Jianpi Qingchang decoction regulates intestinal motility of dextran sulfate sodium-induced colitis through reducing autophagy of interstitial cells of Cajal

AIM To investigate the underlying effect of Jianpi Qingchang decoction(JQD) regulating intestinal motility of dextran sulfate sodium(DSS)-induced colitis in mice. METHODS C57BL/6 mice were randomly divided into four groups: the control group, the DSS group, the JQD group, and the 5-aminosalicylic acid group. Except for the control group, colitis was induced in other groups by giving distilled water containing 5% DSS. Seven days after modeling, the mice were administered corresponding drugs intragastrically. The mice were sacrificed on the 15^(th) day. The disease activity index, macroscopic and histopathologic lesions, and ultrastructure of colon interstitial cells of Cajal(ICC) were observed. The levels of tumor necrosis factor-alpha(TNF-α), interleukin(IL)-1β, IL-10 and interferon gamma(IFN-γ), the expression of nuclear factor-kappa B(NF-κB) p65, c-kit, microtubule-associated protein 1 light chain 3(LC3-Ⅱ) and Beclin-l m RNA, and the colonic smooth muscle tension were assessed. RESULTS Acute inflammation occurred in the mice administered DSS. Compared with the control group, the levels of IL-1β, TNF-α, IL-10 and IFN-γ, the expression of LC3-Ⅱ, Beclin-1 and NF-κB p65 m RNA, and the contractile frequency increased(P < 0.05), the expression of c-kit m RNA and the colonic smooth muscle contractile amplitude decreased in the DSS group(P < 0.05). Compared with the DSS group, the levels of IL-10 and IFN-γ, the expression of c-kit m RNA, and the colonic smooth muscle contractile amplitude increased(P < 0.05), the levels of TNF-α and IL-1β, the expression of LC3-Ⅱ, Beclin-1 and NF-κB p65 m RNA, and the contractile frequency decreased in the JQD group(P < 0.05).CONCLUSION JQD can regulate the intestinal motility of DSS-induced colitis in mice through suppressing intestinal inflammatory cascade reaction, reducing autophagy of ICC, and regulating the network path of ICC/smooth muscle cells.

Effects of prostaglandin F_(2α) on small intestinal interstitial cells of Cajal

AIM：To explore the role of prostaglandin F2α（PGF2α） on pacemaker activity in interstitial cells of Cajal（ICC）from mouse small intestine. METHODS：In this study,effects of PGF2αin the cultured ICC cells were investigated with patch clamp technology combined with Ca 2＋ image analysis. RESULTS：Externally applied PGF2α（10μmol/L）produced membrane depolarization in current-clamp mode and increased tonic inward pacemaker currents in voltage-clamp mode.The application of flufenamic acid（a non-selective cation channel inhibitor）or niflumic acid（aCl channel inhibitor）abolished the generation of pacemaker currents but only flufenamic acid inhibited the PGF2α-induced tonic inward currents.In addition,the tonic inward currents induced by PGF2αwere not inhibited by intracellular application of 5’-[-thio]diphosphate trilithium salt.Pretreatment with Ca 2＋ free solution, U-73122,an active phospholipase C inhibitor,and thapsigargin,a Ca 2＋ -ATPase inhibitor in endoplasmic reticulum,abolished the generation of pacemaker currents and suppressed the PGF2α-induced tonic inward currents.However,chelerythrine or calphostin C,protein kinase C inhibitors,did not block the PGF2α-induced effects on pacemaker currents.When recording intracellular Ca 2＋ （[Ca 2＋ ]i）concentration using fluo-3/AM,PGF2α broadly increased the spontaneous[Ca 2＋ ]i oscillations. CONCLUSION：These results suggest that PGF2αcan modulate pacemaker activity of ICC by acting non-selective action channels through phospholipase C-dependent pathway via[Ca2＋]i regulation

Inhibition of pacemaker activity in interstitial cells of Cajal by LPS via NF-κB and MAP kinase

