电针足三里对大鼠缺血再灌注损伤心肌的保护作用
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摘要
背景:心肌缺血再灌注(ischemia/reperfusion I/R)损伤是一种多因素参与的复杂病理过程,涉及到多个环节。目前认为,心肌I/R损伤是炎症反应过度表达,系统炎症反应和局部炎症反应共同参与的结果,由白细胞(中性粒细胞为主)和细胞因子、趋化因子激活为主的炎症反应在心肌缺血阶段即被激活,再灌注则显著加剧心肌的炎症级联反应。因此防治心肌I/R损伤的有效办法除了尽快恢复心肌血流的再灌注外,如何拮抗炎症的过度表达在心肌中的损伤作用,适时保护心肌是我们目前研究的主要方向。研究表明,刺激外周迷走神经及应用胆碱能递质乙酰胆碱或拟胆碱药物烟碱能抑制内毒素血症导致的全身炎症反应综合征,显著降低细胞因子如TNF-α、IL-1β、I L-6、IL-8等的释放,同时不影响抑炎因子IL-10的释放,并将之命名为“胆碱能抗炎通路”(the cholinergic anti-inflammatorypathway,CAP)。心肌缺血再灌注损伤与内毒素血症、低血容量失血性休克均有相同病理机制,即由许多炎症介质参与、机体失控性过度的炎症反应的病理过程,同时基于传出迷走神经电刺激对上述动物模型均具有抗过度炎症以及器官保护的研究结果,我们假设采取任何措施兴奋迷走神经传出纤维,都有可能激活该通路达到治疗心肌I/R损伤。现有资料表明,针刺足三里能够兴奋迷走神经中枢,并增加其传出纤维的电活动,而有关电针足三里对大鼠缺血再灌注损伤心肌的影响和机制研究目前尚未有人报道,因此本实验拟通过电针足三里,研究该方法对I/R损伤心肌是否也具有保护作用。
目的:通过运用电针足三里刺激或迷走神经电刺激研究兴奋胆碱能抗炎通路对大鼠缺血再灌注损伤心肌的保护作用,探讨其作用机制。
方法:雄性SD大鼠100只,随机分为5组:①手术对照组(SHAM组)②心肌缺血再灌注组(IR组)③迷走神经刺激组(STM组)④电针足三里组(ZSL组)⑤非经非穴组(FJFX组),除SHAM组外,各组均行心肌缺血30min再灌注,STM组于再灌前后各10min,共20min,以5 V、2ms、1HZ强度持续刺激左颈迷走神经,ZSL组于再灌前后各15min,共30min,行电针足三里刺激,FJFX组于再灌前后各15min,共30min,行电针非经非穴刺激。记录心律失常发生率,心率(heart rate,HR),平均动脉压(mean arterial pressure,MAP)变化;再灌注120min后,处死动物,采集标本。常规方法石蜡切片行苏木素一伊红(Hematoxylin and Eosin Staining,HE)染色,光学显微镜下观察心肌的炎症改变;伊文思蓝/氯化三苯基四唑(Evan's Blue/2,3,5-Triphenyl-2H-Tetrazoliumchloride,EB/TTC)测定心肌梗死面积与免疫比浊法测定血浆肌钙蛋白Ⅰ浓度;酶联免疫吸附试验(enzyme-linkedimmunosorbent assay,ELISA)检测心肌和血浆中肿瘤坏死因子(tumornecrosis factor,TNF)含量和白介素-6(interleukin-6,IL-6)含量;分光光度法测定心肌组织髓过氧化物酶(Myeloperoxidas MPO)活性;硫代巴比妥酸法测定心肌组织丙二醛(Malondialdehyde MDA)含量;免疫组化分析心肌核转录因子p65(nulear factor-kappa Bp65 NF-κBp65)表达;原位末端标记法(TUNEL)检测心肌细胞凋亡。
结果:1.血流动力学和心律失常观察:除SHAM组外,再灌120min后各组心率,平均动脉压较缺血前均有下降(p＜0.05),各组之间MAP差异无统计学意义(p＞0.05)。STM组、ZSL组心率在刺激阶段有下降,STM组下降较ZSL组更明显,但波动幅度仍在10%以内,刺激停止后,心率回升。STM组、ZSL组再灌后心律失常发生率明显低于IR组,差异具有统计学意义(p＜0.05);
2、组织形态学观察:光镜下发现SHAM组心肌结构正常,细胞排列紧密、界限清楚,无水肿,无炎性细胞浸润;IR组、FJFX组心肌排列稀疏,不规则,细胞水肿,部分细胞出现明显空泡变性、心肌纤维断裂,细胞间隙明显增宽,大量炎性细胞浸润;STM组、ZSL组心肌细胞排列较规则,细胞轻度水肿,细胞间隙增宽,炎性细胞散在浸润;
3、心肌损伤程度观察:各组心肌行EB/TTC染色显示,各组间缺血范围差异无统计学意义(P＞0.05),与IR组相比,STM组和ZSL组心肌梗死范围差异有统计学意义(p＜0.05),心肌梗死范围减小,而ZSL组和STM组比较,无统计学差异(P＞0.05),FJFX组和IR组比较,无统计学差异(P＞0.05),各组心肌肌钙蛋白(cTnI)在心肌缺血前无明显差别,再灌注120min后,除SHAM组外,其他各组cTnI较缺血前均有不同程度的升高(P＜0.05),STM组和ZSL组cTnI浓度低于IR组(P＜0.05),STM组和ZSL组比较,无统计学差异(P＞0.05);
