中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2011年
14期
996-999
,共4页
赵赞梅%赵金垣%贺蓓%符凤英
趙讚梅%趙金垣%賀蓓%符鳳英
조찬매%조금원%하배%부봉영
黄芩甙%油酸%急性呼吸窘迫综合征%过氧化物酶%动物实验
黃芩甙%油痠%急性呼吸窘迫綜閤徵%過氧化物酶%動物實驗
황금대%유산%급성호흡군박종합정%과양화물매%동물실험
Baicalin%Oleic acid%Acute respiratory distress syndrome%Peroxidase%Animal experiment
目的 探讨黄芩甙对油酸所致急性呼吸窘迫综合征(ARDS)大鼠肺损伤的干预作用.方法 将健康成年雄性SD大鼠随机分为对照组、ARDS模型组和黄芩甙低剂量组(150 mg/kg)、黄芩甙中剂量组(300 mg/kg)、黄芩甙高剂量组(450 mg/kg),经股静脉注射油酸(0.12 ml/kg)复制ARDS模型,黄芩甙各剂量组同时腹腔注射黄芩甙溶液;在注射油酸后10 min及1、2、6 h,分别插管至颈动脉采集动脉血测血氧分压、采用酶联免疫吸附(ELISA)法对肺组织匀浆进行髓过氧化物酶(MPO)定量检测,并进行组织病理学检查.结果 模型组大鼠在注射油酸后10 min,动脉氧分压和氧合指数开始下降,氧合指数最低值平均为190 mm Hg(1 mm Hg=0.133 kPa),达到了ARDS的诊断标准(＜200mm Hg);黄芩甙低剂量组和中剂量组的氧分压和氧合指数也有下降,氧分压最低值分别平均为54.9mm Hg和65.3 mm Hg,与模型组相应时间点比较差异有统计学意义(P＜0.05);黄芩甙高剂量组的氧分压在10 min时明显下降,均值与模型组比较差异有统计学意义(46.8 mm Hg比66.7 mm Hg,P＜0.05),之后略有升高,但与模型组相应时间点比较差异无统计学意义(P＞0.05).模型组和黄芩甙中剂量组大鼠肺组织MPO浓度均高于对照组,但黄芩甙中剂量组在10 min及1、2 h时均低于模型组.肺组织病理检查结果显示,黄芩甙中剂量组肺损伤较模型组轻.结论 适宜剂量的黄芩甙可以改善油酸所致大鼠ARDS的缺氧状态,这一作用可能与抑制MPO活性有关.
目的 探討黃芩甙對油痠所緻急性呼吸窘迫綜閤徵(ARDS)大鼠肺損傷的榦預作用.方法 將健康成年雄性SD大鼠隨機分為對照組、ARDS模型組和黃芩甙低劑量組(150 mg/kg)、黃芩甙中劑量組(300 mg/kg)、黃芩甙高劑量組(450 mg/kg),經股靜脈註射油痠(0.12 ml/kg)複製ARDS模型,黃芩甙各劑量組同時腹腔註射黃芩甙溶液;在註射油痠後10 min及1、2、6 h,分彆插管至頸動脈採集動脈血測血氧分壓、採用酶聯免疫吸附(ELISA)法對肺組織勻漿進行髓過氧化物酶(MPO)定量檢測,併進行組織病理學檢查.結果 模型組大鼠在註射油痠後10 min,動脈氧分壓和氧閤指數開始下降,氧閤指數最低值平均為190 mm Hg(1 mm Hg=0.133 kPa),達到瞭ARDS的診斷標準(＜200mm Hg);黃芩甙低劑量組和中劑量組的氧分壓和氧閤指數也有下降,氧分壓最低值分彆平均為54.9mm Hg和65.3 mm Hg,與模型組相應時間點比較差異有統計學意義(P＜0.05);黃芩甙高劑量組的氧分壓在10 min時明顯下降,均值與模型組比較差異有統計學意義(46.8 mm Hg比66.7 mm Hg,P＜0.05),之後略有升高,但與模型組相應時間點比較差異無統計學意義(P＞0.05).模型組和黃芩甙中劑量組大鼠肺組織MPO濃度均高于對照組,但黃芩甙中劑量組在10 min及1、2 h時均低于模型組.肺組織病理檢查結果顯示,黃芩甙中劑量組肺損傷較模型組輕.結論 適宜劑量的黃芩甙可以改善油痠所緻大鼠ARDS的缺氧狀態,這一作用可能與抑製MPO活性有關.