AIM:To investigate lipopolysaccharide(LPS) related signal transduction in interstitial cells of Cajal(ICCs) from mouse small intestine.METHODS:For this study,primary culture of ICCs was prepared from the small intestine of the mouse.LPS was treated to the cells prior to measurement of the membrane currents by using whole-cell patch clamp technique.Immunocytochemistry was used to examine the expression of the proteins in ICCs.RESULTS:LPS suppressed the pacemaker currents of ICCs and this could be blocked by AH6809,a prostaglandin E2-EP2 receptor antagonist or NG-Nitro-Larginine Methyl Ester,an inhibitor of nitric oxide(NO) synthase.Toll-like receptor 4,inducible NO synthase or cyclooxygenase-2 immunoreactivity by specific antibodies was detected on ICCs.Catalase(antioxidant agent) had no action on LPS-induced action in ICCs.LPS actions were blocked by nuclear factor kB(NF-kB) inhibitor,actinomycin D(a gene transcription inhibitor),PD 98059(a p42/44 mitogen-activated protein kinases inhibitor) or SB 203580 [a p38 mitogen-activated protein kinases(MAPK) inhibitor].SB 203580 also blocked the prostaglandin E2-induced action on pacemaker currents in ICCs but not NO.CONCLUSION:LPS inhibit the pacemaker currents in ICCs via prostaglandin E2-and NO-dependent mechanism through toll-like receptor 4 and suggest that MAPK and NF-kB are implicated in these actions.

Disruption of interstitial cells of Cajal networks after massive small bowel resection

AIM: To investigate the disruptions of interstitial cells of Cajal (ICC) in the remaining bowel in rats after massive small bowel resection (mSBR). METHODS: Thirty male Sprague-Dawley rats fitting entry criteria were divided randomly into three experimental groups (n = 10 each): Group A rats underwent bowel transection and re-anastomosis (sham) and tissue samples were harvested at day 7 post-surgery. Group B and C rats underwent 80% small bowel resection with tissue harvested from Group B rats at day 7 post-surgery, and from Group C rats at day 14 postsurgery. The distribution of ICC at the site of the resid-ual small bowel was evaluated by immunohistochemical analysis of small intestine samples. The ultrastructural changes of ICC in the remnant ileum of model rats 7 and 14 d after mSBR were analyzed by transmission electron microscopy. Intracellular recordings of slow wave oscillations were used to evaluate electrical pacemaking. The protein expression of c-kit, ICC phenotypic markers, and membrane-bound stem cell factor (mSCF) in intestinal smooth muscle of each group were detected by Western blotting. RESULTS: After mSBR, immunohistochemical analysis indicated that the number of c-kit-positive cells was dramatically decreased in Group B rats compared with sham tissues. Significant ultrastructural changes in ICC with associated smooth muscle hypertrophy were also observed. Disordered spontaneous rhythmic contractions with reduced amplitude (8.5 ± 1.4 mV vs 24.8 ± 1.3 mV, P = 0.037) and increased slow wave frequency (39.5 ± 2.1 cycles/min vs 33.0 ± 1.3 cycles/min, P = 0.044) were found in the residual intestinal smooth muscle 7 d post mSBR. The contractile function and electrical activity of intestinal circular smooth muscle returned to normal levels at 14 d post mSBR (amplitude, 14.9 ± 1.6 mV vs 24.8 ± 1.3 mV; frequency, 30.7 ± 1.7 cycles/min vs 33.0 ± 1.3 cycles/min). The expression of Mscf and c-kit protein was decreased at 7 d (P = 0.026), but gradually returned to normal levels at 14 d. The ICC and associated neural networks were disrupted, which was associated with the phenotype alterations of ICC. CONCLUSION: Massive small bowel resection in rats triggered damage to ICC networks and decreased the number of ICC leading to disordered intestinal rhythmicity. The mSCF/c-kit signaling pathway plays a role in the regulation and maintenance of ICC phenotypes.

Interstitial cells of Cajal in the gut-A gastroenterologist’s point of view

Alterations of normal function of interstitial cells of Cajal (ICC) are reported in many intestinal disorders. Diagnosis of their involvement is rare (infrequent), but necessary to propose a specifi c treatment. This article reviews the place of ICC in the pathogenesis of achalasia, gastroesophageal reflux disease, infantile hypertrophic pyloric stenosis, chronic intestinal pseudoobstruction and slow transit constipation. Moreover we discuss the role of the Cajal cells in the development of stromal tumors of the gastrointestinal tract.

