃]비교차이유통계학의의(t=10.178,P＜ 0.01);2h후발열반응축점소퇴,체온하강지37 ℃이하,지속정현저체온반응,2～6 h적체온분별위(37.70±0.10)、(37.23±0.05)、(36.57±0.06)、(36.60±0.10)화(36.57±0.08)℃,여대조조비교[분별위(36.83±0.12)、(36.63±0.12)、(36.71±0.07)、(36.87±0.12)화(36.77±0.08)℃]차이균유통계학의의(t치분별위11.402、11.163、-4.025、-4.000화-4.243,P치균＜ 0.01).(2)궁내감염조태반조직HE염색현시대량중성립세포침윤화혈관강확대、충혈등급성염증표현,대조조태반조직미견대량염성세포침윤.(3)궁내감염조태반조직종류배사인자-α[(0.62±0.02)ng/g]、백세포개소-6[(66.12±5.11) ng/g]화백세포개소-1β[(7.09±1.23) ng/g]표체수평균명현고우대조조[분별위(0.27±0.01)、(16.71±1.55)화(2.86±0.38) ng/g],차이균유통계학의의(t치분별위-26.608、-18.749화-5.714,P치균＜0.01).결론 잉서재임신만기폭로우지다당후,태반존재명현적염증반응,단기발열반응피억제병출현저체온반응.
Objective To explore the febrile response and placental pathological inflammation of pregnant rats exposed to intrauterine infection in late gestation.Methods Pregnant Sprague-Dawley rats at gestational day 18 were randomly divided into control group and intrauterine-infected group with six rats in each.The intrauterine-infected group was intraperitoneally injected with 350 μ g/kg lipopolysaccharide to establish a rat model of intrauterine infection,while the control group was injected with sterile saline of the same dose.Core temperature was measured every 1 h after intraperitoneal injection of lipopolysaccharide or saline for 8 h.At gestational day 19,after anesthesia,the placentas were taken and stained with HE.The expression levels of tumor necrosis factor-α,interleukin-6,and interleukin-1β in the placenta were determined by enzyme linked immunosorbent assay.Student t test was used for statistical analysis.Results (1) There was no temperature difference between the two groups before experimental treatment (P ＞ 0.05).Core temperature was increased 1 h after the lipopolysaccharide injection,reaching (37.67 ±0.08) ℃.The increase of temperature was significant compared with the control group [(37.13 ± 0.08) ℃,t=10.178,P ＜ 0.01].Fever was lowered 2 h later and the rats became hypothermic with body temperature below 37 ℃ in the intrauterine-infected group.The body temperature in the intrauterine-infected group after 2-6 h was (37.70 ± 0.10),(37.23 ± 0.05),(36.57 ± 0.06),(36.60 ± 0.10) and (36.57 ± 0.08) ℃,respectively,compared with the control group [(36.83 ±0.12),(36.63 ± 0.12),(36.71 ± 0.07),(36.87±0.12),and (36.77±0.08) ℃,respectively],the differences being all statistically significant (t=11.402,11.163,-4.025,-4.000 and-4.243,all P ＜ 0.01).(2) HE staining revealed large amounts of neutrophils infiltration,vascular enlargement and congestion in the placenta of the intrauterine-infected rats.No inflammatory cell infiltration was observed in the control placentas.(3) The expression levels of proinflammatory cytokine tumor necrosis factor-α [(0.62 ± 0.02) ng/g],interleukin-6 [(66.12 ± 5.11) ng/g],and interleukin-1β [(7.09± 1.23) ng/g] in the intrauterine-infected group were higher than those in the control group [(0.27±0.01),(16.71 ±1.55) and (2.86 ± 0.38) ng/g,respectively].The differences were all statistically significant (t=-26.608,-18.749 and-5.714,all P ＜ 0.01).Conclusion After exposure to lipopolysaccharide in late gestation,pregnant rats show significant inflammatory response in the placenta,with suppression of febrile response and presence of hypothermia.