목적 탐토황금대대유산소치급성호흡군박종합정(ARDS)대서폐손상적간예작용.방법 장건강성년웅성SD대서수궤분위대조조、ARDS모형조화황금대저제량조(150 mg/kg)、황금대중제량조(300 mg/kg)、황금대고제량조(450 mg/kg),경고정맥주사유산(0.12 ml/kg)복제ARDS모형,황금대각제량조동시복강주사황금대용액;재주사유산후10 min급1、2、6 h,분별삽관지경동맥채집동맥혈측혈양분압、채용매련면역흡부(ELISA)법대폐조직균장진행수과양화물매(MPO)정량검측,병진행조직병이학검사.결과 모형조대서재주사유산후10 min,동맥양분압화양합지수개시하강,양합지수최저치평균위190 mm Hg(1 mm Hg=0.133 kPa),체도료ARDS적진단표준(＜200mm Hg);황금대저제량조화중제량조적양분압화양합지수야유하강,양분압최저치분별평균위54.9mm Hg화65.3 mm Hg,여모형조상응시간점비교차이유통계학의의(P＜0.05);황금대고제량조적양분압재10 min시명현하강,균치여모형조비교차이유통계학의의(46.8 mm Hg비66.7 mm Hg,P＜0.05),지후략유승고,단여모형조상응시간점비교차이무통계학의의(P＞0.05).모형조화황금대중제량조대서폐조직MPO농도균고우대조조,단황금대중제량조재10 min급1、2 h시균저우모형조.폐조직병리검사결과현시,황금대중제량조폐손상교모형조경.결론 괄의제량적황금대가이개선유산소치대서ARDS적결양상태,저일작용가능여억제MPO활성유관.
Objective To investigate the effect of baicalin on pulmonary functions and its mechanism during the development of acute respiratory distress syndrome (ARDS) induced by oleic acid (OA) in rats. Methods Rats were randomized into 5 groups: control, ARDS (OA induction, 0.12 mg/kg),baicalin-treated group ( 150 mg/kg), baicalin-treated group (300 mg/kg) and baicalin-treated group (450mg/kg). The blood samples and lung tissue were collected at 10 min, 1, 2 and 6 h after OA injection. The lung concentration of myeloperoxidase (MPO) was detected by an ELISA (enzyme-linked immunosorbent assay) kit. Meanwhile, blood gas analysis and pulmonary pathological examination were also performed. Results The level of arterial oxygen partial pressure and oxygenation index decreased (P ＜0. 01vs. control) and oxygenation index ( 190 mm Hg, 1 mm Hg =0. 133 kPa) reached the diagnostic standard of ARDS at 2 h in ARDS group. In baicalin-treated group ( 150 mg/kg and 300 mg/kg), the level of arterial oxygen partial pressure and oxygenation index increased versus the ARDS group. In baicalin-treated group (450 mg/kg), the level of arterial oxygen partial pressure was undifferentiated at 1,2 and 6 h (P ＞0. 05)and decreased at 10 min (46. 8 mm Hg, P ＜0. 05 ) versus the ARDS group. The level of MPO increased in baicalin-treated (300 mg/kg) and ARDS groups. Compared with the ARDS group, the level of MPO decreased significantly in baicalin-treated group (300 mg/kg) at 10 min, 1 and 2 h. Meanwhile, the pulmonary pathological damage improved in baicalin-treated group (300 mg/kg). Conclusion An appropriate dose of baicalin may improve hypoxemia of ARDS induced by OA in rats. It may be due to the inhibition of MPO activity.
