中华创伤杂志
中華創傷雜誌
중화창상잡지
Chinese Journal of Traumatology
2015年
4期
347-352
,共6页
马硕%陈冲%曹婷婷%毕玥%欧荀言%佟箫%赵文鑫%周济成%于德钦
馬碩%陳遲%曹婷婷%畢玥%歐荀言%佟簫%趙文鑫%週濟成%于德欽
마석%진충%조정정%필모%구순언%동소%조문흠%주제성%우덕흠
原花青素类%心脏损伤%氧化性应激
原花青素類%心髒損傷%氧化性應激
원화청소류%심장손상%양화성응격
Proanthocyanidins%Heart injuries%Oxidative stress
目的 观察原花青素对机械性创伤(MT)造成大鼠继发性心肌细胞及心脏功能损伤的影响,并探究其作用机制.方法 将120只成年雄性SD大鼠按随机数字表法分为正常组、创伤组、创伤给药组(注射原花青素)和创伤溶剂组(注射等渗盐水),每组30只.制备大鼠MT模型.TUNEL染色后计算心肌细胞凋亡指数,经右颈总动脉向左心室内插管,记录左心室舒缩压力变化,通过流式细胞仪检测H9c2细胞注射原花青素前后活性氧自由基(ROS)数量变化,激光共聚焦显微镜下观察测定经Fluo-4AM标记的心肌细胞内Ca2浓度变化,电子显微镜下观察心肌细胞超微结构改变.结果 (1)创伤组、创伤给药组、创伤溶剂组MT后心肌细胞凋亡指数分别为(7.96±1.16)％、(2.44±0.70)％、(7.76±1.14)％,与正常组(0.64±0.59)％比较均明显增高(P＜0.01);创伤溶剂组与创伤组比较差异无统计学意义,而创伤给药组与创伤组比较差异有统计学意义(P＜0.05).(2)左心室内压上升最大速率(+ dp/dtmax)创伤组、创伤溶剂组分别为(3 294.55±180.95) mmHg/s、(3 337.80±220.11) mmHg/s,与正常组(4 030.04±293.70)mmHg/s比较均明显下降(P＜0.01);创伤给药组为(3 926.72±364.95) mmHg/s,较创伤组升高(P＜0.05).左心室内压下降最大速率(-dp/dtmax)创伤组、创伤溶剂组分别为(2 294.55±298.69) mmHg/s、(2 291.20 ±348.72) mmHg/s,与正常组的(2 830.04±334.63) mmHg/s比较均明显下降(P＜0.05);创伤给药组为(2 801.52±266.25) mmHg/s,较创伤组升高(P＜0.05).(3)与正常组比较,创伤组心肌组织可见染色质边集,颜色变深,肌间毛细血管上皮细胞可见明显空泡形成,原花青素干预后,肌间毛细血管上皮细胞核膜未见明显空泡形成;与创伤组比较,创伤给药组染色质边集,颜色变深的异常改变有所改善.结论 原花青素能减轻MT后心肌细胞超微结构的病理性改变,抑制继发性心肌细胞凋亡,改善心脏功能,发挥心脏保护作用.
目的 觀察原花青素對機械性創傷(MT)造成大鼠繼髮性心肌細胞及心髒功能損傷的影響,併探究其作用機製.方法 將120隻成年雄性SD大鼠按隨機數字錶法分為正常組、創傷組、創傷給藥組(註射原花青素)和創傷溶劑組(註射等滲鹽水),每組30隻.製備大鼠MT模型.TUNEL染色後計算心肌細胞凋亡指數,經右頸總動脈嚮左心室內插管,記錄左心室舒縮壓力變化,通過流式細胞儀檢測H9c2細胞註射原花青素前後活性氧自由基(ROS)數量變化,激光共聚焦顯微鏡下觀察測定經Fluo-4AM標記的心肌細胞內Ca2濃度變化,電子顯微鏡下觀察心肌細胞超微結構改變.結果 (1)創傷組、創傷給藥組、創傷溶劑組MT後心肌細胞凋亡指數分彆為(7.96±1.16)％、(2.44±0.70)％、(7.76±1.14)％,與正常組(0.64±0.59)％比較均明顯增高(P＜0.01);創傷溶劑組與創傷組比較差異無統計學意義,而創傷給藥組與創傷組比較差異有統計學意義(P＜0.05).(2)左心室內壓上升最大速率(+ dp/dtmax)創傷組、創傷溶劑組分彆為(3 294.55±180.95) mmHg/s、(3 337.80±220.11) mmHg/s,與正常組(4 030.04±293.70)mmHg/s比較均明顯下降(P＜0.01);創傷給藥組為(3 926.72±364.95) mmHg/s,較創傷組升高(P＜0.05).左心室內壓下降最大速率(-dp/dtmax)創傷組、創傷溶劑組分彆為(2 294.55±298.69) mmHg/s、(2 291.20 ±348.72) mmHg/s,與正常組的(2 830.04±334.63) mmHg/s比較均明顯下降(P＜0.05);創傷給藥組為(2 801.52±266.25) mmHg/s,較創傷組升高(P＜0.05).(3)與正常組比較,創傷組心肌組織可見染色質邊集,顏色變深,肌間毛細血管上皮細胞可見明顯空泡形成,原花青素榦預後,肌間毛細血管上皮細胞覈膜未見明顯空泡形成;與創傷組比較,創傷給藥組染色質邊集,顏色變深的異常改變有所改善.結論 原花青素能減輕MT後心肌細胞超微結構的病理性改變,抑製繼髮性心肌細胞凋亡,改善心髒功能,髮揮心髒保護作用.