4、炎性标志物和氧化损害程度观察:与SHAM组相比,各组MPO活性和MDA含量显著增高,以IR组升高更为显著(P＜0.01),与ZSL组和STM组相比,差异也有统计学意义(P＜0.05),心肌组织和血浆中的TNF及IL-6的浓度在IR组、STM组、ZSL组、FJFX组明显升高,与SHAM组相比差异均有统计学意义(P＜0.05);其中IR组升高更为显著,与ZSL组相比,差异也有统计学意义(P＜0.05);STM组与ZSL组相比差异无统计学意义(P＞0.05)。免疫组化检测NF-κBp65表达,IR组大部分心肌细胞中,细胞浆染色呈阳性,细胞核染色呈阳性,ZSL组和STM组心肌细胞的胞浆呈弱阳性或阳性,细胞核染色呈弱阳性,核移位细胞数目减少。平均光密度值比较发现STM组、ZSL组NF-κBp65表达低于IR组(P＜0.05);
5、细胞凋亡观察:TUNEL法检测细胞凋亡发现,在SHAM组中,未发现TUNEL阳性细胞,相反,在IR组中,呈现大量TUNEL阳性细胞核呈棕黄色反应,核内染色质浓缩,形成密集颗粒位于核膜下,有的胞核被降解,胞浆不着色。ZSL组、STM组可见散在的阳性细胞。凋亡指数(apoptosis index AI)比较发现,STM组、ZSL组AI值低于IR组(P＜0.05)。
结论:电针足三里能够抑制心肌缺血再灌注损伤引发的炎症反应,对心肌起到保护作用;其机制可能是通过兴奋胆碱能抗炎通路,削弱N F-κB表达,减少TNF、IL-6产生,抑制细胞凋亡有关。
Background:Ischemia-reperfusion injury is a complex pathogenetic process involves multiple signal transductions and inflammatory mediators.At present,it is thought that both systemic and regional inflammatory reaction participat in ischemia-reperfusion injury,leucocyte (neutrophil primarily)、cytokine and chemokine as well as complement is activated during myocardial ischemia and significantly aggravated at reperfusion period,then initiate myocardial inflammatory cascade reaction.Research find that stimulating efferent vagus nervus and applicating neurotransmitter acetylcholine or nicotine can inhibite endotoxemia leading to systemic inflammatory response syndrome,and depress significantly cytokine releasing such as:tumor necrosis factor-α,interleukin-1β,interleukin-6,interleukin-8 meanwhile unaffect of the level of anti-inflammatory factor interleukin-10,which is named "the cholinergic anti-inflammatory pathway"The response of the myocardium to reperfusion is similar to inflammatory responses induced by sepsis.It is a pathogenetic process including some mediators of inflammation participating and excessive inflammatory reaction out of control. Therefore base of above-mentioned finding that electric stimulating efferent vagus nervus can inhibite excessive inflammatory and protect organs in vivo,we hypothesis that any method that can electric stimulating efferent vagus nerve possibly regulate myocardial ischemia- reperfusion injury at direct.Our study is to aim mainly at whether if how to antagonise the injury caused by inflammation overexpression in myocardium,then provide a new and available method for protecting myocardium against ischemia-reperfusion injury.
