Theoretical Study on Drift of Ca^(2+)Spiral Waves Controlled by Electric Field

Based on the Tang-Othmer Ca^2＋ model, the drift behavior of intracellular Ca^2＋ spiral waves under the influence of weak electric field is investigated. Numerical results show that the dependence of drift velocity of the spiral tip on dc electric field is similar to experimental observations in BZ system. When an ac electric field is applied, interesting resonant-drift phenomenon is observed with ω=2ω0. All results can be explained analytically using a proximate method.

Controlling intracellular Ca^(2+) spiral waves by the local agonist in the cell membrane

A modified spatially extended Tang-Othmer Ca2＋ model is used to study intracellular Ca2＋ spiral waves numerically. It is found that, as a local stimulation, the local agonist-binding on the cell membrane, which enhances the local concentration of the messenger molecule inositol 1,4,5-trisphosphate（IP3）, can influence the dynamics of the spiral waves. 1） Strong enough stimuli can change the spiral wave from a meandering to a rigidly rotating one. 2） On the other hand, strong enough stimuli can suppress the spiral wave from the system. It provides the theoretical clue for controlling the spiral waves by stimulating the cell membrane.

Mechanism of Qiliqiangxin capsule on the regulation of IP3Rs/GRP75/VDAC1 gene in myocardial infarction rat heart

Objective:To investigate the regulatory effect of Qiliqiangxin Capsule on mitochondrial Ca^(2+)related genes in rats with myocardial infarction(MI).Methods:The rat model of MI was established by ligation of the left anterior descending coronary artery.After operation,the rats were randomly assigned to the model group,the Qiliqiangxin group and the captopril group;a sham-operated group was also available as a control.After four weeks of treatment,the extent of infarction in rats was observed by gross cardiac structure and the morphological changes of myocardial histopathology were observed by HE staining.Detection of mitochondrial Ca^(2+)transport-related genes such as inositol-1,4,5-trisphosphate receptor 2(IP3R2),glucose regulated protein 75(GRP75),voltage-dependent anion channel 1(VDAC1),and mitofusion 2(Mfn2)and mitochondrial apoptosis-related genes such as B-cell lymphoma-2(Bcl-2)and Bcl-2 related X protein(Bax)mRNA expression changes was measured by RT-PCR in the infarct margins of the heart;Western blot was used to detect changes in Bcl-2,Bax protein expression in myocardial tissue.The rate of apoptosis in cardiac myocardial tissue was detected by TUNEL staining.Results:Compared with the sham group,the anterior left ventricular wall of the model group showed a large area of infarction,and the structure of myocardial tissue was disordered.The mRNA expression level of mitochondrial Ca^(2+)transport-related genes such as IP3R2,GRP75,VDAC1,and Mfn2 were significantly increased(P<0.05,P<0.01);The mRNA and protein expression of Bcl-2,a molecule related to mitochondrial apoptosis,were significantly decreased(P<0.01),while the mRNA and protein expression of Bax were significantly increased(P<0.01);and apoptosis rate was significantly increased(P<0.01).Compared with the model group,the infarct size of cardiac gross specimens in the Qiliqiangxin group and the captopril group was reduced and myocardial fibers were relatively well ordered;The mRNA expression of mitochondrial Ca^(2+)transport-related genes such as IP3R2,GRP75,VDAC1,and Mfn2 were significantly reduced(P<0.01);the mRNA and protein expression of Bcl-2,a molecule related to mitochondrial apoptosis,were increased(P<0.05,P<0.01),and the mRNA and protein expression of Bax were significantly decreased(P<0.05,P<0.01).and apoptosis rate was significantly decreased(P<0.01).Conclusion:Qiliqiangxin Capsule can improve the morphological structure of the heart of rats with MI,and its mechanism is related to regulation of the gene expression of mitochondrial Ca^(2+)transport complex IP3R2/GRP75/VDAC1,thereby inhibiting apoptosis.

