Objective：To observe the protective effects of safflor Injection（SI） and extract of Ginkgo biloba（EGB） on lung ischemia-reperfusion injury（LIRI） and investigate its mechanism.Methods：In vivo rabbit model of LI...Objective：To observe the protective effects of safflor Injection（SI） and extract of Ginkgo biloba（EGB） on lung ischemia-reperfusion injury（LIRI） and investigate its mechanism.Methods：In vivo rabbit model of LIRI was reconstructed.Forty rabbits were randomly and equally divided into four groups：sham-operation group（sham group）,ischemia-reperfusion group（model group）,ischemia-reperfusion plus SI group（safflor group） and ischemia-reperfusion plus EGB injection group（EGB group）.Malondialdehyde（MDA） content,superoxide dismutase（SOD） and xanthine oxidase（XO） activity in serum were measured.The wet/dry weight ratio（W/D） of the lung tissue and activity of myeloperoxidase（MPO） were also tested.Ultrastructure change of the lung tissue was observed by the electron microscope.The expression of intercellular adhesion molecule-1（ICAM-1） was measured by immunohistochemistry（IHC）.Results：In the model group,MDA and XO increased and SOD decreased in serum compared with the sham group（P〈0.01）.The values of W/D,MPO and ICAM-1 of the model group were higher than those of the sham group（P〈0.01）,but those of the safflor group and EGB group were significantly lower than those of the model group（P〈0.01）.The IHC demonstrated that ICAM-1 expression in lung tissue of the model group was significantly higher than those of the safflor group（P〈0.01）.Compared with safflor group,in the EGB group MDA,XO,MPO decreased,SOD and ICAM-1expression increased（P〈0.05）,but the change of W/D was not statistically significant（P〉0.05）.Conclusions：SI and EGB may attenuate LIRI through antioxidation,inhibition of neutrophil aggregation and down-regulation of ICAM-1expression.But EGB had more effect on the antioxidation,while SI did better on regulating ICAM-1 expression.展开更多
Objective： To observe the effect of Safflor Yellow （SY） Injection on acute lung injury （ALl） induced by lipopolysaccharide （LPS） in mice. Methods： Seventy-two mice were divided into six groups： control （sali...Objective： To observe the effect of Safflor Yellow （SY） Injection on acute lung injury （ALl） induced by lipopolysaccharide （LPS） in mice. Methods： Seventy-two mice were divided into six groups： control （saline ＋ saline）; LPS （LPS ＋ saline）; SY Injection [LPS ＋ SY （10, 20 or 40 mg/kg, intravenously）] and anisodamine （AD） （LPS ＋ AD）. Thirty minutes after SY or AD administration, 15 mg/kg LPS was given intraperitoneally. All animals were sacrificed 4 h after LPS injection. Arterial blood gas and lung water content index （LWCI） were measured. Lung tissue myeloperoxidase （MPO） activity was assayed, mRNA expression of inflammatory cytokines was assayed by reverse-transcription polymerase chain reaction. Lung morphological and nuclear factor （NF）- K B p65-positive cell changes were observed by HE and immunohistochemical staining, p38 mitogen-activated protein kinase （MAPK） phosphorylation was observed by Western blotting. Results： After LPS administration, all animals displayed increased arterial carbon dioxide partial pressure （PaCO2） and decreased arterial oxygen partial pressure （PaO2）, arterial oxygen saturation （SO2）, HCOs concentration and pH, and increased LWCI, MPO activity, interleukin （IL）-I β, IL-6 and tumor necrosis factor （TNF）-ot mRNA expression, NF-K B p65 positive staining and p38 MAPK activation compared with normal controls （all P〈0.01）. SY Injection significantly mitigated the LPS-induced increase in arterial PaCO2 and the decreases in arterial PaO2, SO2 and pH, and attenuated increases in LWCI and lung tissue MPO activity （all P〈0.01）. Moreover, SY Injection inhibited the increases in NF- K B p65 staining and in TNF-α, IL-1 β and IL-6 mRNA expression （all P〈0.01）, and promoted the expression of the antiinflammatory cytokine IL-10 （P〈0.05） following LPS injection. LPS-induced pulmonary p38 MAPK phosphorylation was suppressed by pretreatment with SY Injection （P〈0.01）. Conclusion： SY Injection ameliorates inflammatory ALl induced by LPS in mice.展开更多