Comparison of different methods of intestinal obstruction in a rat model

AIM:To investigate different methods of creating incomplete intestinal obstruction in a rat model and to compare their electrophysiologic,morphologic and histologic characteristics. METHODS:Rat ileum was partially obstructed by the respective application of:braided silk(penetrated the mesentery and surrounded intestine);half ligation (penetrated directly and ligated 1/2 cross-section of the intestine);wide pipe(6 mm in width,surrounded the intestine);narrow pipe(2 mm in width,surrounded the intestine).A control was also included(no obstruction). Various behavioral and electrophysiologic variables, as well as morphologic and immunohistochemical observations were recorded by blinded investigators at different time points(12,24,48,72 h),including daily general condition,ileal wet weight and circumference, macromorphous and micromorphous intestine,bowel movement capability in vivo and in vitro,slow wave and neural electrical activity,and the number of c-Kit positive interstitial cells of Cajal(ICC). RESULTS:Despite being of a similar general condition, these methods resulted in different levels of obstruction in each group compared with the control at different time points(12,24,48,72 h).However,these fields of the wide pipe rat showed significantly differences when compared with the other three obstructed groups at 12 to 72 h,including macroscopic and histological presentation,intestinal transit ratio and contractility,circumference and wet weight,amplitude and frequency of nerve electrical discharge and slow wave,and ICC numbers(all P<0.01). CONCLUSION:The wide pipe rat method is significantly more reliable and stable than the other methods of obstruction,demonstrating that use of the wide pipe method can be a useful model of incomplete intestinal obstruction.

New techniques in the tissue diagnosis of gastrointestinal neuromuscular diseases

Gastrointestinal neuromuscular diseases are a clinically heterogeneous group of disorders of children and adults in which symptoms are presumed or proven to arise as a result of neuromuscular (including interstitial cell of Cajal) dysfunction. Common to most of these diseases are symptoms of impaired motor activity which manifest as slowed or obstructed transit with or without evidence of transient or persistent radiological visceral dilatation. A variety of histopathological techniques and allied investigations are being increasingly applied to tissue biopsies from such patients. This review outlines some of the more recent advances in this fi eld, particularly in the most contentious area of small bowel disease manifesting as intestinal pseudo-obstruction.

半夏泻心汤对功能性消化不良大鼠Cajal间质细胞超微结构的影响

目的观察半夏泻心汤对功能性消化不良大鼠Cajal间质细胞超微结构的影响,探讨其可能的作用机制。方法将大鼠随机分成空白对照组、模型组、半夏泻心汤治疗组,采用夹尾刺激法建立功能性消化不良大鼠模型,连续给药15 d后,利用透射电镜观察胃Cajal间质细胞超微结构的变化。结果与对照组比较,模型组大鼠胃Cajal间质细胞的超微结构发生明显改变,线粒体等细胞器明显减少,治疗组Cajal间质细胞的超微结构基本恢复正常,线粒体等细胞器明显增加。结论对Cajal间质细胞超微结构的影响可能是半夏泻心汤治疗功能性消化不良的作用机制之一。

Cajal间质细胞自噬在慢性传输型便秘中的实验研究进展

文章概述Cajal间质细胞（ICC）在慢性传输型便秘中的作用,结合新近相关实验研究,证实ICC过度自噬后的造成的其自身细胞表型的改变、网状结构的破坏及基因表达的减少可造成胃肠动力学紊乱。中医药在基础研究中能在一定程度上改善ICC细胞过度自噬的状态,为临床治疗慢性传输型便秘提供了新思路。

腹部推拿对便秘型肠易激综合征家兔ENS-ICC-SMC结构的影响

目的:验证腹部推拿对肠易激综合征(irritable bowel syndrome,IBS)家兔胃肠动力障碍的调节作用,观察腹部推拿对IBS家兔肠神经细胞、Cajal间质细胞和肠道平滑肌细胞连接结构的影响。方法:将家兔分为空白对照组、模型对照组和腹部推拿组,采用FITC标记微球灌胃,在不同时间点观察胃、小肠、结肠的微球分布情况,免疫荧光染色检测肠组织中C-Kit、nNOS表达情况,电镜观察ENS-ICC-SMC超微结构。结果:空白对照组微球主要分布在小肠,而模型对照组主要分布在胃部,腹部推拿组结肠荧光强度增强;与模型对照组比较,腹部推拿组C-Kit和nNOS表达增加,电镜观察腹部推拿组ENS-ICC-SMC超微结构更接近于空白对照组。结论:腹部推拿对IBS家兔胃肠动力障碍具有调节作用,其作用机制可能与其对肠ENS-ICC-SMC结构的影响有关。