不同频率摩腹法对脾虚型功能性消化不良家兔胃肠平滑肌IP3浓度及Ca^(2+)强度的影响

【目的】探讨不同频率摩腹法对脾虚型功能性消化不良(FD)家兔的治疗作用及机制。【方法】将76只家兔随机分为正常组、模型组、摩法低频组(机械臂摩腹101~150次/min)、摩法高频组(机械臂摩腹201~250次/min)、摩法低频+抑制剂组[机械臂摩腹101~150次/min+腹腔注射肌球蛋白轻链激酶(MLCK)抑制剂ML-92.0 mg·kg^(-1)]、摩法高频+抑制剂组(机械臂摩腹201~250次/min+腹腔注射ML-92.0 mg·kg^(-1))。除正常组外,其余各组采用苦寒泻下法联合饥饱失常法构建FD模型。干预过程中,记录家兔一般情况。干预结束后,采用酶联免疫吸附分析(ELISA)测定胃体、小肠平滑肌组织中三磷酸肌醇(IP3)浓度,采用流式细胞术测定家兔胃体平滑肌细胞中Ca^(2+)强度。【结果】经摩腹法干预后,高、低频组家兔一般情况有不同程度改善。摩法低频组、摩法高频组小肠平滑肌细胞IP3浓度较模型组升高(P<0.05或P<0.01),摩法低频+抑制剂组、摩法高频+抑制剂组IP3浓度较模型组降低(P<0.05)。摩法低频组、摩法高频组、摩法低频+抑制剂组胃体平滑肌细胞Ca^(2+)强度较模型组升高,其中摩法低频组、摩法高频组与模型组间的差异有统计学意义(P<0.01),摩法高频+抑制剂组Ca^(2+)强度较模型组降低(P<0.05);摩法低频组Ca^(2+)强度较摩法高频组升高,摩法低频+抑制剂组Ca^(2+)强度较摩法高频+抑制剂组升高(均P<0.01)。【结论】高、低频率摩腹法干预均可以改善脾虚型FD家兔症状,提高胃肠道平滑肌细胞中IP3浓度与Ca^(2+)强度,低频摩腹法的改善作用优于高频摩腹法。

Numerical study of IP_3-induced Ca^(2+) spiral pattern evolution

The effect of change in concentration of messenger molecule inositol 1,4,5-trisphosphate （IP3） on intracellular Ca^2＋spiral pattern evolution is studied numerically. The results indicate that when the IP3 concentration decreases from 0.27 μM, a physiologically reasonable value, to different values, the spiral centre drifts to the edge of the medium and disappears for a small enough IP3 concentration. The instability of spiral pattern can be understood in terms of excitability-change controlled by the IP3 concentration. On the other hand, when the IP3 concentration increases from 0.27 μM, a homogeneous area with a high Ca^2＋ concentration emerges and competes with the spiral pattern. A high enough IP3 concentration can lead the homogeneous area to occupy the whole medium. The instability of spiral pattern is ascribed to the change in stability of a stationary state with a high Ca^2＋ concentration.

动态IP_3-Ca^(2+)振荡模型的数值分析

通过改进J.W.Shuai和P.Jung钙振荡模型,得到与IP3浓度相关的动态IP3-Ca2+振荡模型。利用改进模型,数值分析依赖性参数#和钙通道数目N对Ca2+振荡的影响,得到Ca2+振荡关于参数#的分叉图、Ca2+振荡与IP3振荡的一致性、钙通道数目N对Ca2+振荡的影响等。这些模型结果显示了Ca2+振荡的特性。

