T-type calcium channel expression in cultured human neuroblastoma cells

Human neuroblastoma cells （SH-SY5Y） have similar structures and functions as neural cells and have been frequently used for cell culture studies of neural cell functions.Previous studies have revealed L-and N-type calcium channels in SH-SY5Y cells.However,the distribution of the low-voltage activated calcium channel （namely called T-type calcium channel,including Cav3.1,Cav3.2,and Cav3.3） in SH-SY5Y cells remains poorly understood.The present study detected mRNA and protein expres-sion of the T-type calcium channel （Cav3.1,Cav3.2,and Cav3.3） in cultured SH-SY5Y cells using real-time polymerase chain reaction （PCR） and western blot analysis.Results revealed mRNA and protein expression from all three T-type calcium channel subtypes in SH-SY5Y cells.Moreover,Cav3.1 was the predominant T-type calcium channel subtype in SH-SY5Y cells.

Differential Effect of Calcium-Activated Potassium and Chloride Channels on Rat Basilar Artery Vasomotion

Spontaneous, rhythmical contractions, or vasomotion, can be recorded from cerebral vessels under both normal physiological and pathophysiological conditions. We investigated the cellular mechanisms underlying vasomotion in the cerebral basilar artery （BA） of Wistar rats. Pressure myograph video microscopy was used to study the changes in cerebral artery vessel diameter. The main results of this study were as follows： （1） The diameters of BA and middle cerebral artery （MCA） were 314.5±15.7 μm （n=15） and 233.3±10.1 μm （n=12） at 10 mmHg working pressure （P〈0.05）, respectively. Pressure-induced vasomotion occurred in BA （22/28, 78.6%）, but not in MCA （4/31, 12.9%） from 0 to 70 mmHg working pressure. As is typical for vasomotion, the contractile phase of the response was more rapid than the relaxation phase; （2） The frequency of vasomotion response and the diameter were gradually increased in BA from 0 to 70 mmHg working pressure. The amplitude of the rhythmic con- tractions was relatively constant once stable conditions were achieved. The frequency of contractions was variable and the highest value was 16.7±4.7 （n=13） per 10 min at 60 mmHg working pressure; （3） The pressure-induced vasomotion of the isolated BA was attenuated by nifedipine, NFA, 181]-GA, TEA or in Ca2＋-free medium. Nifedipine, NFA, 18^-GA or Ca2＋-free medium not only dampened vasomotion, but also kept BA in relaxation state. In contrasts, TEA kept BA in contraction state. These results sug- gest that the pressure-induced vasomotion of the isolated BA results from an interaction between Ca2＋-activated C1- channels （CaCCs） currents and Kca currents. We hypothesize that vasomotion of BA depends on the depolarizing of the vascular smooth muscle cells （VSMCs） to activate CaCCs. Depolarization in turn activates voltage-dependent Ca2＋ channels, synchronizing contractions of adjacent cells through influx of extracellular calcium and the flow of calcium through gap junctions. Subsequent calcium-induced calcium release from ryanodine-sensitive stores activates Kca channels and hyperpo- larizes VSMCs, which provides a negative feedback loop for regenerating the contractile cycle.

Transient Receptor Potential Ion Channels in the Etiology and Pathomechanism of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis

Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a disabling condition of unknown cause having multi-system manifestations. Our group has investigated the potential role of transient receptor potential (TRP) ion channels in the etiology and pathomechanism of this illness. Store-operated calcium entry (SOCE) signaling is the primary intracellular calcium signaling mechanism in non-excitable cells and is associated with TRP ion channels. While the sub-family (Canonical) TRPC has been traditionally associated with this important cellular mechanism, a member of the TRPM sub-family group (Melastatin), TRPM3, has also been recently identified as participating in SOCE in white matter of the central nervous system. We have identified single nucleotide polymorphisms (SNPs) in TRP genes in natural killer (NK) cells and peripheral blood mononuclear cells (PBMCs) in CFS/ME patients. We also describe biochemical pathway changes and calcium signaling perturbations in blood cells from patients. The ubiquitous distribution of TRP ion channels and specific locations of sub-family group members such as TRPM3 suggest a contribution to systemic pathology in CFS/ME.