Objective:To study the protection of myocardium against ischemia-reperfusion injury via activating the cholinergic anti- inflammatory pathway by electric stimulating vagus nerve or electric acupuncture at Zusanli point in rats.
Method:1.100 Sprague-Dawley male rat were randomly divided in 5 groups:①sham-operation control group(SHAM group)②myocardial ischemia-reperfusion group(IR group)③vagus nerve stimulation group(STM group)④electroacupuncture Zusanli point group(ZSL group)⑤electroacupuncture non-acupoints group(FJFX group).Except for SHAM group,each group was subjected to 30 min of myocardial ischemia followed by 2h of reperfusion.In addition,in STM group, electrode continued stimulating left cervical vagus nerve at the intensity of 5 V、2ms、1HZ before and after 10min of reperfusion;in ZSL group, electric acupuncture continued stimulating Zusanli point before and after 10min of reperfusion;in FJFX group,electric acupuncture continued stimulating non-acupoints to exclude the effect of electric stimulus to myocardium injury.To record the incidence rate of arhythmia,and the change of heart rate,mean arterial pressure;sample was collected after 120min of reperfusion.2.Myocardium inflammation were dectected by HE staining and examined under the light microscope;myocardial area at risk and infart region was determined by Evan's blue dye perfusion and triphenyl tetrazolium chloride(TTC) staining;the level of plasma troponinIin was detected by immunoturbidimetry;the level of tissue TNF-αand IL-6 in myocardium and plasm was detected by Elisa;The activity of myeloperoxidase(MPO) in myocardium was detected by chromatometry;the formation of malondialdehyde(MDA) in myocardium was detected by thio-barbituric acid method;the expression of nuclear factor-κB p65(NF-κBp65) in myocardium was analyzed by immunohistochemical technique;myocardial apoptotic cells were examined by the TUNEL assay.
Results:1.Vital signs and arhythmia:compared with SHAM group,MAP decreased in IR group,ZSL group,STM group and FJFX group.there is no difference in these groups.HR in these group decreased during reperfusion period and STM group dereased more rapidly at the sitmulation period.When stimulation stopped,HR recovered.The incidence rate of arhythmia in STM group and ZSL group decreased more significantly than IR group(P＜0.05).2.Histodiagnosis by light microscope:myocardium structure is normal and cardiocyte rank tightly,no edma and inflammtory cell infiltrate in SHAM group.IR group and FJFX group have more significantly change than STM group and ZSL group.Extensive cloudy swelling,lamellar necrosis,many inflammatory cells infiltration existed in IR group.3.Area at risk and infarct size were detected by EB/TTC staining.There is a significant difference between IR group and STM group in%infart size.the levels of cTnI in each group before ischmia are similar.after 120min of reperfusion,there is a increase in each group,compared with SHAM group(P＜0.05),the level of cTnI in STM group and ZSL group are lower than IR group(P＜0.05);there is no difference in ST group and ZSL group(P＜0.05).4.Injury caused by inflammation and oxidation:MPO activity and MDA formation in other 4 groups increase more significantly than SHAM group.The MPO activity and MDA formation in IR group are higher than STM group and ZSL group,compared to SHAM group,TNF and IL-6 concentration in plasma and myocardium are higher in IR group,STM group,ZSL group and FJFX group(P＜0.05).IR group caused a farther increase of TNF an IL-6 compared to ZSL group.There is no difference between STM group and ZSL group.The immuno-histochemical stain of NF-κB demonstrated that compared with SHAM group,the colour in cytoplasma was obviously deeper in IR group.there is positive staining in cytoplasma and nuclei,indicating that NF-κB was activated from cytoplasma into nuclei;vagus nerve stimulation(VNS) and eclectroacupuncture Zusanli point can reduce its expression,however which was still higher than SHAM group.5.Cardiocyte apoptosis index:There were hardly any TUNEL-positive nuclei in myocardium of SHAM group.numerous TUNEL-positive nuclei in the myocardium were observed in the IR group. Electric vagus nerve stimulation and electroacupuncture Zusanli reduced the amout of TUNEL-positive cells as AI(apoptosis index ) are lower in STM group and ZSL group than in IR group.(P＜0.05).
