中华临床营养杂志
中華臨床營養雜誌
중화림상영양잡지
CHINESE JOURNAL OF CLINICAL NUTRITION
2014年
1期
49-52
,共4页
殷宗宝%向群%计超%谢斌%侯宇
慇宗寶%嚮群%計超%謝斌%侯宇
은종보%향군%계초%사빈%후우
慢性阻塞性肺疾病%ω-3鱼油脂肪乳%干扰素-γ%核转录因子-κB%白细胞介素-6
慢性阻塞性肺疾病%ω-3魚油脂肪乳%榦擾素-γ%覈轉錄因子-κB%白細胞介素-6
만성조새성폐질병%ω-3어유지방유%간우소-γ%핵전록인자-κB%백세포개소-6
Chronic obstructive pulmonery disease%ω-3 fatty acids%Interferon-γ%Nuclear factor-κB%Interleukin-6
目的 探讨ω-3鱼油脂肪乳对烟熏加气管注入脂多糖法致慢性阻塞性肺疾病(COPD)大鼠干预的作用机制.方法 清洁级雄性大鼠90只,完全随机分成生理盐水对照组、烟熏加气管注入脂多糖法致大鼠COPD模型组、烟熏加气管注入脂多糖法致大鼠COPD模型+ω-3鱼油脂肪乳干预组.在第7、21、28天分别取左肺下叶供免疫组化检测核转录因子-κB (NF-κB)、干扰素-γ(IFN-γ)的表达,右肺下叶供HE染色病理观察；用ELISA双抗体夹心法测定各组大鼠血清白细胞介素-6(IL-6)、IFN-γ浓度.结果 (1)肺组织病理变化示第28天COPD模型组肺泡腔有大量炎性渗出,壁增厚,血管平滑肌增生,肺泡结构破坏；ω-3鱼油脂肪乳干预组肺组织结构部分破坏,肺泡腔少许炎性渗出；对照组大鼠几乎无肺泡炎发生.(2)第28天模型组大鼠肺组织NF-κB累计吸光度为18.91 ±3.07,显著高于对照组和干预组的5.47-±-4.86与7.23±2.21,差异均有统计学意义(均P＜0.01)；第28天模型组大鼠肺组织IFN-γ累计吸光度为7.12±3.37,显著低于干预组的18.74 ±2.65,差异有统计学意义(P＜0.01).(3)第28天模型组大鼠血清IL-6为(13.43 ±2.47) ng/L,显著高于对照组和干预组的(4.78±1.93)和(4.98±1.89) ng/L,差异均有统计学意义(均P＜0.01)；第28天模型组大鼠血清IFN-γ为(2.23 ±0.63) ng/L,显著低于对照组和干预组的(4.51±0.71)和(7.05±0.52)ng/L,差异均有统计学意义(均P＜0.01).结论 ω-3鱼油脂肪乳可以下调大鼠肺组织NF-κB,降低其血清含量和IL-6含量；上调肺组织1FN-γ表达,增加其血清含量,从两减轻COPD肺部炎症.
目的 探討ω-3魚油脂肪乳對煙熏加氣管註入脂多糖法緻慢性阻塞性肺疾病(COPD)大鼠榦預的作用機製.方法 清潔級雄性大鼠90隻,完全隨機分成生理鹽水對照組、煙熏加氣管註入脂多糖法緻大鼠COPD模型組、煙熏加氣管註入脂多糖法緻大鼠COPD模型+ω-3魚油脂肪乳榦預組.在第7、21、28天分彆取左肺下葉供免疫組化檢測覈轉錄因子-κB (NF-κB)、榦擾素-γ(IFN-γ)的錶達,右肺下葉供HE染色病理觀察；用ELISA雙抗體夾心法測定各組大鼠血清白細胞介素-6(IL-6)、IFN-γ濃度.結果 (1)肺組織病理變化示第28天COPD模型組肺泡腔有大量炎性滲齣,壁增厚,血管平滑肌增生,肺泡結構破壞；ω-3魚油脂肪乳榦預組肺組織結構部分破壞,肺泡腔少許炎性滲齣；對照組大鼠幾乎無肺泡炎髮生.(2)第28天模型組大鼠肺組織NF-κB纍計吸光度為18.91 ±3.07,顯著高于對照組和榦預組的5.47-±-4.86與7.23±2.21,差異均有統計學意義(均P＜0.01)；第28天模型組大鼠肺組織IFN-γ纍計吸光度為7.12±3.37,顯著低于榦預組的18.74 ±2.65,差異有統計學意義(P＜0.01).(3)第28天模型組大鼠血清IL-6為(13.43 ±2.47) ng/L,顯著高于對照組和榦預組的(4.78±1.93)和(4.98±1.89) ng/L,差異均有統計學意義(均P＜0.01)；第28天模型組大鼠血清IFN-γ為(2.23 ±0.63) ng/L,顯著低于對照組和榦預組的(4.51±0.71)和(7.05±0.52)ng/L,差異均有統計學意義(均P＜0.01).結論 ω-3魚油脂肪乳可以下調大鼠肺組織NF-κB,降低其血清含量和IL-6含量；上調肺組織1FN-γ錶達,增加其血清含量,從兩減輕COPD肺部炎癥.