목적 관찰원화청소대궤계성창상(MT)조성대서계발성심기세포급심장공능손상적영향,병탐구기작용궤제.방법 장120지성년웅성SD대서안수궤수자표법분위정상조、창상조、창상급약조(주사원화청소)화창상용제조(주사등삼염수),매조30지.제비대서MT모형.TUNEL염색후계산심기세포조망지수,경우경총동맥향좌심실내삽관,기록좌심실서축압력변화,통과류식세포의검측H9c2세포주사원화청소전후활성양자유기(ROS)수량변화,격광공취초현미경하관찰측정경Fluo-4AM표기적심기세포내Ca2농도변화,전자현미경하관찰심기세포초미결구개변.결과 (1)창상조、창상급약조、창상용제조MT후심기세포조망지수분별위(7.96±1.16)％、(2.44±0.70)％、(7.76±1.14)％,여정상조(0.64±0.59)％비교균명현증고(P＜0.01);창상용제조여창상조비교차이무통계학의의,이창상급약조여창상조비교차이유통계학의의(P＜0.05).(2)좌심실내압상승최대속솔(+ dp/dtmax)창상조、창상용제조분별위(3 294.55±180.95) mmHg/s、(3 337.80±220.11) mmHg/s,여정상조(4 030.04±293.70)mmHg/s비교균명현하강(P＜0.01);창상급약조위(3 926.72±364.95) mmHg/s,교창상조승고(P＜0.05).좌심실내압하강최대속솔(-dp/dtmax)창상조、창상용제조분별위(2 294.55±298.69) mmHg/s、(2 291.20 ±348.72) mmHg/s,여정상조적(2 830.04±334.63) mmHg/s비교균명현하강(P＜0.05);창상급약조위(2 801.52±266.25) mmHg/s,교창상조승고(P＜0.05).(3)여정상조비교,창상조심기조직가견염색질변집,안색변심,기간모세혈관상피세포가견명현공포형성,원화청소간예후,기간모세혈관상피세포핵막미견명현공포형성;여창상조비교,창상급약조염색질변집,안색변심적이상개변유소개선.결론 원화청소능감경MT후심기세포초미결구적병이성개변,억제계발성심기세포조망,개선심장공능,발휘심장보호작용.
Objective To evaluate the effect of proanthocyanidins on cardiocyte apoptosis and cardiac dysfunction following mechanical trauma (MT) in rats and discuss its mechanism.Methods A total of 120 SD rats were allocated to normal group,trauma group,and trauma solvent group (treated with proanthocyanidins) and trauma vehicle group (treated with saline solution) according to the random number table,with 30 rats per group.Small animal quantitative wound instrument was used to prepare the MT model in rats.Cardiocyte apoptosis was measured by TUNEL staining.Changes in left ventricular diastolic pressure were recorded by left ventricular intubation via the right common carotid artery.Reactive oxygen species (ROS) produced by H9c2 cells before and after proanthocyanidins administration was detected with flow cytometry.Level of Ca2 + in cardiocytes marked by Fluo-4AM was determined with laser scanning confocal microscope.Ultrastructure changes in cardiocytes were observed under electronic microscope.Results After the induction of MT,apoptosis index of cardiocytes in trauma group,trauma solvent group and trauma vehicle group was (7.96 ± 1.16) ％,(2.44 ±0.70) ％,and (7.76 ± 1.14) ％ respectively,far higher than (0.64 ± 0.59) ％ in normal group (P ＜ 0.01).By comparison with the trauma group,apoptosis index did not differ significantly in trauma vehicle group (P ＞ 0.05) but substantial reduction was detected in trauma solvent group (P ＜ 0.05).The + dp/dtmax of cardiac function in trauma and trauma vehicle groups was (3294.55 ± 180.95) mmHg/s and (3337.80 ±220.11) mmHg/s respectively lowered from (4030.04 ±293.70) mmHg/s in normal group (P ＜0.01),and was (3926.72 ± 364.95) mmHg/s in trauma solvent group lowered in contrast with trauma group (P ＜ 0.05).The-dp/dtmax in trauma and trauma vehicle groups was (2294.55 ± 298.69)mmHg/s and (2291.20-± 348.72)mmHg/s respectively lowered significantly from (2830.04 ± 334.63) mmHg/s in normal group (P ＜ 0.05),and was (2801.52 ± 266.25) mmHg/s increased significantly in contrast with trauma group (P ＜ 0.05).Compared with normal group,trauma group showed chromatin margination and condensation as well as marked vacuolization in the epithelium from intramuscular capillaries.However,the pathological changes were improved after proanthocyanidins therapy.Conclusion Proanthocyanidins is effective in heart protection after the mechanical trauma by attenuating the pathological changes of myocardial ultrastructure and myocardial apoptosis and improving cardiac function.