Conclusion:Electroacupuncture Zusanli point can inhibite the inflammtion induced by myocardial I/R injury and protect myocardium without vagus nerve dissection;The mechanism is invovled about activation of cholinergic anti-inflammatory pathway,blunting NF-κB p65 expression,down-regulation TNF and IL-6 release,inhibiting apoptosis.
目的:通过运用电针足三里刺激或迷走神经电刺激研究兴奋胆碱能抗炎通路对大鼠缺血再灌注损伤心肌的保护作用,探讨其作用机制。
方法:雄性SD大鼠100只,随机分为5组:①手术对照组(SHAM组)②心肌缺血再灌注组(IR组)③迷走神经刺激组(STM组)④电针足三里组(ZSL组)⑤非经非穴组(FJFX组),除SHAM组外,各组均行心肌缺血30min再灌注,STM组于再灌前后各10min,共20min,以5 V、2ms、1HZ强度持续刺激左颈迷走神经,ZSL组于再灌前后各15min,共30min,行电针足三里刺激,FJFX组于再灌前后各15min,共30min,行电针非经非穴刺激。记录心律失常发生率,心率(heart rate,HR),平均动脉压(mean arterial pressure,MAP)变化;再灌注120min后,处死动物,采集标本。常规方法石蜡切片行苏木素一伊红(Hematoxylin and Eosin Staining,HE)染色,光学显微镜下观察心肌的炎症改变;伊文思蓝/氯化三苯基四唑(Evan's Blue/2,3,5-Triphenyl-2H-Tetrazoliumchloride,EB/TTC)测定心肌梗死面积与免疫比浊法测定血浆肌钙蛋白Ⅰ浓度;酶联免疫吸附试验(enzyme-linkedimmunosorbent assay,ELISA)检测心肌和血浆中肿瘤坏死因子(tumornecrosis factor,TNF)含量和白介素-6(interleukin-6,IL-6)含量;分光光度法测定心肌组织髓过氧化物酶(Myeloperoxidas MPO)活性;硫代巴比妥酸法测定心肌组织丙二醛(Malondialdehyde MDA)含量;免疫组化分析心肌核转录因子p65(nulear factor-kappa Bp65 NF-κBp65)表达;原位末端标记法(TUNEL)检测心肌细胞凋亡。
结果:1.血流动力学和心律失常观察:除SHAM组外,再灌120min后各组心率,平均动脉压较缺血前均有下降(p＜0.05),各组之间MAP差异无统计学意义(p＞0.05)。STM组、ZSL组心率在刺激阶段有下降,STM组下降较ZSL组更明显,但波动幅度仍在10%以内,刺激停止后,心率回升。STM组、ZSL组再灌后心律失常发生率明显低于IR组,差异具有统计学意义(p＜0.05);
2、组织形态学观察:光镜下发现SHAM组心肌结构正常,细胞排列紧密、界限清楚,无水肿,无炎性细胞浸润;IR组、FJFX组心肌排列稀疏,不规则,细胞水肿,部分细胞出现明显空泡变性、心肌纤维断裂,细胞间隙明显增宽,大量炎性细胞浸润;STM组、ZSL组心肌细胞排列较规则,细胞轻度水肿,细胞间隙增宽,炎性细胞散在浸润;
3、心肌损伤程度观察:各组心肌行EB/TTC染色显示,各组间缺血范围差异无统计学意义(P＞0.05),与IR组相比,STM组和ZSL组心肌梗死范围差异有统计学意义(p＜0.05),心肌梗死范围减小,而ZSL组和STM组比较,无统计学差异(P＞0.05),FJFX组和IR组比较,无统计学差异(P＞0.05),各组心肌肌钙蛋白(cTnI)在心肌缺血前无明显差别,再灌注120min后,除SHAM组外,其他各组cTnI较缺血前均有不同程度的升高(P＜0.05),STM组和ZSL组cTnI浓度低于IR组(P＜0.05),STM组和ZSL组比较,无统计学差异(P＞0.05);
4、炎性标志物和氧化损害程度观察:与SHAM组相比,各组MPO活性和MDA含量显著增高,以IR组升高更为显著(P＜0.01),与ZSL组和STM组相比,差异也有统计学意义(P＜0.05),心肌组织和血浆中的TNF及IL-6的浓度在IR组、STM组、ZSL组、FJFX组明显升高,与SHAM组相比差异均有统计学意义(P＜0.05);其中IR组升高更为显著,与ZSL组相比,差异也有统计学意义(P＜0.05);STM组与ZSL组相比差异无统计学意义(P＞0.05)。免疫组化检测NF-κBp65表达,IR组大部分心肌细胞中,细胞浆染色呈阳性,细胞核染色呈阳性,ZSL组和STM组心肌细胞的胞浆呈弱阳性或阳性,细胞核染色呈弱阳性,核移位细胞数目减少。平均光密度值比较发现STM组、ZSL组NF-κBp65表达低于IR组(P＜0.05);