芪苈强心胶囊对心肌梗死大鼠心脏IP3Rs/GRP75/VDAC1基因调控的机制研究

目的:探讨芪苈强心胶囊对心肌梗死大鼠线粒体Ca^(2+)转运相关基因的调控作用。方法:采用冠状动脉左前降支结扎术建立心肌梗死大鼠模型。术后随机将动物分到模型组、芪苈强心组和卡托普利组;同时设有假手术组作为对照。治疗四周后,通过心脏大体结构观察大鼠心脏梗死范围,HE染色观察大鼠心肌组织病理形态变化;实时荧光(Real⁃Time)PCR检测大鼠心脏梗死边缘区线粒体Ca^(2+)转运相关基因三磷酸肌醇受体2(IP3R2),葡萄糖调节蛋白75(GRP75),电压依赖性阴离子通道1(VDAC1),线粒体融合蛋白2(Mfn2),以及线粒体凋亡相关基因B淋巴细胞瘤⁃2(Bcl⁃2),Bcl⁃2相关X蛋白(Bax)mRNA表达变化;Western blot检测心肌组织Bcl⁃2,Bax蛋白表达变化;TUNEL染色检测心肌组织细胞凋亡率。结果:与假手术组相比,模型组大鼠心脏左室前壁呈现大面积梗死区域,心肌组织结构紊乱;线粒体Ca^(2+)转运相关基因IP3R2,GRP75,VDAC1,Mfn2 mRNA表达显著升高(P<0.05,P<0.01);线粒体凋亡相关分子Bcl⁃2 mRNA和蛋白表达均明显下降(P<0.01),Bax mRNA和蛋白表达均显著升高(P<0.01),心肌细胞凋亡率显著增加(P<0.01)。与模型组相比,芪苈强心组和卡托普利组心脏大体标本的梗死范围缩小,心肌纤维排列相对规整;线粒体Ca^(2+)转运相关基因IP3R2,GRP75,VDAC1,Mfn2 mRNA表达显著降低(P<0.01);线粒体凋亡相关分子Bcl⁃2 mRNA和蛋白表达有所提高(P<0.05,P<0.01),Bax mRNA和蛋白表达显著降低(P<0.05,P<0.01),心肌细胞凋亡率明显下降(P<0.01)。结论:芪苈强心胶囊能够改善心肌梗死大鼠心脏形态结构,其作用机制与调节线粒体Ca^(2+)转运复合体IP3R2/GRP75/VDAC1基因表达,进而抑制细胞凋亡有关。

钙库操纵的Ca^(2+)内流在神经退行性疾病中的研究进展

Ca^(2+)作为重要的第二信使,在分化、增殖、生长、生存、凋亡、基因转录和膜兴奋性等方面起到至关重要的作用[1]。细胞内Ca^(2+)浓度升高通过细胞外流入和细胞内存储释放两种方式。细胞外Ca^(2+)流入主要是由电压依赖的Ca^(2+)通道(voltage-gated Ca^(2+)channels,VGCCs)或受体作用的通道(receptor-operated Ca^(2+)channels,ROCs)等介导的,如谷氨酸敏感的N-甲基-D天冬氨酸受体(N-methyl-D-aspartic acid receptor,NMDARs)等[2];细胞内存储释放最常见的Ca^(2+)信号产生途径是细胞表面受体的激活,从而产生第二信使肌醇1,4,5-三磷酸(inositol 1,4,5-triphosphate,IP3),内质网上IP3受体(inositol 1,4,5-triphosphate receptors,IP3Rs)被激活后向胞浆释放Ca^(2+)[3]。

动物受精过程中卵子Ca^(2+)释放机制

Ca2+是动物受精过程中卵内重要的第二信使,它对于皮质颗粒的排放、减数分裂的恢复、原核形成等过程具有重要的作用,受精过程中Ca2+的释放机制研究是当今受精生物学研究的热点之一,已有的研究结果表明动物卵子在受精过程中有三种Ca2+释放机制:由1,4,5,三磷酸肌醇引发内质网中储存的Ca2+释放、由环腺苷酸二核苷酸磷核糖引发与其相关联的钙库Ca2+释放和烟酸腺嘌呤二核苷酸磷酸引发的与其相关联的钙库Ca2+释放.

心肌细胞核Ca^(2+)库特点及其调节的离体研究

研究核外Ca^(2+)浓度对核Ca^(2+)的影响,及细胞核Ca^(2+)摄取和释放的关系,以探讨核Ca^(2+)转运的调节机制。采用差速离心和密度梯度离心法分离纯化心肌细胞核,以Fluo-4/AM荧光指示剂负载心肌细胞核,应用激光共聚焦扫描显微镜和荧光分光光度计进行观察和测定。结果显示,分离纯化的成年大鼠心肌细胞核内自由[Ca^(2+)]随着核外[Ca^(2+)]的增加而逐渐增加,孵育液[Ca^(2+)]为1000 nmol/L达高峰,但二者增加的程度并不一致,之后随核外[Ca^(2+)]浓度的增加而呈降低趋势。ATP和100—600nmol/L的核外游离Ca^(2+),使心肌细胞核显示核被膜腔Ca^(2+)荧光,ATP和1000nmol/L的核外游离Ca^(2+)则进一步引起核浆内的Ca^(2+)荧光强度升高。荧光染色观察可见IP_3受体染色主要位于核内膜,而钙泵和ryanodine受体染色主要位于核外膜。IP_3和Ryancodine使核Ca^(2+)短暂升高1.68倍和1.93倍(P<0.001),而钙泵抑制剂Thapsigargin和IP_3受体抑制剂Heparin则分别使核Ca^(2+)降低64%和35.6%(p<0.05)。ryanodine使IP_3升高的核Ca^(2+)显著回落至正常水平以下(p<0.001)。Thapsigargin不能阻断IP_3和Ryanodine所致的核Ca^(2+)释放增加(p<0.05),但事先采用钙泵抑制剂Thapsigargin预处理心肌细胞核,则能显著的阻断IP_3和Ryanodine所致的核Ca^(2+)升高作用(Ca^(2+)释放作用)(p<0.05)。结果提示大鼠心肌细胞核可能也是细胞内的钙库之一,心肌细胞核上存在Ca^(2+)-ATPase、ryanodine受体和IP_3受体等Ca^(2+)转运系统,可能参与核Ca^(2+)摄取和释放的调节。

