实用药物与临床
實用藥物與臨床
실용약물여림상
Practical Pharmacy and Clinical Remedies
2015年
9期
1011-1014
,共4页
袁红%周慧霞%兰秋艳%王晓琴%刘卫名
袁紅%週慧霞%蘭鞦豔%王曉琴%劉衛名
원홍%주혜하%란추염%왕효금%류위명
芦丁%脂多糖%急性肺损伤%氧化应激%炎症
蘆丁%脂多糖%急性肺損傷%氧化應激%炎癥
호정%지다당%급성폐손상%양화응격%염증
Rutin%LPS%Acute lung injury%Oxidative stress%Inflammation
目的 探讨芦丁( Rutin)对脂多糖( Lipopolysaccharide,LPS)诱导的小鼠急性肺损伤( ALI)氧化应激失衡的作用. 方法 将30只雄性C57 小鼠随机分为3 组:对照组( C组)、脂多糖组( LPS组)和芦丁组( R组),每组10只. R组在LPS注射前0.5 h给予芦丁(100 μmol/kg)腹腔注射,C组和LPS组在LPS注射前0.5 h给予等量生理盐水腹腔注射,LPS组和R组给予脂多糖(20 mg/kg)腹腔注射,C组给予等浓度生理盐水腹腔注射. 脂多糖或生理盐水注射后6 h 测小鼠血气,取肺组织进行病理观察,测定肺组织湿干比( W/D)、丙二醛(MDA)含量,检测过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)、超氧化物歧化酶(SOD)活性,血清和肺组织中肿瘤坏死因子-α( TNF-α)、白介素( IL)-6和IL-1β的表达. 结果 与C组比较,LPS组肺组织病理改变和肺组织湿干比、二氧化碳分压( PaCO2 )、呼吸频率( RR)、MDA含量及IL-6、IL-1β和TNF-α表达明显增加,而氧分压( PaO2 )、pH值及CAT、GPx、SOD活性明显降低. 与LPS组比较,R组肺组织病理改变和肺组织湿干比、PaCO2、RR、MDA含量及IL-6、IL-1β、TNF-α表达明显减少,而PaO2、pH值及CAT、GPx、SOD活性明显增高. 结论 芦丁可通过抑制氧化应激和炎症而减轻脂多糖诱导的急性肺损伤.
目的 探討蘆丁( Rutin)對脂多糖( Lipopolysaccharide,LPS)誘導的小鼠急性肺損傷( ALI)氧化應激失衡的作用. 方法 將30隻雄性C57 小鼠隨機分為3 組:對照組( C組)、脂多糖組( LPS組)和蘆丁組( R組),每組10隻. R組在LPS註射前0.5 h給予蘆丁(100 μmol/kg)腹腔註射,C組和LPS組在LPS註射前0.5 h給予等量生理鹽水腹腔註射,LPS組和R組給予脂多糖(20 mg/kg)腹腔註射,C組給予等濃度生理鹽水腹腔註射. 脂多糖或生理鹽水註射後6 h 測小鼠血氣,取肺組織進行病理觀察,測定肺組織濕榦比( W/D)、丙二醛(MDA)含量,檢測過氧化氫酶(CAT)、穀胱甘肽過氧化物酶(GPx)、超氧化物歧化酶(SOD)活性,血清和肺組織中腫瘤壞死因子-α( TNF-α)、白介素( IL)-6和IL-1β的錶達. 結果 與C組比較,LPS組肺組織病理改變和肺組織濕榦比、二氧化碳分壓( PaCO2 )、呼吸頻率( RR)、MDA含量及IL-6、IL-1β和TNF-α錶達明顯增加,而氧分壓( PaO2 )、pH值及CAT、GPx、SOD活性明顯降低. 與LPS組比較,R組肺組織病理改變和肺組織濕榦比、PaCO2、RR、MDA含量及IL-6、IL-1β、TNF-α錶達明顯減少,而PaO2、pH值及CAT、GPx、SOD活性明顯增高. 結論 蘆丁可通過抑製氧化應激和炎癥而減輕脂多糖誘導的急性肺損傷.
목적 탐토호정( Rutin)대지다당( Lipopolysaccharide,LPS)유도적소서급성폐손상( ALI)양화응격실형적작용. 방법 장30지웅성C57 소서수궤분위3 조:대조조( C조)、지다당조( LPS조)화호정조( R조),매조10지. R조재LPS주사전0.5 h급여호정(100 μmol/kg)복강주사,C조화LPS조재LPS주사전0.5 h급여등량생리염수복강주사,LPS조화R조급여지다당(20 mg/kg)복강주사,C조급여등농도생리염수복강주사. 지다당혹생리염수주사후6 h 측소서혈기,취폐조직진행병리관찰,측정폐조직습간비( W/D)、병이철(MDA)함량,검측과양화경매(CAT)、곡광감태과양화물매(GPx)、초양화물기화매(SOD)활성,혈청화폐조직중종류배사인자-α( TNF-α)、백개소( IL)-6화IL-1β적표체. 결과 여C조비교,LPS조폐조직병리개변화폐조직습간비、이양화탄분압( PaCO2 )、호흡빈솔( RR)、MDA함량급IL-6、IL-1β화TNF-α표체명현증가,이양분압( PaO2 )、pH치급CAT、GPx、SOD활성명현강저. 여LPS조비교,R조폐조직병리개변화폐조직습간비、PaCO2、RR、MDA함량급IL-6、IL-1β、TNF-α표체명현감소,이PaO2、pH치급CAT、GPx、SOD활성명현증고. 결론 호정가통과억제양화응격화염증이감경지다당유도적급성폐손상.
Objective To investigate the effects of rutin on oxidative stress of acute lung injury induced by li-popolysaccharide (LPS). Methods 30 male C57 mice were randomly divided into control group (group C),group LPS,and rutin group (group R). Group R was pretreated with rutin (100 μmol/kg)by intraperitoneal injection at 0.5 h before LPS injection,and the equal volume of saline was administered in the other 2 groups. Group R and group LPS were treated with LPS (20 mg/kg)by intraperitoneal injection and group C were treated with the saline (20 mg/kg)by intraperitoneal injection. After 6 h of LPS injection,arterial blood was collected for blood gas analysis and lung tissue to exmanine pathological change,Wet/Dry,the expression of MDA,the activity of CAT,GPx and SOD and the expression of IL-6,IL-1β and TNF-α in lung and serum. Results Compared with group C,the pathological change and Wet/Dry of lung tissue,the PaCO2 and RR,the expression of MDA in lung tissue and the expression of IL-6,IL-1β and TNF-αsignificantly increased,while the PaCO2 ,pH and the activity of CAT,GPx and SOD decreased. Compared with group LPS,the pathological change and Wet/Dry of lung tissue,the PaCO2 and RR,the expression of MDA in lung tissue and the expression of IL-6,IL-1β and TNF-α in group R significantly decreased and the PaCO2,pH and the activity of CAT,GPx and SOD increased. Conclusion Rutin pretreatment can significantly decrease LPS-induced acute lung inju-ry by suppressing oxidative stress and inflammation.
