中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
1期
118-120
,共3页
脂多糖类%成纤维细胞%细胞存活%肺
脂多糖類%成纖維細胞%細胞存活%肺
지다당류%성섬유세포%세포존활%폐
Lipopolysaccharides%Fibroblasts%Cell survival%Lung
目的 评价脂多糖(LPS)对小鼠肺成纤维细胞活化的影响.方法 原代培养的小鼠肺成纤维细胞,接种于96孔培养板,采用随机数字表法,将其随机分为2组,正常对照组(C组,外=6)不作任何处理,LPS组(n=24)加入LPS 1μg/ml,分别于LPS孵育3、6、24、72 h时取6孔(C组于培养72 h时),收集细胞,采用实时PCR法测定Ⅰ型前胶原mRNA、α-平滑肌肌动蛋白(α-SMA)mRNA、Toll样受体4(TLR4)mRNA和整合素β1 mRNA的表达水平.结果 与C组比较,LPS组LPS孵育3、6和24 h时Ⅰ型前胶原mRNA、α-SMA mRNA、TLR4 mRNA和整合素β1 mRNA的表达水平差异无统计学意义(P＞0.05),LPS孵育72 h时上述指标表达水平上调(P＜0.05).结论 在急性肺损伤的早期LPS一方面可直接活化小鼠肺成纤维细胞,导致肺纤维化;另一方面可上调TLR4和整合素β1的表达,增加细胞对LPS的反应性,从而加速小鼠肺成纤维细胞的活化,促进肺纤维化.
目的 評價脂多糖(LPS)對小鼠肺成纖維細胞活化的影響.方法 原代培養的小鼠肺成纖維細胞,接種于96孔培養闆,採用隨機數字錶法,將其隨機分為2組,正常對照組(C組,外=6)不作任何處理,LPS組(n=24)加入LPS 1μg/ml,分彆于LPS孵育3、6、24、72 h時取6孔(C組于培養72 h時),收集細胞,採用實時PCR法測定Ⅰ型前膠原mRNA、α-平滑肌肌動蛋白(α-SMA)mRNA、Toll樣受體4(TLR4)mRNA和整閤素β1 mRNA的錶達水平.結果 與C組比較,LPS組LPS孵育3、6和24 h時Ⅰ型前膠原mRNA、α-SMA mRNA、TLR4 mRNA和整閤素β1 mRNA的錶達水平差異無統計學意義(P＞0.05),LPS孵育72 h時上述指標錶達水平上調(P＜0.05).結論 在急性肺損傷的早期LPS一方麵可直接活化小鼠肺成纖維細胞,導緻肺纖維化;另一方麵可上調TLR4和整閤素β1的錶達,增加細胞對LPS的反應性,從而加速小鼠肺成纖維細胞的活化,促進肺纖維化.
목적 평개지다당(LPS)대소서폐성섬유세포활화적영향.방법 원대배양적소서폐성섬유세포,접충우96공배양판,채용수궤수자표법,장기수궤분위2조,정상대조조(C조,외=6)불작임하처리,LPS조(n=24)가입LPS 1μg/ml,분별우LPS부육3、6、24、72 h시취6공(C조우배양72 h시),수집세포,채용실시PCR법측정Ⅰ형전효원mRNA、α-평활기기동단백(α-SMA)mRNA、Toll양수체4(TLR4)mRNA화정합소β1 mRNA적표체수평.결과 여C조비교,LPS조LPS부육3、6화24 h시Ⅰ형전효원mRNA、α-SMA mRNA、TLR4 mRNA화정합소β1 mRNA적표체수평차이무통계학의의(P＞0.05),LPS부육72 h시상술지표표체수평상조(P＜0.05).결론 재급성폐손상적조기LPS일방면가직접활화소서폐성섬유세포,도치폐섬유화;령일방면가상조TLR4화정합소β1적표체,증가세포대LPS적반응성,종이가속소서폐성섬유세포적활화,촉진폐섬유화.
Objective To investigate the effect of lipopolysaccharide (LPS) on the activation of mouse lung fibroblasts. Methods Primary cultured mouse lung fibroblasts were incubated in 96 well plates and randomly divided into 2 groups: control group ( group C, n = 6) and LPS group ( n = 24). The fibroblasts were cultured for 72 h in group C. LPS 1 μg/ml was added and then the fibroblasts were incubated for 72 h in group LPS. The expression of type Ⅰ procollagen mRNA, α-smooth muscle actin (α-SMA) mRNA, Toll-like receptor 4 (TLR4)mRNA and integrin β1 mRNA was determined using real-time PCR at 3, 6, 24 and 72 h of incubation (6 wells at each time point). Results Compared with group C, there was no significant change in the expression of type Ⅰ procollagen mRNA, α-SMA mRNA, TLR4 mRNA and integrin β1 mRNA at 3, 6 and 24 h of incubation ( P ＞0.05), but the parameters mentioned above were significantly up-regulated at 72 h of incubation in group LPS ( P ＜ 0.05). Conclusion In the early acute lung injury, LPS leads to pulmonary fibrosis through activating lung fibroblasts directly, and also accelerates the activation of lung fibroblasts and promotes the process of pulmonary fibrosis through up-regulating the expression of TLR4 and integrin β1 in mice.