小儿腹泻外敷散对腹泻大鼠小肠Cajal细胞超微结构及血管活性肠肽受体1表达的影响

目的探讨小儿腹泻外敷散对腹泻大鼠小肠Cajal间质细胞(ICC)和血管活性肠肽受体1(VIP-R1)表达的影响。方法 30只Wistar大鼠随机分为对照组、模型组、药物组,每组10只。采用番泻叶水煎液灌胃(2ml/100g)的方法建立腹泻模型,药物组给予小儿腹泻外敷散贴敷。采用透射电镜观察药物对腹泻大鼠小肠ICC超微结构的影响,免疫组化法观察VIP-R1在腹泻大鼠小肠内的分布,RT-PCR和Western blotting测定VIP-R1 m RNA和蛋白表达水平。结果药物贴敷可使ICC形态和缝隙连接基本恢复正常。VIP-R1主要分布在小肠组织环形肌与纵形肌之间、小肠组织肌间神经丛处、结肠黏膜层上皮细胞及固有层细胞的周围。小儿腹泻外敷散可抑制VIP-R1分泌并下调VIP-R1 m RNA及蛋白表达。结论小儿腹泻外敷散可修复腹泻大鼠损伤的ICC细胞,同时可通过下调VIP-R1表达而治疗腹泻。

“双固一通”电针法对糖尿病胃轻瘫大鼠胃电图及胃窦Cajal间质细胞表达的影响

目的:探讨"双固一通"电针法对糖尿病胃轻瘫大鼠胃电图及胃窦Cajal间质细胞的影响。方法:20周龄清洁级SD雄性大鼠30只,随机分为正常组、糖尿病胃轻瘫模型组(简称模型组)、"双固一通"电针组(简称电针组);除正常组大鼠外,一次性腹腔注射链脲佐菌素及高脂饮食不规则喂养,诱导糖尿病胃轻瘫模型。以"双固一通"电针法为治疗手段,采用神经电生理、免疫组化方法检测模型大鼠胃排空、胃电图以及胃窦Cajal间质细胞数量的变化。结果:与正常组大鼠胃电慢波主频率(4.12±1.04)次/min、主功率(53.21±1.71)decibel(dB)比较,模型组大鼠胃电慢波主频率(2.34±0.83)次/min、主功率(35.64±1.74)dB,组间差异显著(P<0.05,P<0.01);电针组胃电慢波主频率(3.42±0.76)次/min、主功率(46.04±2.43)dB,电针组与模型组比较具有统计学意义(P<0.05或P<0.01)。正常组胃排空率(79.6±6.4)%、模型组(50.4±6.9)%,两组比较有显著差异(P<0.05);而电针组胃排空率为(65.5±4.3)%,与模型组比较具有显著差异(P<0.01)。光镜下C-kit阳性表达为肌层之间夹杂的深浅不一的棕黄色,形状为圆形或边缘不规则。正常组C-kit阳性细胞数量较多,模型组相对明显减少,散在分布于肌层之间,与模型组比较,电针组C-kit阳性细胞则增多,且分布较为均匀。正常组大鼠胃窦组织中ICC阳性细胞的灰度值(IOD)为3825.82±376.58、模型组为(2424.07±294.86),两组间比较差异显著(P<0.05);电针组ICC阳性细胞的灰度值(IOD)(3225.37±284.43),与模型组比较差异有统计学意义(P<0.05)。结论:"双固一通"电针法可以提高糖尿病胃轻瘫模型大鼠胃排空率,改善胃电节律紊乱,减少胃窦ICC细胞的丢失。

重型颅脑损伤对小鼠小肠平滑肌自主节律运动和Cajal间质细胞的影响

目的通过观察重型颅脑损伤(severe head injury,SHI)后小鼠离体小肠平滑肌自主节律运动和小肠肠肌丛Cajal间质细胞(interstitial cells of cajal,ICC)数量及功能的变化,探讨重型颅脑损伤后肠动力障碍的可能机制。方法选取36只6～8周龄清洁级健康雄性昆明小鼠,体质量(35±5)g。重型颅脑损伤组(n=18)参照Feeney自由落体法制作小鼠SHI模型,假伤对照组(n=18)只开颅骨不致颅脑伤。于伤后1、3、7 d取材检测离体末端回肠平滑肌肌条运动的模式、幅度、频率及末端回肠ICC数量变化。结果①SHI后平滑肌自主节律运动的幅度1 d[(0.16±0.04)gvs(0.31±0.05)g]、3 d[(0.16±0.04)gvs(0.23±0.06)g]、7 d[(0.22±0.07)gvs(0.27±0.05)g]均显著低于假伤对照组(P<0.05);平滑肌自主节律运动的频率1 d[(30.23±3.71)min-1vs(34.55±1.99)min-1]、7 d[(30.34±4.56)min-1vs(33.10±0.81)min-1]显著低于假伤对照组(P<0.05),2组3 d时差异无统计学意义[(31.46±4.64)min-1vs(33.39±2.17)min-1,P>0.05];肌条运动模式紊乱、不规律。②SHI后各时相点ICC细胞数量较假伤对照组显著减少[1 d:(189±41)/mm2vs(303±10)/mm2;3 d:(156±39)/mm2vs(305±9)/mm2;7 d:(215±28)/mm2vs(325±42)/mm2;P<0.05],网络明显受损变稀薄。结论小鼠SHI后存在严重的小肠ICC受损,平滑肌自主节律运动紊乱,从而导致胃肠动力障碍的发生。