5、细胞凋亡观察:TUNEL法检测细胞凋亡发现,在SHAM组中,未发现TUNEL阳性细胞,相反,在IR组中,呈现大量TUNEL阳性细胞核呈棕黄色反应,核内染色质浓缩,形成密集颗粒位于核膜下,有的胞核被降解,胞浆不着色。ZSL组、STM组可见散在的阳性细胞。凋亡指数(apoptosis index AI)比较发现,STM组、ZSL组AI值低于IR组(P＜0.05)。
结论:电针足三里能够抑制心肌缺血再灌注损伤引发的炎症反应,对心肌起到保护作用;其机制可能是通过兴奋胆碱能抗炎通路,削弱N F-κB表达,减少TNF、IL-6产生,抑制细胞凋亡有关。
Background:Ischemia-reperfusion injury is a complex pathogenetic process involves multiple signal transductions and inflammatory mediators.At present,it is thought that both systemic and regional inflammatory reaction participat in ischemia-reperfusion injury,leucocyte (neutrophil primarily)、cytokine and chemokine as well as complement is activated during myocardial ischemia and significantly aggravated at reperfusion period,then initiate myocardial inflammatory cascade reaction.Research find that stimulating efferent vagus nervus and applicating neurotransmitter acetylcholine or nicotine can inhibite endotoxemia leading to systemic inflammatory response syndrome,and depress significantly cytokine releasing such as:tumor necrosis factor-α,interleukin-1β,interleukin-6,interleukin-8 meanwhile unaffect of the level of anti-inflammatory factor interleukin-10,which is named "the cholinergic anti-inflammatory pathway"The response of the myocardium to reperfusion is similar to inflammatory responses induced by sepsis.It is a pathogenetic process including some mediators of inflammation participating and excessive inflammatory reaction out of control. Therefore base of above-mentioned finding that electric stimulating efferent vagus nervus can inhibite excessive inflammatory and protect organs in vivo,we hypothesis that any method that can electric stimulating efferent vagus nerve possibly regulate myocardial ischemia- reperfusion injury at direct.Our study is to aim mainly at whether if how to antagonise the injury caused by inflammation overexpression in myocardium,then provide a new and available method for protecting myocardium against ischemia-reperfusion injury.
Objective:To study the protection of myocardium against ischemia-reperfusion injury via activating the cholinergic anti- inflammatory pathway by electric stimulating vagus nerve or electric acupuncture at Zusanli point in rats.
