临床儿科杂志
臨床兒科雜誌
림상인과잡지
2014年
3期
250-253
,共4页
石计朋%黄丽密%钱燕%尚云
石計朋%黃麗密%錢燕%尚雲
석계붕%황려밀%전연%상운
脂肪乳剂%脂多糖%急性肺损伤%大鼠
脂肪乳劑%脂多糖%急性肺損傷%大鼠
지방유제%지다당%급성폐손상%대서
lipid emulsion%lipopolysaccharide%acute lung injury%rat
目的:比较3种脂肪乳剂对脂多糖(LPS)诱导的急性肺损伤(ALI)大鼠IL-1β和IL-6分泌的影响。方法100只SD幼年大鼠分为对照组、LPS组、ω-9组、ω-6组和ω-3组。日龄28 d时连续7 d,对照组大鼠经尾静脉注射生理盐水;ω-6组注射脂肪乳(C14~24)、ω-9组注射长链脂肪乳、ω-3组注射ω-3鱼油脂肪乳注射液;随后对照组气管内滴入生理盐水,另4组大鼠均喷洒LPS溶液。8 h后处死大鼠观察各组肺组织的病理改变,并测定IL-1β和IL-6 mRNA及蛋白等水平。结果各组大鼠肺组织病理切片均可见明显炎症细胞浸润和出血;4组ALI大鼠的肺系数、肺损伤评分均高于对照组,差异均有统计学意义(P均<0.005);ω-9组和ω-3组两组肺组织中IL-1β和IL-6 mRNA表达均较LPS组和ω-6组降低,差异均有统计学意义(P均<0.005);支气管肺泡灌洗液中ω-9组和ω-3组IL-1β和IL-6蛋白水平均低于其余组,差异均有统计学意义(P均<0.005)。ω-9组和ω-3组IL-1β和IL-6 mRNA表达及其相应的蛋白水平差异均无统计学意义(P均>0.005)。结论ω-6 PUFAs可增加IL-1β和IL-6的产生加重ALI大鼠炎症反应;而ω-9 MUFAs和ω-3 PUFAs可降低IL-1β和IL-6减轻ALI大鼠炎症反应,具有一定的抗炎作用。
目的:比較3種脂肪乳劑對脂多糖(LPS)誘導的急性肺損傷(ALI)大鼠IL-1β和IL-6分泌的影響。方法100隻SD幼年大鼠分為對照組、LPS組、ω-9組、ω-6組和ω-3組。日齡28 d時連續7 d,對照組大鼠經尾靜脈註射生理鹽水;ω-6組註射脂肪乳(C14~24)、ω-9組註射長鏈脂肪乳、ω-3組註射ω-3魚油脂肪乳註射液;隨後對照組氣管內滴入生理鹽水,另4組大鼠均噴灑LPS溶液。8 h後處死大鼠觀察各組肺組織的病理改變,併測定IL-1β和IL-6 mRNA及蛋白等水平。結果各組大鼠肺組織病理切片均可見明顯炎癥細胞浸潤和齣血;4組ALI大鼠的肺繫數、肺損傷評分均高于對照組,差異均有統計學意義(P均<0.005);ω-9組和ω-3組兩組肺組織中IL-1β和IL-6 mRNA錶達均較LPS組和ω-6組降低,差異均有統計學意義(P均<0.005);支氣管肺泡灌洗液中ω-9組和ω-3組IL-1β和IL-6蛋白水平均低于其餘組,差異均有統計學意義(P均<0.005)。ω-9組和ω-3組IL-1β和IL-6 mRNA錶達及其相應的蛋白水平差異均無統計學意義(P均>0.005)。結論ω-6 PUFAs可增加IL-1β和IL-6的產生加重ALI大鼠炎癥反應;而ω-9 MUFAs和ω-3 PUFAs可降低IL-1β和IL-6減輕ALI大鼠炎癥反應,具有一定的抗炎作用。
목적:비교3충지방유제대지다당(LPS)유도적급성폐손상(ALI)대서IL-1β화IL-6분비적영향。방법100지SD유년대서분위대조조、LPS조、ω-9조、ω-6조화ω-3조。일령28 d시련속7 d,대조조대서경미정맥주사생리염수;ω-6조주사지방유(C14~24)、ω-9조주사장련지방유、ω-3조주사ω-3어유지방유주사액;수후대조조기관내적입생리염수,령4조대서균분쇄LPS용액。8 h후처사대서관찰각조폐조직적병리개변,병측정IL-1β화IL-6 mRNA급단백등수평。결과각조대서폐조직병리절편균가견명현염증세포침윤화출혈;4조ALI대서적폐계수、폐손상평분균고우대조조,차이균유통계학의의(P균<0.005);ω-9조화ω-3조량조폐조직중IL-1β화IL-6 mRNA표체균교LPS조화ω-6조강저,차이균유통계학의의(P균<0.005);지기관폐포관세액중ω-9조화ω-3조IL-1β화IL-6단백수평균저우기여조,차이균유통계학의의(P균<0.005)。ω-9조화ω-3조IL-1β화IL-6 mRNA표체급기상응적단백수평차이균무통계학의의(P균>0.005)。결론ω-6 PUFAs가증가IL-1β화IL-6적산생가중ALI대서염증반응;이ω-9 MUFAs화ω-3 PUFAs가강저IL-1β화IL-6감경ALI대서염증반응,구유일정적항염작용。
Objective To compare the effect of three types of lipid emulsions on the IL-1βand IL-6 expressions in acute lung injury induced by lipopolysaccharide (LPS) in rats. Methods One hundred young SD rats were divided into control,LPS,ω-6,ω-9 andω-3 group. Age 29 days, the control group were intravenously injected with saline,ω-6 group injected lipid emu-sion (C14-24),ω-9 group injected long chain fat emusion,ω-3 group injected fish oil fat emusion. Then the control group fol-lowed by intratracheal instillation of saline, and the reamining four groups were sprayed with LPS. Pathologic changes in lung tissue section were observed. The expression levels of IL-1βmRNA and IL-6 mRNA were determined by RT-PCR,and the con-centrations of IL-1βand IL-6 in bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immune-specific assay. Results Infiltration and bleeding were observed in lung tissue under light microscopy in ALI rats. The lung indexes and patho-logical scores of ALI model groups were significantly higher than those of control group (P<0.005). The expressions of IL-1βand IL-6 mRNA in groupsω-9 andω-3 were significantly higher than those in groups LPS andω-6 (P<0.005). The levels of IL-1βand IL-6 in BALF in groupsω-9 andω-3 were significantly higher than those in groups LPS andω-6 (P<0.005). There was no significant difference (P>0.005) of the expressions of IL-1βand IL-6 mRNA betweenω-9 andω-3 group. Conclusions ω-6 PUFAs can accentuate inflammation by up-regulating the levels of IL-1βand IL-6 whileω-9 PUFAs andω-3 PUFAs can relieve inflammation by down-regulating the levels of IL-1βand IL-6.