心脑血管病防治
心腦血管病防治
심뇌혈관병방치
PREVENTION AND TREATMENT OF CARDIO-CEREBRAL-VASCULAR DISEASE
2014年
2期
102-104,143
,共4页
陈上仲%李莉%胡才宝%龚仕金%蔡国龙%王国付%陈日萍%朱颖%王倩倩%严静
陳上仲%李莉%鬍纔寶%龔仕金%蔡國龍%王國付%陳日萍%硃穎%王倩倩%嚴靜
진상중%리리%호재보%공사금%채국룡%왕국부%진일평%주영%왕천천%엄정
脓毒症%p38MAPK%清热解毒通腑中药液%心肌损伤%炎症因子
膿毒癥%p38MAPK%清熱解毒通腑中藥液%心肌損傷%炎癥因子
농독증%p38MAPK%청열해독통부중약액%심기손상%염증인자
Sepsis%P38MAPK%Heat_clearing and detoxicating drug%Myocardial injury%Inflammatory factors
目的探讨清热解毒通腑中药液对脓毒症大鼠心肌损伤的作用及其可能机制。方法采用盲肠结扎穿孔法（CLP）制备脓毒症动物模型。180只雄性wistar大鼠，随机分为对照组（control）60只、脓毒症组（sepsis）60只、治疗组（treatment）60只。治疗组从造模前96小时（96h）开始按10ml/（kg-1·d-1）灌胃给予清热解毒通腑中药液，脓毒症组及对照组按相同方法予等量0.9％氯化钠注射液。分别于造模后3h ，6h ，12h ，24h ，48h ，72h六个时间点检测各亚组大鼠心功能、血清炎症因子（TNF_a、IL_6、IL_10）、心肌p38丝裂原活化蛋白激酶（p38mitogen_activated protein kinase ，p38MAPK ）等指标。结果与对照组比较，脓毒症组在造模后3h心肌p38MAPK磷酸化水平出现升高并达高峰（ P＜0.01）；血清炎症因子在3h出现升高（ P＜0.05），其中TNF_a在造模后3h达高峰（ P＜0.01），IL_6于造模后12h达高峰（ P＜0.01）；心功能指标从3h即出现下降（ P＜0.05），至12h下降最明显（ P＜0.01）。与脓毒症组比较，治疗组各项指标均有所改善（ P＜0.05）。结论清热解毒通腑中药液对脓毒症大鼠心肌损伤具有保护作用，其作用机制可能是通过p38MAPK信号途径，调控机体免疫炎症反应，从而对脓毒症大鼠心肌损伤起到保护作用。
目的探討清熱解毒通腑中藥液對膿毒癥大鼠心肌損傷的作用及其可能機製。方法採用盲腸結扎穿孔法（CLP）製備膿毒癥動物模型。180隻雄性wistar大鼠，隨機分為對照組（control）60隻、膿毒癥組（sepsis）60隻、治療組（treatment）60隻。治療組從造模前96小時（96h）開始按10ml/（kg-1·d-1）灌胃給予清熱解毒通腑中藥液，膿毒癥組及對照組按相同方法予等量0.9％氯化鈉註射液。分彆于造模後3h ，6h ，12h ，24h ，48h ，72h六箇時間點檢測各亞組大鼠心功能、血清炎癥因子（TNF_a、IL_6、IL_10）、心肌p38絲裂原活化蛋白激酶（p38mitogen_activated protein kinase ，p38MAPK ）等指標。結果與對照組比較，膿毒癥組在造模後3h心肌p38MAPK燐痠化水平齣現升高併達高峰（ P＜0.01）；血清炎癥因子在3h齣現升高（ P＜0.05），其中TNF_a在造模後3h達高峰（ P＜0.01），IL_6于造模後12h達高峰（ P＜0.01）；心功能指標從3h即齣現下降（ P＜0.05），至12h下降最明顯（ P＜0.01）。與膿毒癥組比較，治療組各項指標均有所改善（ P＜0.05）。結論清熱解毒通腑中藥液對膿毒癥大鼠心肌損傷具有保護作用，其作用機製可能是通過p38MAPK信號途徑，調控機體免疫炎癥反應，從而對膿毒癥大鼠心肌損傷起到保護作用。
목적탐토청열해독통부중약액대농독증대서심기손상적작용급기가능궤제。방법채용맹장결찰천공법（CLP）제비농독증동물모형。180지웅성wistar대서，수궤분위대조조（control）60지、농독증조（sepsis）60지、치료조（treatment）60지。치료조종조모전96소시（96h）개시안10ml/（kg-1·d-1）관위급여청열해독통부중약액，농독증조급대조조안상동방법여등량0.9％록화납주사액。분별우조모후3h ，6h ，12h ，24h ，48h ，72h륙개시간점검측각아조대서심공능、혈청염증인자（TNF_a、IL_6、IL_10）、심기p38사렬원활화단백격매（p38mitogen_activated protein kinase ，p38MAPK ）등지표。결과여대조조비교，농독증조재조모후3h심기p38MAPK린산화수평출현승고병체고봉（ P＜0.01）；혈청염증인자재3h출현승고（ P＜0.05），기중TNF_a재조모후3h체고봉（ P＜0.01），IL_6우조모후12h체고봉（ P＜0.01）；심공능지표종3h즉출현하강（ P＜0.05），지12h하강최명현（ P＜0.01）。여농독증조비교，치료조각항지표균유소개선（ P＜0.05）。결론청열해독통부중약액대농독증대서심기손상구유보호작용，기작용궤제가능시통과p38MAPK신호도경，조공궤체면역염증반응，종이대농독증대서심기손상기도보호작용。
Objective To investigate the effects of p38MAPK on heat_clearing and detoxicating drug in septic rats with myocardial in-jury and the possible mechanism.Methods Male adult rats were subjected to sepsis by cecal ligation and puncture (CLP).Total 180 male adult wistar rats were randomly divided into control group (n=60) ,sepsis group(n=60) and treatment group(n=60).The rats in treatment group were pretreated with decoction by 10ml/(kg-1 ·d-1 ) 96h before CLP ,and rats in other two groups were pretreated with normal saline in the same way.Cardiac function was assessed at 3h ,6h ,12h ,24h ,48h and 72h after CLP or sham surgery ,and the detections of the level of phosphorylation of p38MAPK、the level of inflammatory cytokines (TNF_a ,IL_6 ,IL_10) were tested re-spectively. Results Compared with control group ,the expression of p38MAPK protein are increased significantly and peaked 3h after the surgery ( P<0.01 ) ,cardiac function in sepsis group decreased significantly since 3h after the surgery ,while a remarkable de-crease could be observed at post_challenge of 12h( P<0.01);serum inflammatory factors including TNF_a ,IL_6 in sepsis group in-creased significantly since 3h after the surgery. TNF_a reached peaked at 3h ( P<0.01 ) ,the IL_6 reached peaked at 12h ( P<0.01) . Compared with sepsis group , cardiac function ,the level of inflammatory cytokines and the level of phosphorylation of p38MAPK were all improved in treatment group. Conclusions Heat_clearing and detoxicating drug may decrease myocardial injury in septic rats.Further ,p38MAPK signaling pathway may play an important role through regulating the inflammation reaction during sepsis .
