东南国防医药
東南國防醫藥
동남국방의약
Military Medical Journal of Southeast China
2015年
5期
467-470
,共4页
张严高%余磊%王建莉%尹戴佳佳%朱闽湘%祝春华%范洁
張嚴高%餘磊%王建莉%尹戴佳佳%硃閩湘%祝春華%範潔
장엄고%여뢰%왕건리%윤대가가%주민상%축춘화%범길
地塞米松%异丙肾上腺素%心肌损伤%肿瘤坏死因子-α
地塞米鬆%異丙腎上腺素%心肌損傷%腫瘤壞死因子-α
지새미송%이병신상선소%심기손상%종류배사인자-α
Dexamethasone%isoproterenol%myocardial injury%TNF-α
目的:观察地塞米松( Dexamethasone,DEX)对异丙肾上腺素( Isoprotereno,ISO)致小鼠急性心肌缺血损伤的影响并探讨其作用机制。方法16只昆明种小鼠随机分成正常对照( control,CON)组、ISO组、地塞米松预处理( Dexamethasone pretreatment,DEX-pre)组、DEX组,每组4只。 CON组、ISO组首次处理前30 min给予等量0.9%氯化钠注射液腹腔注射预处理,然后CON组给予等量0.9%氯化钠注射液腹腔注射处理,ISO组小鼠给予ISO(5 mg/kg),每日腹腔注射1次,连续3 d;DEX-pre组在首次ISO注射前30 min给予DEX(1.25 mg/kg)腹腔注射,余同ISO组;DEX组在第2天、第3天ISO注射30 min后给予DEX(1.25 mg/kg)腹腔注射,余同ISO组。检测血清谷草转氨酶(AST)、乳酸脱氢酶(LDH)、肌酸激酶(CK)、肌酸激酶同工酶( CK-MB)了解心肌损伤;观察心肌组织的病理学改变并检测细胞因子TNF-α的变化。结果①与CON组比较,ISO组ASL、LDH、CK均明显升高(P<0.01),CK-MP无明显改变(P>0.05);ISO组心肌损伤明显加重,形态学计分为4.0比0.0(P<0.01);ISO组血清TNF-α明显升高(P<0.05); DEX-pre组TNF-α明显下降(P<0.01)。②与ISO组比较,EX-pre组ASL、CK下降非常显著(P<0.01),LDH、CK-MP轻度下降(P<0.05);DEX-pre组心肌损伤得到明显改善,形态学计分为2.0比4.0(P<0.01);DEX-pre组血清TNF-α下降非常显著(P<0.01)。③与ISO组比较,DEX组ASL、LDH、CK、CK-MP均无明显改变(P>0.05);DEX组心肌损伤无明显变化,形态学计分为3.5比4.0(P>0.05);DEX组血清TNF-α升高非常显著(P<0.01)。结论地塞米松预处理对异丙肾上腺素致小鼠急性心肌损伤的心肌具有明显保护作用,TNF-α等细胞因子改变可能是其机制之一。
目的:觀察地塞米鬆( Dexamethasone,DEX)對異丙腎上腺素( Isoprotereno,ISO)緻小鼠急性心肌缺血損傷的影響併探討其作用機製。方法16隻昆明種小鼠隨機分成正常對照( control,CON)組、ISO組、地塞米鬆預處理( Dexamethasone pretreatment,DEX-pre)組、DEX組,每組4隻。 CON組、ISO組首次處理前30 min給予等量0.9%氯化鈉註射液腹腔註射預處理,然後CON組給予等量0.9%氯化鈉註射液腹腔註射處理,ISO組小鼠給予ISO(5 mg/kg),每日腹腔註射1次,連續3 d;DEX-pre組在首次ISO註射前30 min給予DEX(1.25 mg/kg)腹腔註射,餘同ISO組;DEX組在第2天、第3天ISO註射30 min後給予DEX(1.25 mg/kg)腹腔註射,餘同ISO組。檢測血清穀草轉氨酶(AST)、乳痠脫氫酶(LDH)、肌痠激酶(CK)、肌痠激酶同工酶( CK-MB)瞭解心肌損傷;觀察心肌組織的病理學改變併檢測細胞因子TNF-α的變化。結果①與CON組比較,ISO組ASL、LDH、CK均明顯升高(P<0.01),CK-MP無明顯改變(P>0.05);ISO組心肌損傷明顯加重,形態學計分為4.0比0.0(P<0.01);ISO組血清TNF-α明顯升高(P<0.05); DEX-pre組TNF-α明顯下降(P<0.01)。②與ISO組比較,EX-pre組ASL、CK下降非常顯著(P<0.01),LDH、CK-MP輕度下降(P<0.05);DEX-pre組心肌損傷得到明顯改善,形態學計分為2.0比4.0(P<0.01);DEX-pre組血清TNF-α下降非常顯著(P<0.01)。③與ISO組比較,DEX組ASL、LDH、CK、CK-MP均無明顯改變(P>0.05);DEX組心肌損傷無明顯變化,形態學計分為3.5比4.0(P>0.05);DEX組血清TNF-α升高非常顯著(P<0.01)。結論地塞米鬆預處理對異丙腎上腺素緻小鼠急性心肌損傷的心肌具有明顯保護作用,TNF-α等細胞因子改變可能是其機製之一。
목적:관찰지새미송( Dexamethasone,DEX)대이병신상선소( Isoprotereno,ISO)치소서급성심기결혈손상적영향병탐토기작용궤제。방법16지곤명충소서수궤분성정상대조( control,CON)조、ISO조、지새미송예처리( Dexamethasone pretreatment,DEX-pre)조、DEX조,매조4지。 CON조、ISO조수차처리전30 min급여등량0.9%록화납주사액복강주사예처리,연후CON조급여등량0.9%록화납주사액복강주사처리,ISO조소서급여ISO(5 mg/kg),매일복강주사1차,련속3 d;DEX-pre조재수차ISO주사전30 min급여DEX(1.25 mg/kg)복강주사,여동ISO조;DEX조재제2천、제3천ISO주사30 min후급여DEX(1.25 mg/kg)복강주사,여동ISO조。검측혈청곡초전안매(AST)、유산탈경매(LDH)、기산격매(CK)、기산격매동공매( CK-MB)료해심기손상;관찰심기조직적병이학개변병검측세포인자TNF-α적변화。