CB_1 Cannabinoid Receptor-Dependent and-Independent Inhibition of Depolarization-Induced Calcium Influx in Oligodendrocytes

Ca2+稳态平衡的调节在少突胶质细胞功能和存活中起重要作用。大麻素CB1和CB2受体在许多细胞中调节Ca2+水平和/或K+电流。本文利用培养的少突胶质细胞中,通过增高细胞外K+浓度(50 mM诱导膜去极化,研究大麻素复合物在此过程引发钙内流中的作用。CB2受体激动剂ACEA导致去极化诱导的少突胶质细胞胞浆的Ca2+瞬变表达浓度依赖性抑制,最大效应为(94±3)%,半效应浓度(EC50)为(1.3±0.03)μM。这种作用可被CB2/CB2激动剂CP55、940、内源性大麻素类AEA和2-AG所模拟,但是CB2受体选择性激动剂J WH133没有作用。CB2受体拮抗剂AM251(1μM)也可减少细胞外高K+诱导的Ca2+反应,但不能防止ACEA(3μM)诱发的抑制效应。然而,ACEA和AEA减少去极化诱导的Ca2+瞬变的能力在CB2受体敲除小鼠和经百日咳毒素预处理的少突胶质细胞中明显降低。内流性K+通道阻断剂BaCl2(300μM)和CsCl2(1 mM)降低电压诱导的Ca2+内流并部分阻断ACEA的抑制效应。本文表明,大麻素抑制少突胶质细胞中去极化诱导的Ca2+瞬变是通过包括PTX-敏感的Gi/o蛋白和阻断K+内流通道的CB2受体依赖性和非依赖性机制。

Does closure of acid-sensing ion channels reduce ischemia/reperfusion injury in the rat brain?

Acidosis is a common characteristic of brain damage. Because studies have shown that permeable Ca2＋-acid-sensing ion channels can mediate the toxic effects of calcium ions, they have become new targets against pain and various intracranial diseases. However, the mechanism associated with expression of these channels remains unclear. This study sought to observe the expression characteristics of permeable Ca2＋-acid-sensing ion channels during different reperfusion inflows in rats after cerebral ischemia. The rat models were randomly divided into three groups： adaptive ischemia/reperfusion group, one-time ischemia/reperfusion group, and severe cerebral ischemic injury group. Western blot assays and immunofluorescence staining results exhibited that when compared with the one-time ischemia/reperfusion group, acid-sensing ion channel 3 and Bcl-x/I expression decreased in the adaptive ischemia/reperfusion group. Calmodulin expression was lowest in the adaptive ischemia/reperfusion group. Following adaptive reperfusion, common carotid artery flow was close to normal, and the pH value improved. Results verified that adaptive reperfusion following cerebral ischemia can suppress acid-sensing ion channel 3 expression, significantly reduce Ca2＋ influx, inhibit calcium overload, and diminish Ca2＋ toxicity. The effects of adaptive ischemia/reperfusion on suppressing cell apoptosis and relieving brain damage were better than that of one-time ischemia/reperfusion.

压电型机械门控离子通道组件1在大鼠压力性损伤中的作用机制

背景:压力性损伤的发生机制复杂,哪些因素在其发生中起到核心作用,这些因素具体又是如何发生的尚不完全清楚。目的:探讨压电型机械门控离子通道组件1(piezo-type mechanosensitive ion channel component 1,PIEZO1)与压力性损伤发生的关系。方法:①细胞实验:采用不同浓度的PIEZO1激动剂Yoda1干预人永生化角质形成细胞(HaCaT),检测细胞活性、钙离子内流及PIEZO1、凋亡相关蛋白的表达。②动物实验:采用随机数字表法将12只SD大鼠随机分为4组,每组3只:对照组大鼠不进行任何处理,1,2,3 mm组分别采用厚度1,2,3 mm的磁铁在大鼠背部两侧压迫1 h,建立压力性损伤模型,造模后切除全部创面组织,分别进行苏木精-伊红、Masson、免疫荧光染色及Western blot检测。结果与结论:①细胞实验:活/死细胞染色结果显示,随着Yoda1浓度(0,2.5,5,10μmol/L)的升高,HaCaT细胞凋亡增加;随着Yoda1浓度(0,5,10μmol/L)的升高,HaCaT细胞钙离子内流增加,并且随着处理时间的延长,钙离子内流增多;Western blot检测结果显示,与对照组(0μmol/L Yoda1干预)比较,5,10μmol/L Yoda1干预可提升HaCaT细胞中BAX、TG2、PIEZO1蛋白的表达,降低Bcl-2蛋白的表达;②动物实验:苏木精-伊红与Masson染色结果显示,3个实验组压迫部位皮肤结构被破坏,皮下脂肪液化坏死,胶原蛋白稀疏且排列紊乱,并且随着磁铁厚度(压力)的增加,压迫部位皮肤组织结构破坏程度加重;免疫荧光染色与Western blot检测结果显示,与对照组比较,3个实验组大鼠BAX、TG2、Yap1与PIEZO1蛋白表达升高,Bcl-2蛋白表达降低,并且随着磁铁厚度(压力)的增加,相关蛋白表达值改变更加明显;③结果表明:皮肤受压会激活PIEZO1使钙离子大量内流,随着所受压力的不断增加,最终导致钙超载后的细胞凋亡。