bFGF对人晶状体上皮细胞系内钙离子及IP3R、RyR的作用

目的:探讨碱性成纤维细胞生长因子(bFGF)对人晶状体上皮细胞系LEC-B3内静息Ca2+浓度及三磷酸肌醇受体(IP3R)、ryanodine受体(RyR)表达的影响。方法:LEC-B3细胞系传代培养,分别以1,10,100μg/L bFGF诱导第3代细胞的增殖,MTT法检测其增殖度,激光扫描共聚焦显微镜测细胞内静息钙浓度;RT-PCR(reverse-transcriptase,PCR)方法检测10μg/L bFGF作用后细胞内IP3R和RyRmRNA的表达。结果:与对照组相比,3个浓度的bFGF对LEC-B3都有促增殖作用(P<0.01),其中10μg/L作用最强;bFGF作用后细胞内Ca2+浓度呈bFGF浓度依赖性增高,10μg/L,100μg/LP<0.01,1μg/L<0.05;10μg/L bFGF作用后的细胞IP3RI mRNA表达无明显变化,III型表达明显减弱(P<0.01),ryan-odineRI,IIImRNA表达升高(P<0.05,0.01)。结论:bFGF诱导LEC-B3细胞增殖引起细胞内钙离子浓度增加。Ca2+升高呈bFGF浓度依赖性,并不与细胞增殖度平行。bFGF对IP3R和RyR亚型的mRNA表达有一定影响,并且细胞内Ca2+浓度升高与bFGF刺激RyRmRNA表达升高有关。

阿尔茨海默病与内质网Ca^2+紊乱的研究进展

阿尔茨海默病(Alzheimer’s disease,AD)是一种以学习记忆能力障碍为主要表现的渐进性神经系统退行性疾病,主要累及患者的海马体和大脑皮质区。AD的主要病理特点是该病患者脑内普遍的神经元凋亡、大脑皮质内出现神经原纤维缠结(neurofibrillary tangles,NFTs)和老年斑(senile plaque,SP)。据报道,世界上每3 s就会出现一个该病患者[1],然而令人惋惜的是至今尚无有效缓解和完全治愈的药物问世。其发病机制复杂,目前为大多数学者所认可的假说主要有:遗传学因素、Aβ学说、兴奋性氨基酸毒性作用、钙离子(Ca^2+)稳态失调、胰岛素相关代谢异常、中枢胆碱能系统受损、微管相关蛋白异常学说、自由基与氧化应激、炎症与免疫机制等,其中Ca^2+失调假说受到广泛关注,该假说提出在AD发病早期Ca^2+失调使得细胞信号通道异常进而造成细胞功能瘫痪,导致突触传递功能障碍和神经元受损。本文将对这一假说延伸的新型预防或治疗性药物的机制及其临床指导价值做一综述。

Primary evidence for involvement of IP_(3) in heat-shock signal transduction in Arabidopsis

