国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2013年
18期
1395-1398,封3
,共5页
陈伟%何振华%谭小武%欧阳劭
陳偉%何振華%譚小武%歐暘劭
진위%하진화%담소무%구양소
肺纤维化%细胞凋亡%Bid%Bcl-xl%姜黄素
肺纖維化%細胞凋亡%Bid%Bcl-xl%薑黃素
폐섬유화%세포조망%Bid%Bcl-xl%강황소
Pulmonary fibrosis%Apoptosis%Bid%Bcl-xl%Cucumin
目的 研究姜黄素对博莱霉素诱导的大鼠肺纤维化形成上皮细胞凋亡及Bcl-2家族部分蛋白的影响,探讨姜黄素治疗肺纤维化的可能机制.方法 选取SD大鼠72只,随机分为4组,每组18只:空白组、模型组、姜黄素组、泼尼松龙组.应用博莱霉素(5 mg/kg)气管内注入建立实验性大鼠肺纤维化模型,空白组注入等量生理盐水,造模后第2天起,姜黄素组和泼尼松龙组分别给予姜黄素(300mg/kg)和泼尼松(5mg/kg)每日灌胃1次,其余两组每日给予1％羧甲基纤维素钠(10ml/kg)灌胃1次.各组动物于7d、14d、28 d随机处死6只,取肺组织行HE、Masson染色评价肺组织病理变化,消化法测定肺组织羟脯氨酸(HYP),TUNEL法检测肺组织细胞凋亡.SABC法检测Bid及Bcl-xl蛋白的表达.结果 姜黄素组肺纤维化程度、病理改变及HYP含量及上皮细胞凋亡指数较同时期模型组降低(P值均＜0.01)；姜黄素组肺组织肺泡上皮细胞Bid表达较同时期模型组比较差异无统计学意义.姜黄素组肺组织肺泡上皮细胞Bcl-xl表达较同时期模型组升高(P值均＜0.01).结论 在博莱霉素诱导的大鼠肺纤维化形成阶段应用姜黄素干预能有效减轻肺纤维化程度,可能机制为姜黄素上调Bcl-xl的表达而非下调Bid表达来抑制上皮细胞凋亡.
目的 研究薑黃素對博萊黴素誘導的大鼠肺纖維化形成上皮細胞凋亡及Bcl-2傢族部分蛋白的影響,探討薑黃素治療肺纖維化的可能機製.方法 選取SD大鼠72隻,隨機分為4組,每組18隻:空白組、模型組、薑黃素組、潑尼鬆龍組.應用博萊黴素(5 mg/kg)氣管內註入建立實驗性大鼠肺纖維化模型,空白組註入等量生理鹽水,造模後第2天起,薑黃素組和潑尼鬆龍組分彆給予薑黃素(300mg/kg)和潑尼鬆(5mg/kg)每日灌胃1次,其餘兩組每日給予1％羧甲基纖維素鈉(10ml/kg)灌胃1次.各組動物于7d、14d、28 d隨機處死6隻,取肺組織行HE、Masson染色評價肺組織病理變化,消化法測定肺組織羥脯氨痠(HYP),TUNEL法檢測肺組織細胞凋亡.SABC法檢測Bid及Bcl-xl蛋白的錶達.結果 薑黃素組肺纖維化程度、病理改變及HYP含量及上皮細胞凋亡指數較同時期模型組降低(P值均＜0.01)；薑黃素組肺組織肺泡上皮細胞Bid錶達較同時期模型組比較差異無統計學意義.薑黃素組肺組織肺泡上皮細胞Bcl-xl錶達較同時期模型組升高(P值均＜0.01).結論 在博萊黴素誘導的大鼠肺纖維化形成階段應用薑黃素榦預能有效減輕肺纖維化程度,可能機製為薑黃素上調Bcl-xl的錶達而非下調Bid錶達來抑製上皮細胞凋亡.
목적 연구강황소대박래매소유도적대서폐섬유화형성상피세포조망급Bcl-2가족부분단백적영향,탐토강황소치료폐섬유화적가능궤제.방법 선취SD대서72지,수궤분위4조,매조18지:공백조、모형조、강황소조、발니송룡조.응용박래매소(5 mg/kg)기관내주입건립실험성대서폐섬유화모형,공백조주입등량생리염수,조모후제2천기,강황소조화발니송룡조분별급여강황소(300mg/kg)화발니송(5mg/kg)매일관위1차,기여량조매일급여1％최갑기섬유소납(10ml/kg)관위1차.각조동물우7d、14d、28 d수궤처사6지,취폐조직행HE、Masson염색평개폐조직병리변화,소화법측정폐조직간포안산(HYP),TUNEL법검측폐조직세포조망.SABC법검측Bid급Bcl-xl단백적표체.결과 강황소조폐섬유화정도、병리개변급HYP함량급상피세포조망지수교동시기모형조강저(P치균＜0.01)；강황소조폐조직폐포상피세포Bid표체교동시기모형조비교차이무통계학의의.강황소조폐조직폐포상피세포Bcl-xl표체교동시기모형조승고(P치균＜0.01).결론 재박래매소유도적대서폐섬유화형성계단응용강황소간예능유효감경폐섬유화정도,가능궤제위강황소상조Bcl-xl적표체이비하조Bid표체래억제상피세포조망.
Objective To investigate the expression of Bcl-2 family protein and apoptosis in epithelial cells of pulmonary fibrosis rats induced by bleomycin on different times,and observe the curcumin intervention in the formation stage of pulmonary fibrosis and explore its possible mechanism.Methods Seventy-two Sprague Dawley rats were randomly divided into four groups:control group,model group,cucumin group,and prednisone group.Model group,cucumin group,and prednisone group were induced to produce pulmonary fibrosis with bleomycin endotracheally while control group was given with normal saline instead in the same condition.From the second day after bleomycin administration,the curcumin group was given with curcumin (300 mg/kg) while prednisone group with prednisone (5 mg/kg) per day by intragastric administration,respectively.The control group and model group were given with 1％ sodium carboxymethyl cellulose (10 ml/kg).Six rats of each group were randomly sacrificed on 7th,14th,and 28th day after bleomycin administration,respectively.The histological changes of the lung were evaluated by HE and Masson staining.The level of hydroxyproline in lung tissue was assessed by digestion method.The immunohistochemical method was used to investigate the changes of Bid and Bcl-xl protein.TUNEL was used to detect the change of cell apoptosis.Results The cell apoptosis index,hydroxyproline and histological changes of the lung in cucumin group were lower than those in model group (P ＜0.01).There was no significant difference in the expression of Bid protein between model group and cucumin group.The expression of Bcl-xl protein in model group was lower than that in cucumin group (P ＜0.01).Conclusions Cucumin can reduce the expression of pulmonary fibrosis through inhibition of apoptosis of epithelial cells.It may up-regulate the expression of Bcl-xl in alveolar epithelial cells and bronchial cells of pulmonary fibrosis rats but not down-regulate the expression of Bid.