文摘Objective：To observe the protective effects of safflor Injection（SI） and extract of Ginkgo biloba（EGB） on lung ischemia-reperfusion injury（LIRI） and investigate its mechanism.Methods：In vivo rabbit model of LIRI was reconstructed.Forty rabbits were randomly and equally divided into four groups：sham-operation group（sham group）,ischemia-reperfusion group（model group）,ischemia-reperfusion plus SI group（safflor group） and ischemia-reperfusion plus EGB injection group（EGB group）.Malondialdehyde（MDA） content,superoxide dismutase（SOD） and xanthine oxidase（XO） activity in serum were measured.The wet/dry weight ratio（W/D） of the lung tissue and activity of myeloperoxidase（MPO） were also tested.Ultrastructure change of the lung tissue was observed by the electron microscope.The expression of intercellular adhesion molecule-1（ICAM-1） was measured by immunohistochemistry（IHC）.Results：In the model group,MDA and XO increased and SOD decreased in serum compared with the sham group（P〈0.01）.The values of W/D,MPO and ICAM-1 of the model group were higher than those of the sham group（P〈0.01）,but those of the safflor group and EGB group were significantly lower than those of the model group（P〈0.01）.The IHC demonstrated that ICAM-1 expression in lung tissue of the model group was significantly higher than those of the safflor group（P〈0.01）.Compared with safflor group,in the EGB group MDA,XO,MPO decreased,SOD and ICAM-1expression increased（P〈0.05）,but the change of W/D was not statistically significant（P〉0.05）.Conclusions：SI and EGB may attenuate LIRI through antioxidation,inhibition of neutrophil aggregation and down-regulation of ICAM-1expression.But EGB had more effect on the antioxidation,while SI did better on regulating ICAM-1 expression.
基金Supported by National Natural Science Foundation of China(No.30572344)Natural Science Foundation of Beijing(No.7102025)Science and Technology Personnel ServeEnterprise Action(No.2009GJA30001)
文摘Objective： To observe the effect of Safflor Yellow （SY） Injection on acute lung injury （ALl） induced by lipopolysaccharide （LPS） in mice. Methods： Seventy-two mice were divided into six groups： control （saline ＋ saline）; LPS （LPS ＋ saline）; SY Injection [LPS ＋ SY （10, 20 or 40 mg/kg, intravenously）] and anisodamine （AD） （LPS ＋ AD）. Thirty minutes after SY or AD administration, 15 mg/kg LPS was given intraperitoneally. All animals were sacrificed 4 h after LPS injection. Arterial blood gas and lung water content index （LWCI） were measured. Lung tissue myeloperoxidase （MPO） activity was assayed, mRNA expression of inflammatory cytokines was assayed by reverse-transcription polymerase chain reaction. Lung morphological and nuclear factor （NF）- K B p65-positive cell changes were observed by HE and immunohistochemical staining, p38 mitogen-activated protein kinase （MAPK） phosphorylation was observed by Western blotting. Results： After LPS administration, all animals displayed increased arterial carbon dioxide partial pressure （PaCO2） and decreased arterial oxygen partial pressure （PaO2）, arterial oxygen saturation （SO2）, HCOs concentration and pH, and increased LWCI, MPO activity, interleukin （IL）-I β, IL-6 and tumor necrosis factor （TNF）-ot mRNA expression, NF-K B p65 positive staining and p38 MAPK activation compared with normal controls （all P〈0.01）. SY Injection significantly mitigated the LPS-induced increase in arterial PaCO2 and the decreases in arterial PaO2, SO2 and pH, and attenuated increases in LWCI and lung tissue MPO activity （all P〈0.01）. Moreover, SY Injection inhibited the increases in NF- K B p65 staining and in TNF-α, IL-1 β and IL-6 mRNA expression （all P〈0.01）, and promoted the expression of the antiinflammatory cytokine IL-10 （P〈0.05） following LPS injection. LPS-induced pulmonary p38 MAPK phosphorylation was suppressed by pretreatment with SY Injection （P〈0.01）. Conclusion： SY Injection ameliorates inflammatory ALl induced by LPS in mice.