The role of inositol 1,4,5-trisphosphate （IP3） in transducing heat-shock （HS） signals was examined in Arabidopsis. The whole-plant IP3 level increased within 1 min of HS at 37℃. After 3 min of HS, the IP3 level reached a maximum 2.5 fold increase. Using the transgenic Arabidopsis plants that have AtHsp 18.2 promoter-β-glucuronidase （GUS） fusion gene, it was found that the level of GUS activity was up-regulated by the addition of caged IP3 at both non-HS and HS temperatures and was down-regulated by the phospholipase C （PLC） inhibitors {1-[6-（（ 1713-3-Methoxyestra-1,3,5（10）-trien- 7-yl）amino）hexyl]-2,5-pyrrolidinedione } （U-73122）. The intracellular-free calcium ion concentration （[Ca^2＋]i） increased during HS at 37℃ in suspension-cultured Arabidopsis cells expressing apoaequorin. Treatment with U-73122 prevented the increase of [Ca^2＋]i to some extent. Above results provided primary evidence for the possible involvement of IP3 in HS signal transduction in higher plants.

p53 siRNA promotes autophagy of U2OS cells through its target gene Rap2B

The present study aims to explore the effects of p53 and its target gene Rap2B on the autophagy of U2OS cells.U2OS cells were treated with siRNA against p53,Rap2B,and PLCε.Relative expressions of p53,Rap2B,and PLCεwere determined using quantitative polymerase chain reaction(qPCR)and Western blotting,respectively.Levels of IP3 in the cells were determined using Enzyme-linked Immunosorbent Assay(ELISA).Levels of Ca^(2+) were detected using Flow cytometry.Fluorescence microscopy was used to observe the autophagy of cells.Knockdown of p53 significantly decreased the expressions of Rap2B protein.Additionally,knockdown of p53 significantly decreased the mRNA levels of PLCε.The knockdown of p53,Rap2B,and PLCεsignificantly decreased the levels of intracellular IP3 and Ca^(2+) and promoted autophagy of U2OS cells.Our results demonstrated that p53-Rap2B-PLCε-IP3 signaling pathway regulated autophagy of U2OS cells.

Inositol 1,4,5-trisphosphate 3-kinases:functions and regulations

Inositol 1,4,5-trisphosphate 3-kinase (IP3 3-kinase/IP3K) plays an important role in signal transduction in animal cellsby phosphorylating inositol 1,4,5-trisphosphate (IP3) to inositol 1,3,4,5-tetrakisphosphate (IP4). Both IP3 and IP4 arecritical second messengers which regulate calcium (Ca2+) homeostasis. Mammalian IP3Ks are involved in many biologicalprocesses, including brain development, memory, learning and so on. It is widely reported that Ca2+ is a canonicalsecond messenger in higher plants. Therefore, plant IP3K should also play a crucial role in plant development. Recently,we reported the identification of plant IP3K gene (AtIpk2β/AtIP3K) from Arabidopsis thaliana and its characterization.Here, we summarize the molecular cloning, biochemical properties and biological functions of IP3Ks from animal, yeastand plant. This review also discusses potential functions of IP3Ks in signaling crosstalk, inositol phosphate metabolism,gene transcriptional control and so on.

铅对小鼠学习记忆及脑海马细胞内钙库释放的影响

目的探讨铅对小鼠学习记忆和海马细胞内钙库Ca2+释放的影响。方法用水迷宫实验测定小鼠的空间学习记忆能力;采用低浓度胰蛋白酶消化法分离小鼠海马细胞,用IP3敏感钙库和IP3非敏感钙库的特异性拮抗剂肝素和普鲁卡因刺激海马细胞,以弗拉吐(Fura2)作Ca2+荧光探针测定铅对海马细胞[Ca2+]i的影响。结果在水迷宫实验中,结果表明慢性铅暴露可明显损伤仔鼠的空间定位航行能力,损伤程度与饮用铅的浓度成正相关。与对照组比较,25μmol·L-1铅可致分离的小鼠海马细胞在胞外无钙静息状态下[Ca2+]i显著性增高(P<0.05);而30μg·ml-1的三磷酸肌醇(IP3)敏感钙库特异性拮抗剂Heparin和0.1mg·ml-1的非IP3敏感钙库的特异性拮抗剂procaine可拮抗铅引起的海马细胞[Ca2+]i增高。结论慢性铅暴露可致小鼠空间学习记忆能力下降;高水平的铅可促进小鼠海马细胞内IP3敏感和非IP3敏感的两种内质网钙库释放,致海马细胞在胞外无钙静息状态下[Ca2+]i升高。