결과①여CON조비교,ISO조ASL、LDH、CK균명현승고(P<0.01),CK-MP무명현개변(P>0.05);ISO조심기손상명현가중,형태학계분위4.0비0.0(P<0.01);ISO조혈청TNF-α명현승고(P<0.05); DEX-pre조TNF-α명현하강(P<0.01)。②여ISO조비교,EX-pre조ASL、CK하강비상현저(P<0.01),LDH、CK-MP경도하강(P<0.05);DEX-pre조심기손상득도명현개선,형태학계분위2.0비4.0(P<0.01);DEX-pre조혈청TNF-α하강비상현저(P<0.01)。③여ISO조비교,DEX조ASL、LDH、CK、CK-MP균무명현개변(P>0.05);DEX조심기손상무명현변화,형태학계분위3.5비4.0(P>0.05);DEX조혈청TNF-α승고비상현저(P<0.01)。결론지새미송예처리대이병신상선소치소서급성심기손상적심기구유명현보호작용,TNF-α등세포인자개변가능시기궤제지일。
Objective To investigate potential protective effect of glucocorticoid receptor (GR) agonist dexamethasone on isoproterenol-induced myocardial injury and the possible mechanism.Methods The sixteen mice were randomly divided into control (CON) group (n=4), ISO group (n=4), Dexamethasone pretreatment (DEX-pre) group (n=4) and Dexamethasone treatment (DEX) group (n=4).The mice in CON group and ISO group were given the same amount of 0.9% sodium chloride and DEX-pre group given dexamethasone (1.25 mg/kg) injection by intraperitoneal injection as a pretreatment before treatment 30 minutes.CON group was given the same amount of 0.9%sodium chloride injection by intraperitoneal injection.ISO group, DEX-pre group and DEX group received 5 mg/kg isoproterenol hydrochloride with daily intraperitoneal injection and continuous 3 days.At the two and three days, dexamethasone (1.25 mg/kg) was given after ISO injected 30 minutes in DEX group.Observe the serum ASL, LDH, CK, and CK-MP.Myocardial tissue injury was assessed by HE staining.The expression of TNF-αon serum was detected by ELISA.Results①Compared with control group, the levels of ASL, LDH and CK was significantly increased; the degree of myocardial injury were greatly deteriorated in ISO group (P<0.01).The expression of TNF-αon serum was greatly increased (P<0.05) in ISO group. The expression of TNF-αon serum was significantly reduced (P<0.01) in DEX-pre group.②Compared with ISO group, the levels of ASL and CK was significantly reduced (P<0.01) and the levels of LDH and CK-MP was reduced (P<0.05).The degree of myo-cardial injury were greatly improved ( P<0.01) in DEX-pre group.The expression of TNF-αon serum was significantly reduced ( P<0.01) in DEX-pre group.③Compared with ISO group, the levels of ASL, LDH, CK, CK-MP and the degree of myocardial injury weren′t significantly difference in DEX group (P>0.05).The expression of TNF-αon serum was significantly increased (P<0.01) in DEX group.Conclusion DEX pretreatment has protective effect against ISO-induced myocardial injury.The mechanism might be the changes of inflammatory cytokinesthe.