中国急救医学
中國急救醫學
중국급구의학
CHINESE JOURNAL OF CRITICAL CARE MEDICINE
2009年
11期
973-977
,共5页
王平%巩建平%张建新%金普乐
王平%鞏建平%張建新%金普樂
왕평%공건평%장건신%금보악
硫化氢(H_2S)%急性肺损伤(ALI)%白细胞介素-1β%白细胞介素-10%核内转录因子-κB%细胞间黏附分子-1
硫化氫(H_2S)%急性肺損傷(ALI)%白細胞介素-1β%白細胞介素-10%覈內轉錄因子-κB%細胞間黏附分子-1
류화경(H_2S)%급성폐손상(ALI)%백세포개소-1β%백세포개소-10%핵내전록인자-κB%세포간점부분자-1
Hydrogen sulfide%Acute lung injure%Interleukin-1β%Interleukin-10%Nuclear factor-ΚB%Intercellular adhesion molecule-1
目的 观察硫化氢(H_2S)对脂多糖(LPS)所致大鼠内毒素性急性肺损伤(ALI)炎性细胞因子的影响,探讨其对肺脏的作用机制.方法 雄性SD 大鼠共48只,随机分为六组,每组8只:空白对照组、LPS 组、LPS+NaHS 低剂量组、LPS+NaHS 中剂量组、LPS+NaHS 高剂量组及LPS+PPG 组.所有大鼠均检测血清中白细胞介素-1β(IL-1β)和IL-10浓度的变化,取肺组织检测肺组织中IL-1β、IL-10、黏附分子-1(ICAM-1)mRNA基因表达变化及肺组织NF-κB p65活性变化.结果 与空白对照组比较,LPS组大鼠血清中IL-1β和IL-10浓度,肺组织中IL-1β、IL-10和ICAM-1 mRNA基因表达和NF-κB p65活性均明显升高(P<0.01).与LPS组比较,LPS+NaHS低、中、高剂量组血清中IL-1β浓度、肺组织中IL-1βmRNA基因表达和NF-κB p65活性均明显降低;LPS+NaHS中、高剂量组血清中IL-10浓度和IL-10 mRNA基因表达明显升高,ICAM-1 mRNA基因表达明显降低(P<0.05或P<0.01).与LPS组比较,LPS+PPG组血清中IL-1β浓度、肺组织中IL-1β和ICAM-1 mRNA基因表达及NF-κB p65活性均明显升高,血清中IL- 10浓度和肺组织中IL-10 mRNA基因表达明显降低(P<0.05或P<0.01).结论 H_2S对内毒素诱导的ALI大鼠有保护性作用,其作用机制可能与H_2S调节炎性细胞因子的生成有关.
目的 觀察硫化氫(H_2S)對脂多糖(LPS)所緻大鼠內毒素性急性肺損傷(ALI)炎性細胞因子的影響,探討其對肺髒的作用機製.方法 雄性SD 大鼠共48隻,隨機分為六組,每組8隻:空白對照組、LPS 組、LPS+NaHS 低劑量組、LPS+NaHS 中劑量組、LPS+NaHS 高劑量組及LPS+PPG 組.所有大鼠均檢測血清中白細胞介素-1β(IL-1β)和IL-10濃度的變化,取肺組織檢測肺組織中IL-1β、IL-10、黏附分子-1(ICAM-1)mRNA基因錶達變化及肺組織NF-κB p65活性變化.結果 與空白對照組比較,LPS組大鼠血清中IL-1β和IL-10濃度,肺組織中IL-1β、IL-10和ICAM-1 mRNA基因錶達和NF-κB p65活性均明顯升高(P<0.01).與LPS組比較,LPS+NaHS低、中、高劑量組血清中IL-1β濃度、肺組織中IL-1βmRNA基因錶達和NF-κB p65活性均明顯降低;LPS+NaHS中、高劑量組血清中IL-10濃度和IL-10 mRNA基因錶達明顯升高,ICAM-1 mRNA基因錶達明顯降低(P<0.05或P<0.01).與LPS組比較,LPS+PPG組血清中IL-1β濃度、肺組織中IL-1β和ICAM-1 mRNA基因錶達及NF-κB p65活性均明顯升高,血清中IL- 10濃度和肺組織中IL-10 mRNA基因錶達明顯降低(P<0.05或P<0.01).結論 H_2S對內毒素誘導的ALI大鼠有保護性作用,其作用機製可能與H_2S調節炎性細胞因子的生成有關.