气孔保卫细胞信号转导中的第二信使

介绍了保卫细胞信号转导中第二信使的种类、特征、调控机制以及第二信使之间的相互作用 ,特别是钙信使和质子信使之间的相互关系。

心房颤动时心房肌细胞T型钙通道对肌浆网RyR、IP_3R表达及功能的影响

目的 探讨房颤时心房肌细胞膜上T型Ca2 + 通道对肌浆网上IP3 R和RyR表达及功能的影响。方法 杂种犬 15条 ,随机分为正常对照组、单纯房颤组和房颤 +Mibefradil组。房颤组用起搏器进行右心房快速起搏(5 2 0 /min)。房颤 +Mibefradil组在起搏术后第 2天开始给mibefradil。正常对照组不植入起搏器。胶原酶Ⅱ型分离心房肌细胞 ,用激光共聚焦显微镜检测T型Ca2 + 通道阻滞剂对肌浆网上三磷酸肌醇受体 (IP3 R)和兰尼碱受体(RyR)表达及功能的影响。结果 房颤 +Mibefradil组的RyR/IP3 比值 (0 2 96 5± 0 0 812 )比正常对照组 (2 70 4 3±0 2 2 93)明显减少 (P <0 0 5 ) ,而与单纯房颤组 (0 2 4 72± 0 135 5 )比较无统计学意义 ;房颤 +Mibefradil组的心房肌细胞在给予caffeine刺激时细胞内Ca2 + 浓度增高不明显 (1 30 31± 0 10 5 6 ) ,与正常对照组 (1 74 10± 0 15 6 6 )比较有统计学意义 (P <0 0 5 ) ,而与单纯房颤组 (1 2 5 6 1± 0 0 6 4 6 )比较无统计意义 ;房颤 +Mibefradil组的心房肌细胞在给予ATP刺激时细胞内Ca2 + 浓度增高不明显 (1 186 6± 0 6 6 91) ,与正常对照组 (1 2 319± 0 2 2 73)比较无统计学意义 ,而比单纯房颤组 (2 2 90 4± 0 6 4 71)明显减少 (P <0 0 5 )。

经络实质辨析——关于经络本质与生物学基础的研究

本文是对作者近年关于经络本质研究工作的小结。作者首先对十余年来我国经络本质研究方面的工作进行了简略的回顾和评价,突出强调了:经络本质的研究,重点应当放在对调控人体经络生理网络的信息载体(messenger)的研究上。作者应用细胞信号转导的理论和相关实验数椐指出:当针刺穴位时,细胞产生Ca2+振荡(-在胞内)和Ca2+波(-在胞间),其幅频信号中可能蕴含有相关经络通路和生理功能调节信息;Ca2+通过与其结合的蛋白(如钙调素CaM等)参与了人体从受精、代谢、肌缩运动,直至认知、记忆等几乎所有生命过程。因此,作者猜想钙离子(Ca2+)以及配合针刺实现在细胞间Ca2+波接力传递的三磷酸肌醇(IP3)可能便是人们长期探寻的调控人体经络网络的信息载体,它们联同在经线上的细胞缝隙连接蛋白(connexon)熏构成了经络的物质基础。作者最后指出了今后进一步研究的途径和实验方法。

探索经络本质的新途径

作者首先对近20年来我国在经络本质方面的研究工作进行了回顾与评价。指出若长期在宏观(组织解剖学)层面上难以找到经络的物质存在,应努力在多层面、多学科交叉领域系统开展研究;特别是在微观层面,只有充分借助细胞分子生物学、基因组学、生物物理学、生物化学的理论和实验成果,构筑研究平台,方能有所创新和突破。作者强调经络本质的研究重点应放在对调控人体经络生理网络的信息载体上,并且根椐细胞信号转导的理论和相关实验数据指出,当针刺穴位时,细胞所产生的Ca2+振荡(在胞内)和Ca2+波(在胞间)的幅频信号中可能蕴含有经络通路和生理功能调节信息;Ca2+通过与其结合的蛋白(如钙调素CaM等)参与了人体从生殖、代谢、肌缩运动,直至认知、记忆的几乎所有生命过程。因此,作者认为Ca2+以及配合针刺实现在细胞间Ca2+波接力传递的三磷酸肌醇(IP3),可能就是人们长期探寻的调控人体经络网络的信息载体,它们联同在经线上的细胞缝隙连接蛋白,构成了经络的物质基础。作者最后指出了进一步研究的途径和实验方法。