Exploiting MCF-7 Cells’ Calcium Dependence with Interlaced Therapy

The purpose of this study is to demonstrate MCF-7 cells’ dependence on calcium for growth and to exploit that dependence to improve chemotherapy efficacy. Fura-2 fluorescence imaging shows that MCF-7 cells maintain a higher basal intracellular calcium concentration than non-tumorigenic MCF-10A cells. Blocking T-type calcium channels with mibefradil reduced MCF-7 intracellular calcium concentration. Flow cytometry shows that knocking down T-type calcium channel expression with siRNA caused an increase in MCF-7 cells in G1 phase and a decrease in cells in S phase. Proliferation assays of MCF-7 cells treated with EGTA and thapsigargin reveal the dependence of MCF-7 cell growth on extracellular and intracellular calcium sources, respectively. In vitro, interlaced treatment that alternated the T-type calcium channel blocker NNC-55-0396 with paclitaxel more effectively reduced MCF-7 cell number than chemotherapy alone. In a mouse in vivo model, interlaced mibefradil and paclitaxel more effectively reduced MCF-7 xenograft size than chemotherapy alone. These findings indicate that MCF-7 cells are dependent on calcium for proliferation, particularly in passing the G1/S cell cycle checkpoint. Further, this dependence on calcium can be exploited by alternating treatment with T-type calcium channel blockers with paclitaxel in an interlaced therapy scheme that increases the efficacy of the chemotherapy.

The changes of neuronal Ca^（2＋） channel and its effects on BBB permeability and cerebral edema associated with brain injury

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环核苷酸门控离子通道及其功能的研究进展

环核苷酸门控(CNG)离子通道是一种非选择性的四聚体阳离子通道,可以直接被细胞内信使小分子——环核苷酸活化,是钙离子进入细胞的主要通道之一。CNG通道蛋白由6种不同基因编码:4个A亚单位和2个B亚单位。CNG离子通道的活性可被钙离子/钙调素(Ca2+/CaM)及磷酸化或膜上磷酸肌醇作用调节,从而改变细胞内钙离子浓度,参与多种生物学功能的调控。自从在视杆细胞中发现CNG离子通道以来,经历了对其生理功能、克隆相关基因、理解调控方式、解析晶体结构和开发相关的基因治疗方法等研究过程,在视觉和嗅觉感觉神经元(OSNs)的信号转导中发挥着重要作用。现就CNG离子通道的功能、结构、调控机制及其与相关疾病关系等方面进行简要综述,以期为CNG离子通道相关疾病的治疗提供理论依据。

Transient Receptor Potential Melastatin 3 and Intracellular Calcium in Natural Killer Cells in Multiple Sclerosis