목적 관찰류화경(H_2S)대지다당(LPS)소치대서내독소성급성폐손상(ALI)염성세포인자적영향,탐토기대폐장적작용궤제.방법 웅성SD 대서공48지,수궤분위륙조,매조8지:공백대조조、LPS 조、LPS+NaHS 저제량조、LPS+NaHS 중제량조、LPS+NaHS 고제량조급LPS+PPG 조.소유대서균검측혈청중백세포개소-1β(IL-1β)화IL-10농도적변화,취폐조직검측폐조직중IL-1β、IL-10、점부분자-1(ICAM-1)mRNA기인표체변화급폐조직NF-κB p65활성변화.결과 여공백대조조비교,LPS조대서혈청중IL-1β화IL-10농도,폐조직중IL-1β、IL-10화ICAM-1 mRNA기인표체화NF-κB p65활성균명현승고(P<0.01).여LPS조비교,LPS+NaHS저、중、고제량조혈청중IL-1β농도、폐조직중IL-1βmRNA기인표체화NF-κB p65활성균명현강저;LPS+NaHS중、고제량조혈청중IL-10농도화IL-10 mRNA기인표체명현승고,ICAM-1 mRNA기인표체명현강저(P<0.05혹P<0.01).여LPS조비교,LPS+PPG조혈청중IL-1β농도、폐조직중IL-1β화ICAM-1 mRNA기인표체급NF-κB p65활성균명현승고,혈청중IL- 10농도화폐조직중IL-10 mRNA기인표체명현강저(P<0.05혹P<0.01).결론 H_2S대내독소유도적ALI대서유보호성작용,기작용궤제가능여H_2S조절염성세포인자적생성유관.
Objective To study the effect of hydrogen sulfide ( H_2S) on inflammatory factor in acute lung injury induced by lipopolysaccharide (LPS) in rats and to explore the mechanism. Methods Fourty - eight male rats were randomly divided into six groups ( n = 8) ; control group, LPS group, LPS + NaHS Low dose group,LPS + NaHS Middle dose group, LPS + NaHS High dose group, and LPS + PPG group. The contents of interleukin-1β (IL-1β) and interleukin -10 (IL-10) in serum, and their mRNA expression in lung tissue were respectively measured. The expression of intercellular adhe-sion molecule - 1 (ICAM - 1) mRNA and the nuclear factor -ΚB p65 ( NF - ΚB p65) activity in lung tissue were respectively detected. Results Compared with control group, the contents of IL -1β and IL - 10 in serum, the expression of IL - 1β, IL - 10 and ICAM - 1 mRNA, and the activity of NF-ΚB p65 in lung tissue were significantly increased in LPS group. Compared with LPS group, the content of IL-1β in serum, the expression of IL-1β mRNA and the activity of NF-ΚB p65 in lung tissue were significantly decreased in LPS + NaHS Low, Middle and High dose groups. The expression of ICAM - 1 mRNA was significantly decreased, the content of IL-10 in serum and the expression of IL-10 mRNA were significantly increased in LPS + NaHS Middle and High dose groups. Compared with LPS group, the content of IL - 1β in serum, the expression of IL-1β and ICAM - 1 mRNA, and the activity of NF - ΚB p65 in lung tissue were significantly increased, while the content of IL-10 in serum and the expression of IL - 10 mRNA were significantly decreased in the LPS + PPG group. Conclusion H_2S could ameliorate the ALI induced by LPS in rats, the mechanism may be H_2S could regulate the inflam-matory factors formation.
