重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2013年
26期
3139-3141
,共3页
矽肺%N-乙酰基-丝氨酰-天门冬酰-赖氨酰-脯氨酸 ,核转录因子κB p65
矽肺%N-乙酰基-絲氨酰-天門鼕酰-賴氨酰-脯氨痠 ,覈轉錄因子κB p65
석폐%N-을선기-사안선-천문동선-뢰안선-포안산 ,핵전록인자κB p65
silicosis%N-acetyl-seryl-aspartyl-lysyl-proline%NF-κB p65
目的研究N-乙酰基-丝氨酰-天门冬酰-赖氨酰-脯氨酸（AcSDKP）对硅肺纤维化大鼠肺内胶原合成及核转录因子κB（NF-κB）p65的影响。方法将大鼠分为3组：对照组（每只大鼠支气管内灌注生理盐水1mL，8周后处死）、硅肺模型组（每只大鼠支气管内灌注SiO2混悬液1mL，8周后处死）、AcSDKP治疗组（每只大鼠支气管内灌注SiO2混悬液1mL，并持续给予AcS-DKP800μg·kg-1·d-1，8周后处死）。从HE染色、VG染色和羟脯氨酸胶原测定法检测各组大鼠肺纤维化程度及胶原含量，用免疫组化法和免疫印迹法检测NF-κBp65蛋白的表达。结果与对照组比较，硅肺模型组硅结节的数量、胶原含量和NF-κBp65的表达增高。与硅肺模型组相比，AcSDKP治疗组矽结节的数量、胶原含量和NF-κBp65的表达降低。结论AcSDKP可能会通过增加B抑制蛋白（I-κB）的稳定性来抑制NF-κBp65的活性及表达，进而影响着肺泡炎与硅肺纤维化的进展。
目的研究N-乙酰基-絲氨酰-天門鼕酰-賴氨酰-脯氨痠（AcSDKP）對硅肺纖維化大鼠肺內膠原閤成及覈轉錄因子κB（NF-κB）p65的影響。方法將大鼠分為3組：對照組（每隻大鼠支氣管內灌註生理鹽水1mL，8週後處死）、硅肺模型組（每隻大鼠支氣管內灌註SiO2混懸液1mL，8週後處死）、AcSDKP治療組（每隻大鼠支氣管內灌註SiO2混懸液1mL，併持續給予AcS-DKP800μg·kg-1·d-1，8週後處死）。從HE染色、VG染色和羥脯氨痠膠原測定法檢測各組大鼠肺纖維化程度及膠原含量，用免疫組化法和免疫印跡法檢測NF-κBp65蛋白的錶達。結果與對照組比較，硅肺模型組硅結節的數量、膠原含量和NF-κBp65的錶達增高。與硅肺模型組相比，AcSDKP治療組矽結節的數量、膠原含量和NF-κBp65的錶達降低。結論AcSDKP可能會通過增加B抑製蛋白（I-κB）的穩定性來抑製NF-κBp65的活性及錶達，進而影響著肺泡炎與硅肺纖維化的進展。
목적연구N-을선기-사안선-천문동선-뢰안선-포안산（AcSDKP）대규폐섬유화대서폐내효원합성급핵전록인자κB（NF-κB）p65적영향。방법장대서분위3조：대조조（매지대서지기관내관주생리염수1mL，8주후처사）、규폐모형조（매지대서지기관내관주SiO2혼현액1mL，8주후처사）、AcSDKP치료조（매지대서지기관내관주SiO2혼현액1mL，병지속급여AcS-DKP800μg·kg-1·d-1，8주후처사）。종HE염색、VG염색화간포안산효원측정법검측각조대서폐섬유화정도급효원함량，용면역조화법화면역인적법검측NF-κBp65단백적표체。결과여대조조비교，규폐모형조규결절적수량、효원함량화NF-κBp65적표체증고。여규폐모형조상비，AcSDKP치료조석결절적수량、효원함량화NF-κBp65적표체강저。결론AcSDKP가능회통과증가B억제단백（I-κB）적은정성래억제NF-κBp65적활성급표체，진이영향착폐포염여규폐섬유화적진전。
Objective To investigate the effect of N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) on the synthesis of collagen and the expression of NF-κB p65 in lung of rats with silicosis fibrosis .Methods Rats were divided into 3 groups randomly :the control group(each rat was intratracheally instilled with 1 mL normal saline and killed after 8 weeks ,the silicotic model group(each rat was intratracheally instilled with 1 mL silica suspension and killed after 8 weeks ,the AcSDKP treated group(each rat was intra-tracheally instilled with 1 mL silica suspension and AcSDKP (800 μg · kg -1 · d-1 ) was administered into every rat ,then rats were killed after 8 weeks .Lung fibrosis in morphology and collagen content was observed by HE and vg staining and hydroxyproline as-say .The expression of NF-κB p65 was detected with the immunohistochemistry and Western blot .Results Compared with the con-trol group ,the quantity of silicon nodules ,collagen content and the expression of NF-κB p65were increased in the silicotic model group .Compared with the silicotic model group ,the quantity of silicon nodules ,collagen content and the expression of NF-κB p65 were decreased in the AcSDKP-treated group .Conclusion AcSDKP could inhibit the activity and expression of NF-κB p65 by strengthening the stability of I-κB ,which may influence the progress of alveolar inflammation and silicosis fibrosis .