Method:1.100 Sprague-Dawley male rat were randomly divided in 5 groups:①sham-operation control group(SHAM group)②myocardial ischemia-reperfusion group(IR group)③vagus nerve stimulation group(STM group)④electroacupuncture Zusanli point group(ZSL group)⑤electroacupuncture non-acupoints group(FJFX group).Except for SHAM group,each group was subjected to 30 min of myocardial ischemia followed by 2h of reperfusion.In addition,in STM group, electrode continued stimulating left cervical vagus nerve at the intensity of 5 V、2ms、1HZ before and after 10min of reperfusion;in ZSL group, electric acupuncture continued stimulating Zusanli point before and after 10min of reperfusion;in FJFX group,electric acupuncture continued stimulating non-acupoints to exclude the effect of electric stimulus to myocardium injury.To record the incidence rate of arhythmia,and the change of heart rate,mean arterial pressure;sample was collected after 120min of reperfusion.2.Myocardium inflammation were dectected by HE staining and examined under the light microscope;myocardial area at risk and infart region was determined by Evan's blue dye perfusion and triphenyl tetrazolium chloride(TTC) staining;the level of plasma troponinIin was detected by immunoturbidimetry;the level of tissue TNF-αand IL-6 in myocardium and plasm was detected by Elisa;The activity of myeloperoxidase(MPO) in myocardium was detected by chromatometry;the formation of malondialdehyde(MDA) in myocardium was detected by thio-barbituric acid method;the expression of nuclear factor-κB p65(NF-κBp65) in myocardium was analyzed by immunohistochemical technique;myocardial apoptotic cells were examined by the TUNEL assay.
Results:1.Vital signs and arhythmia:compared with SHAM group,MAP decreased in IR group,ZSL group,STM group and FJFX group.there is no difference in these groups.HR in these group decreased during reperfusion period and STM group dereased more rapidly at the sitmulation period.When stimulation stopped,HR recovered.The incidence rate of arhythmia in STM group and ZSL group decreased more significantly than IR group(P＜0.05).2.Histodiagnosis by light microscope:myocardium structure is normal and cardiocyte rank tightly,no edma and inflammtory cell infiltrate in SHAM group.IR group and FJFX group have more significantly change than STM group and ZSL group.Extensive cloudy swelling,lamellar necrosis,many inflammatory cells infiltration existed in IR group.3.Area at risk and infarct size were detected by EB/TTC staining.There is a significant difference between IR group and STM group in%infart size.the levels of cTnI in each group before ischmia are similar.after 120min of reperfusion,there is a increase in each group,compared with SHAM group(P＜0.05),the level of cTnI in STM group and ZSL group are lower than IR group(P＜0.05);there is no difference in ST group and ZSL group(P＜0.05).4.Injury caused by inflammation and oxidation:MPO activity and MDA formation in other 4 groups increase more significantly than SHAM group.The MPO activity and MDA formation in IR group are higher than STM group and ZSL group,compared to SHAM group,TNF and IL-6 concentration in plasma and myocardium are higher in IR group,STM group,ZSL group and FJFX group(P＜0.05).IR group caused a farther increase of TNF an IL-6 compared to ZSL group.There is no difference between STM group and ZSL group.The immuno-histochemical stain of NF-κB demonstrated that compared with SHAM group,the colour in cytoplasma was obviously deeper in IR group.there is positive staining in cytoplasma and nuclei,indicating that NF-κB was activated from cytoplasma into nuclei;vagus nerve stimulation(VNS) and eclectroacupuncture Zusanli point can reduce its expression,however which was still higher than SHAM group.5.Cardiocyte apoptosis index:There were hardly any TUNEL-positive nuclei in myocardium of SHAM group.numerous TUNEL-positive nuclei in the myocardium were observed in the IR group. Electric vagus nerve stimulation and electroacupuncture Zusanli reduced the amout of TUNEL-positive cells as AI(apoptosis index ) are lower in STM group and ZSL group than in IR group.(P＜0.05).
Conclusion:Electroacupuncture Zusanli point can inhibite the inflammtion induced by myocardial I/R injury and protect myocardium without vagus nerve dissection;The mechanism is invovled about activation of cholinergic anti-inflammatory pathway,blunting NF-κB p65 expression,down-regulation TNF and IL-6 release,inhibiting apoptosis.
引文
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