목적 탐토ω-3어유지방유대연훈가기관주입지다당법치만성조새성폐질병(COPD)대서간예적작용궤제.방법 청길급웅성대서90지,완전수궤분성생리염수대조조、연훈가기관주입지다당법치대서COPD모형조、연훈가기관주입지다당법치대서COPD모형+ω-3어유지방유간예조.재제7、21、28천분별취좌폐하협공면역조화검측핵전록인자-κB (NF-κB)、간우소-γ(IFN-γ)적표체,우폐하협공HE염색병리관찰；용ELISA쌍항체협심법측정각조대서혈청백세포개소-6(IL-6)、IFN-γ농도.결과 (1)폐조직병리변화시제28천COPD모형조폐포강유대량염성삼출,벽증후,혈관평활기증생,폐포결구파배；ω-3어유지방유간예조폐조직결구부분파배,폐포강소허염성삼출；대조조대서궤호무폐포염발생.(2)제28천모형조대서폐조직NF-κB루계흡광도위18.91 ±3.07,현저고우대조조화간예조적5.47-±-4.86여7.23±2.21,차이균유통계학의의(균P＜0.01)；제28천모형조대서폐조직IFN-γ루계흡광도위7.12±3.37,현저저우간예조적18.74 ±2.65,차이유통계학의의(P＜0.01).(3)제28천모형조대서혈청IL-6위(13.43 ±2.47) ng/L,현저고우대조조화간예조적(4.78±1.93)화(4.98±1.89) ng/L,차이균유통계학의의(균P＜0.01)；제28천모형조대서혈청IFN-γ위(2.23 ±0.63) ng/L,현저저우대조조화간예조적(4.51±0.71)화(7.05±0.52)ng/L,차이균유통계학의의(균P＜0.01).결론 ω-3어유지방유가이하조대서폐조직NF-κB,강저기혈청함량화IL-6함량；상조폐조직1FN-γ표체,증가기혈청함량,종량감경COPD폐부염증.
Objective To explore the effectiveness of ω-3 fatty acids in intervening rat models of chronic obstructive pulmonery disease (COPD).Methods The rat COPD models were established by cigarette smoking and intratracheal lipopolysaccharide instillation.Totally 90 rats were randomly divided into 3 groups:normal control group (treated with normal saline),COPD group,and intervention group (the COPD rat models treated with ω-3 fatty acids).Lung tissues were obtained on the 7th,21st,and 28th day.The left lower lobes were analyzed to determine the expressions of nuclear factor-kappa beta (NF-κB) and interferon-γ (IFN-γ)and the right lung lobes were sliced for detecting the cell apoptosis.Double antibody sandwich enzyme-linked immunosorbent assay (DAS-ELISA) was used to detect the serum IFN-γ and interleukin-6 (IL-6).Results (1) The pathological changes of lung tissue:there were a large number of inflammatory exudation,alveolar wall thickening,hyperplasia of vascular smooth muscle and the alveolar structure destruction in the COPD model group,but the lung tissue were part of alveolar cavity and a little inflammatory exudate in ω-3 fatty fish acids treatment group,control rats were almost no alveolar inflammation on the 28th days.(2) On the 28th day,NF-κB protein expression of the lung tissue (18.91 ± 3.07) in rats of COPD model group was significantly higher than the control group and the intervention group (5.47 ±4.86 and 7.23 ±2.21) (P ＜0.01).On the 28th day,IFN-γ protein expression in lung tissue of the rats in the model group was 7.12 ±3.37,significantly lower than the intervention group (18.74 ± 2.65),the difference was statistically significant (P ＜ 0.01).(3) The IL-6 levels of the blood-serum of model group rats were (13.43 ± 2.47) ng/L,significantly higher than the control group and the intervention group [(4.78 ± 1.93) and (4.98 ± 1.89) ng/L],the differences were statistically significant (P ＜ 0.01) on the 28th day,,but the IFN-γ level [(2.23 ± 0.63) ng/L] in COPD group was more poorer than ω-3 fatty acids group and the intervention group [(4.51 ± 0.71) and (7.05 ± 0.52) ng/L] (P ＜ 0.01).Conclusions The ω-3 fatty acids can lower NF-κB protein expressions in lung tissues and serum and IL-6 levels in COPD rats; aslo,it can increase the IFN-γ protein expression in lung tissue and serum.Thus,it can prevent the lung inflammation in COPD rats.