Background: Natural killer (NK) cell phenotypes have reported to be implicated in the pathomechanism of Multiple Sclerosis (MS). Several investigators have observed reduced peripheral numbers, reduced cytotoxic activity, and altered CD56Dim and CD56Bright NK cell phenotypes. This current project, for the first time, investigates the NK cell cytotoxicity, calcium mobilisation and transient receptor potential melastatin 3 (TRPM3) surface expression. Methods: NK cell cytotoxic activity and calcium signaling were examined in CD56Dim and CD56Bright NK cells before and after stimulation using Ionomycin, Pregnenolone sulphate, 2-Aminoethoxydiphenyl borate and Thapsigargin. Purified NK cells were labelled with antibodies to determine TRPM3, CD69 and CD107a surface expression using flow cytometry. Results: Twenty-two MS patients and 22 healthy controls were recruited for this project. Twelve of the 22 previously received Alemtuzumab (Lemtrada®) and the remaining ten reported nil medication. We report TRPM3 was significantly increased in untreated MS patients compared with healthy controls and treated MS patients (p-value 0.034). There was a significant decrease in CD69 surface expression on CD56Dim NK cell phenotype for untreated MS patients (p-value 0.031) and treated MS patients (p-value 0.036). We report altered calcium mobilisation in CD56Bright NK cells and to a lesser extent CD56Dim NK cells between healthy controls, treated and untreated MS patients. Conclusion: This investigation suggests variations in TRPM3 expression and calcium mobilisation of NK cells may be implicated in the pathogenesis of MS. Further investigation is required to determine the mechanism by which alemtuzumab alters calcium signaling in NK cells.

Piezo1通道激活促进大鼠冠脉平滑肌细胞内钙浓度升高的机制研究

目的:探讨机械敏感性离子通道Piezo1激活促进冠状动脉平滑肌细胞(CASMCs)内Ca^(2+)浓度([Ca^(2+)]i)升高的机制。方法:采用原代成年大鼠CASMCs为研究对象,用细胞免疫荧光技术观察Piezo1在CASMCs中的表达与亚细胞定位情况;利用Western blot检测用si RNA敲减CASMCs中Piezo1和基质相互作用分子1(STIM1)后CASMCs中的蛋白表达情况;利用激光共聚焦显微镜,通过基于Flou-4 AM负载的细胞内Ca^(2+)成像技术,测量CASMCs[Ca^(2+)]i的变化。结果:细胞免疫荧光染色结果显示,Piezo1在原代大鼠CASMCs中表达;Piezo1与肌浆/内质网Ca^(2+)-ATP酶2(SERCA2)、线粒体外膜蛋白TOM20和核膜蛋白lamin B1共定位程度较高。Western blot结果表明,si RNA转染后STIM1和Piezo1蛋白表达下调(P<0.05)。激光共聚焦显微镜检测[Ca^(2+)]i结果表明:与对照组相比,Piezo1激动剂Yoda1诱导CASMCs的胞外Ca^(2+)内流增加(P<0.01),抑制L型钙通道不影响Yoda1诱导的Ca^(2+)内流;Yoda1诱导CASMCs胞内Ca^(2+)释放增加(P<0.01),抑制内质网上的钙通道(雷诺丁受体和1,4,5-三磷酸肌醇受体)不影响Yoda1诱导的胞内Ca^(2+)释放;使用毒胡萝卜素(TG)排空内质网中Ca^(2+)后,Yoda1仍能诱导CASMCs中其它细胞器的Ca^(2+)释放(P<0.01);抑制L型钙通道后,使用钙库操纵性钙通道(SOCC)抑制剂BTP2或敲减STIM1使Yo‐da1诱导CASMCs胞外Ca^(2+)内流减少(P<0.01);敲减Piezo1使TG诱导的CASMCs内质网Ca^(2+)释放增加(P<0.05),但不影响TG诱导的胞外Ca^(2+)内流;抑制L型钙通道和SOCC后,敲减Piezo1导致Yoda1诱导的CASMCs胞内Ca^(2+)释放以及胞外Ca^(2+)内流均减少(P<0.01)。结论:Piezo1激动剂诱导CASMCs胞外Ca^(2+)内流主要通过细胞膜上的Piezo1通道和间接激活的SOCC,也可触发胞内细胞器Ca^(2+)释放,共同升高[Ca^(2+)]i。

FRACTIONAL TIME SCALE IN CALCIUM ION CHANNELS MODEL

We propose a fractional time scale to model the calcium ion channels model which is retarded with injection of calcium-chelator Ethylene Glycol Tetraacetic Acid （EGTA）. By using this nonlinear time scale and Modified Riemann-Liouville fractional derivative, we convert the integer-order calcium ion channels model into fractional-order differential equations. We also analyze the range of order of fractional-order differentiM equations to ensure the equilibria of it are asymptotically stable. The simulation results are given to demonstrate the solutions of this model coincide with the real experiment data.

