目的:比较不同给氧方案对脂多糖(lipopolysaccharide,LPS)诱导的急性肾损伤(acute kidney injury,AKI)模型小鼠肾组织炎症性损伤及外周血炎症因子的影响。方法:采用ICR雌性小鼠,腹腔注射LPS(5 mg/kg)建立小鼠AKI模型,随机分成:(1)空白组...目的:比较不同给氧方案对脂多糖(lipopolysaccharide,LPS)诱导的急性肾损伤(acute kidney injury,AKI)模型小鼠肾组织炎症性损伤及外周血炎症因子的影响。方法:采用ICR雌性小鼠,腹腔注射LPS(5 mg/kg)建立小鼠AKI模型,随机分成:(1)空白组(Control组),注射同等量的生理盐水;(2)模型组(LPS组);(3)纯氧治疗组(LPS+100%O_(2)组);(4)2.0绝对大气压(atmosphere absolute,ATA)高压氧(hyperbaric oxygen,HBO)治疗组(LPS+2.0 ATA HBO组);(5)3.0 ATA HBO治疗组(LPS+3.0 ATA HBO组),治疗后24 h,通过流式微球技术及实时荧光定量PCR(real-time PCR,RT-PCR)实验分别检测肾组织和外周血中促炎因子IL-1β、IL-6和TNF-α,以及抑炎因子IL-10水平。此外,通过HE染色法观察肾组织炎症性损伤的组织形态变化。结果:IL-1β、IL-6和TNF-α在LPS诱导24 h后均显著增加;100%O_(2)和2.0 ATA HBO治疗均可抑制促炎因子IL-1β、IL-6和TNF-α的释放,且2.0 ATA HBO抑制作用更显著(P<0.05或P<0.01);此外,LPS+2.0ATA HBO组抑炎因子IL-10水平显著增高(P<0.01)。HE染色结果表明,与LPS组相比,100%O_(2)和2.0 ATA HBO治疗后,肾组织炎症性损伤均有所减轻,且LPS+2.0 ATA HBO组改善效果最好(P<0.05或P<0.01),而LPS+3.0 ATA HBO组肾组织损伤未改善。结论:100%O_(2)和2.0 ATA HBO治疗均可明显改善AKI小鼠炎症性损伤,且2.0 ATA HBO改善作用更好。展开更多
Oxygen inhalation has been shown to increase oxygen supply to tissues after cerebral ischemia/ reperfusion injury, protecting injured neural cells. However, hyperbaric oxygen may aggravate oxi- dative stress. By contr...Oxygen inhalation has been shown to increase oxygen supply to tissues after cerebral ischemia/ reperfusion injury, protecting injured neural cells. However, hyperbaric oxygen may aggravate oxi- dative stress. By contrast, normobaric oxygen has the rapid and non-invasive characteristics and may have therapeutic effects on ischemic/hypoxic disease. Rats inhaled normobaric oxygen （95% 02） for 6 consecutive days, and then a rat model of focal cerebral ischemia was established. Nisst and 2,3,5-triphenyltetrazolium chloride （TTC） staining revealed that normobaric oxygen pretreat- ment improved neurological deficits and reduced infarct volume. Immunohistochemical staining and western blot assay revealed that the expression of hypoxia-inducible factor-la, Notch-l, vascular endothelial growth factor and erythropoietin were increased. Behavioral studies also verified that neurological deficit scores increased. The hypoxia-inducible factor inhibitor 2-methoxyestradiol treatment at 1 hour before administration of normobaric oxygen could suppress the protective effect of normobaric oxygen. Given these observations, normobaric oxygen pretreatment may alleviate cerebral ischemic injury via the hypoxia-inducible factor signal pathway.展开更多
文摘目的:比较不同给氧方案对脂多糖(lipopolysaccharide,LPS)诱导的急性肾损伤(acute kidney injury,AKI)模型小鼠肾组织炎症性损伤及外周血炎症因子的影响。方法:采用ICR雌性小鼠,腹腔注射LPS(5 mg/kg)建立小鼠AKI模型,随机分成:(1)空白组(Control组),注射同等量的生理盐水;(2)模型组(LPS组);(3)纯氧治疗组(LPS+100%O_(2)组);(4)2.0绝对大气压(atmosphere absolute,ATA)高压氧(hyperbaric oxygen,HBO)治疗组(LPS+2.0 ATA HBO组);(5)3.0 ATA HBO治疗组(LPS+3.0 ATA HBO组),治疗后24 h,通过流式微球技术及实时荧光定量PCR(real-time PCR,RT-PCR)实验分别检测肾组织和外周血中促炎因子IL-1β、IL-6和TNF-α,以及抑炎因子IL-10水平。此外,通过HE染色法观察肾组织炎症性损伤的组织形态变化。结果:IL-1β、IL-6和TNF-α在LPS诱导24 h后均显著增加;100%O_(2)和2.0 ATA HBO治疗均可抑制促炎因子IL-1β、IL-6和TNF-α的释放,且2.0 ATA HBO抑制作用更显著(P<0.05或P<0.01);此外,LPS+2.0ATA HBO组抑炎因子IL-10水平显著增高(P<0.01)。HE染色结果表明,与LPS组相比,100%O_(2)和2.0 ATA HBO治疗后,肾组织炎症性损伤均有所减轻,且LPS+2.0 ATA HBO组改善效果最好(P<0.05或P<0.01),而LPS+3.0 ATA HBO组肾组织损伤未改善。结论:100%O_(2)和2.0 ATA HBO治疗均可明显改善AKI小鼠炎症性损伤,且2.0 ATA HBO改善作用更好。
基金supported by the National Natural Science Foundation of China,No.81000523the grant from Peking University Health Science Center for the New Teacher Funding,No.BMU20090463
文摘Oxygen inhalation has been shown to increase oxygen supply to tissues after cerebral ischemia/ reperfusion injury, protecting injured neural cells. However, hyperbaric oxygen may aggravate oxi- dative stress. By contrast, normobaric oxygen has the rapid and non-invasive characteristics and may have therapeutic effects on ischemic/hypoxic disease. Rats inhaled normobaric oxygen （95% 02） for 6 consecutive days, and then a rat model of focal cerebral ischemia was established. Nisst and 2,3,5-triphenyltetrazolium chloride （TTC） staining revealed that normobaric oxygen pretreat- ment improved neurological deficits and reduced infarct volume. Immunohistochemical staining and western blot assay revealed that the expression of hypoxia-inducible factor-la, Notch-l, vascular endothelial growth factor and erythropoietin were increased. Behavioral studies also verified that neurological deficit scores increased. The hypoxia-inducible factor inhibitor 2-methoxyestradiol treatment at 1 hour before administration of normobaric oxygen could suppress the protective effect of normobaric oxygen. Given these observations, normobaric oxygen pretreatment may alleviate cerebral ischemic injury via the hypoxia-inducible factor signal pathway.