山奈酚对缺氧/复氧损伤诱导心肌细胞凋亡的影响及机制研究

目的:探究山奈酚对缺氧/复氧损伤诱导心肌细胞凋亡的影响和机制。方法:利用随机数字法将H9C2大鼠心肌细胞随机分为三组,对照组细胞在常规孵箱培养,缺氧/复氧组细胞利用缺氧孵箱和常规孵箱交替培养,山奈酚组细胞在缺氧/复氧培养的基础上应用30μmol/L山奈酚。分别利用流式细胞仪和多核苷酸链断裂技术检测各组细胞凋亡水平,利用蛋白印迹技术检测凋亡相关蛋白和钙离子通道蛋白含量,利用免疫荧光技术检测细胞中钙离子浓度。结果:和对照组比较,缺氧/复氧组细胞凋亡增加,钙离子通道蛋白Cav1.2表达和细胞中钙离子含量增加(均P<0.05);和缺氧/复氧组比较,山奈酚组细胞凋亡减少,钙离子通道蛋白Cav1.2表达和胞内钙离子浓度减少(均P<0.05)。结论:山奈酚可能通过减少钙离子通道蛋白Cav1.2表达和胞内钙离子浓度抑制缺氧/复氧损伤诱导的大鼠心肌细胞H9C2凋亡。

谷氨酸受体蛋白调控植物生长与胁迫应答的研究进展

植物谷氨酸受体(glutamate receptor-like,GLRs)是动物离子型谷氨酸受体(inotropic glutamate receptors,iGluRs)的同源蛋白,在开花植物中具有多个拷贝,常以功能冗余的基因家族形式共同调节植物生长发育和逆境应答过程。GLRs在植物中发挥作用的机制与其动物同源蛋白既有类似之处,但又表现出植物特异性。iGluRs在哺乳动物的神经系统中发挥重要作用。在iGluRs介导的神经传导中,由突触前膜释放的神经递质识别并结合突触后膜的iGluRs,iGluRs介导的阳离子内流引起突触后膜的去极化,形成动作电位的传递,构成神经传导的基础。过去20多年的研究发现,植物GLRs也可以作为离子通道蛋白,通过调节跨膜离子流行使功能。本文系统综述了植物谷氨酸受体的蛋白结构和演化特征,并对已报道的重要功能位点进行阐释;总结了近些年来对植物谷氨酸受体蛋白在植物生长发育不同时期,以及多种生物和非生物逆境应答中的功能的研究进展,并比较了其与动物iGluRs作用机制的异同;提出并梳理了该领域仍待解决的重要科学问题;最后展望了该蛋白家族在作物耐逆育种中的重要应用前景和价值,以期为改良作物耐逆性状提供线索。

结肠运动与离子通道的研究进展

结肠运动障碍是导致肠道疾病的重要因素,且也常并发于其他器质性疾病。离子通道作为细胞膜上的一种跨膜受体蛋白,可介导离子被动流入/流出细胞,控制细胞质/细胞器内离子浓度、膜电位和细胞体积,是调控结肠运动的关键因素。文章围绕结肠运动与Ca^(2+)、Na^(+)、K^(+)、TRPV1离子通道关系进行综述,可能为高效治疗结肠疾病提供研究基础。

多机制多通路参与哮喘新说

目的哮喘发病机制十分复杂,涉及许多方面,对哮喘发病机制的最新研究成果进行综述。方法参阅国外公开发表的相关文献26篇,从炎症及神经体液机制、气道高反应性及气道重塑机制、主要的离子通道等方面阐述了哮喘的发病机制。结果哮喘的发生发展涉及支气管炎症、机体的免疫反应、神经体液信号分子、平滑肌细胞膜及浆膜钙离子通道和钾离子通道等。结论对哮喘发病机制的阐明将为其治疗提供新的思路,同时也为抗哮喘药物的研发奠定基础。

锌对心肌保护作用机理的探讨

应用电镜、电子示踪技术和立体计量测试法，从形态学上观察异丙基肾上腺素对心肌膜系统的影响及锌的保护作用，同时应用标准玻璃微电极技术和微机实时分析方法，研究异丙基肾上腺素致心肌损伤及锌对心肌保护作用的机理。实验结果表明：异丙基肾上腺素可引起心肌细胞膜系统损伤，此时心肌细胞的去极化和复极化过程均发生改变；经锌前处理后，心肌损伤程度明显减轻，心肌细胞的复极化过程得到明显改善。锌对心肌的保护作用，主要是通过阻断心肌细胞膜慢通道、减少平台期钙离子内流、防止细胞内钙超载来实现。

内皮素对离体大鼠心肌细胞的影响

本文应用离体成年大鼠心肌细胞,研究内皮素作用的细胞机制,发现10^(-9)—10^(-7)mol/L内皮素可引起心肌细胞挛缩、胞浆乳酸脱氢酶漏出和细胞总钙量增加,且具有剂量-效应关系。内皮素可促进^(45)Ca内流,其作用为钙通道阻断剂维拉帕米所拮抗。预先用负载荧光染料Fura-2的心肌细胞与内皮素孵育,可见胞浆游离钙显著增加,其作用亦可为维拉帕米抑制。结果提示:内皮素主要通过电位依赖的钙通道促进心肌细胞Ca^(2+)内流,产生其生物学效应。

牛磺酸镁对缺氧/复氧致大鼠心肌细胞钙离子通道异常的影响

目的观察牛磺酸镁配合物(taurine magnesium coordination compound,TMCC)对缺氧/复氧损伤所致大鼠心室细胞异常L-型钙电流(ICa,L)的影响,以探讨其抗心律失常作用机制。方法酶解法分离大鼠单个心室肌细胞,应用全细胞膜片钳技术记录低(100μmol·L-1)、中(200μmol·L-1)、高(400μmol·L-1)3个浓度的牛磺酸镁及胺碘酮(24.24μmol·L-1)对缺氧/复氧大鼠心室细胞ICa,L的影响。结果缺氧/复氧使大鼠心室肌细胞ICa,L峰值从(3.35±0.50)pA/pF增大到(5.69±0.25)pA/pF(n=6,P<0.01),TMCC(100、200、400μmol·L-1)可使缺氧/复氧损伤模型增大的ICa,L峰值分别恢复到(5.28±0.18)pA/pF(n=6,P>0.05)、(4.41±0.22)pA/pF、(3.82±0.21)pA/pF(n=6,P<0.01)。24.24μmol·L-1胺碘酮使其恢复为(3.66±0.27)pA/pF(n=6,P<0.01)。与正常对照组相比,缺氧/复氧使钙激活曲线左移,激活加快,失活曲线右移,失活减慢,TMCC(200、400μmol·L-1)和胺碘酮(24.24μmol·L-1)可恢复左移的激活曲线,使激活减慢,恢复右移的失活曲线,使失活加快。结论 TMCC可通过促进钙通道的失活以及抑制钙通道的激活过程,浓度依赖性地恢复缺氧/复氧损伤引起的钙电流增大,其作用与胺碘酮相当,TMCC对钙电流的抑制作用可能是其发挥抗心律失常的机制之一。

参松养心胶囊对心梗后心肌的保护作用及机制研究

目的探讨参松养心胶囊(SSYX)对心肌梗死后心律失常发生和心功能不全的影响及其作用机制。方法将40只新西兰大耳白兔行冠状动脉前降支结扎术后随机分为正常对照组(Control组)10只、心梗组(MI组)10只、心梗+胺碘酮组(MI+A组,0.4 g·kg^(^(-1))·d^(^(-1)))10只、心梗+参松组(MI+S组,0.5 g·kg^(^(-1))·d^(^(-1)))10只。正常对照组开胸后在冠状动脉下穿线,但不结扎。术后,分别以普食、普食+胺碘酮粉末、普食+参松养心胶囊原粉喂食。8周后将家兔处死,在心梗周边区取材,检测各组白兔缝隙连接蛋白43(CX43)、钠钙交换体(NCX)和兰尼碱受体蛋白(Ry R2)m RNA的相对表达量。结果与Control组比较,MI组CX43、Ry R2 m RNA相对表达量显著下降(P<0.05),而NCX m RNA相对表达量虽然有所下降,但其差异无统计学意义(P>0.05);与MI组比较,MI+A组CX43、Ry R2 m RNA相对表达量显著升高(P<0.05),MI+S组CX43、NCX、Ry R2 m RNA的相对表达量也显著升高(P<0.05);与MI+A组比较,MI+S组CX43、NCX m RNA的相对表达量均显著升高(P<0.05)。结论参松养心胶囊可以改善心肌梗死后心律失常以及心功能不全,其机制可能与调控各钙离子通道的开放,抑制钙超载有关。