卡巴胆碱对缺血/再灌注损伤肠道Cajal间质细胞的影响

目的:观察缺血/再灌注损伤肠道Cajal间质细胞、炎症因子、氧自由基变化以及拟胆碱药卡巴胆碱对上述指标的影响。方法:成年雄性SD大鼠,随机分为手术对照(S)组、肠缺血再灌注(I/R)组和I/R+卡巴胆碱(I/R+CAR)组。制备肠I/R模型,于夹闭后2.5 h处死动物,取肠袋组织测定TNF-α含量、SOD活性和MDA含量;另取肠组织制作病理切片、进行Cajal间质细胞免疫组化染色。结果:I/R组肠组织中Cajal间质细胞阳性表达量比S组显著降低(P<0.01),I/R+CAR组Cajal间质细胞阳性表达量显著高于I/R组(P<0.01)。I/R组MDA和TNF-α含量较S组显著升高(P<0.01)、SOD活性显著降低(P<0.01)。I/R+CAR组MDA和TNF-α含量与I/R组比较明显减少(P<0.01),SOD活性有所回升(P<0.05)。结论:肠缺血/再灌注损伤时炎症因子及氧自由基增加,导致Cajal间质细胞损伤;卡巴胆碱可通过减少炎症因子释放及氧自由基损伤,减轻Cajal间质细胞的损伤。

胚胎小肠Cajal细胞的发育研究

目的 研究人胚胎小肠Cajal细胞的发育变化规律。方法 采用全层铺片结合切片的免疫细胞化学技术。结果 Cajal细胞呈酪氨酸激酶受体 (Kit)和波形蛋白 (vimentin)免疫反应阳性。在胚胎发育早期 ,Cajal细胞较少 ,为单层 ,稀疏分布于肌间神经丛周围 ,细胞为梭形 ,可见两个短而小的突起 ,未见分支 ;随着胎龄的增加 ,Cajal细胞数量增多 ,胞体增大 ,突起伸长 ,并出现分支。此时 ,肌间神经丛周围的Cajal细胞出现两层 ,其长轴彼此垂直 ,分别平行于环行肌和纵行肌。与此同时环行肌层内亦可见少许Cajal细胞 ;出生前 ,肌间神经丛部位的Cajal细胞接近成熟 ,两层细胞的突起进一步增多、伸长 ,彼此间形成与成人相似的完整的细胞网络。此时深肌丛附近亦可见少量Cajal细胞。结论 人的小肠Cajal细胞发育有一定的时间顺序 ,即肌间神经丛周围最先出现 ,肌内次之 ,深肌丛较晚 ,出生前肌间神经丛周围的Cajal细胞已经接近成熟。这种发育演变若发生异常 ,可能导致某些胃肠动力障碍性疾病。

豚鼠空肠吻合术后ICCs的再生及细胞网络再形成研究

目的 探讨豚鼠空肠壁内ICCs再生及细胞网络重新形成过程。方法 利用手术切断的方法 ,制造ICCs损伤丢失、网络断裂动物模型 ,冰冻切片和全层铺片免疫细胞化学染色观察。结果 术后 3 0～ 5 0d ,断端KIT阳性细胞开始增多 ;术后 70d左右 ,KIT阳性细胞在断端形成以正常肠壁为底面 ,顶端向吻合部位的三角形增生区域 ,在该区域中部KIT阳性细胞的数量较多 ,且排列不规则 ,呈团状 ,突起较短 ,胞浆丰富 ,细胞核较大 ;而靠近三角形底部的KIT阳性细胞逐渐与肌间神经丛周围和深肌丛附近的ICCs相延续。在术后 6个月 ,近端和远端的肠壁已逐渐恢复延续性 ,肠壁各层结构基本正常 ,此时KIT阳性细胞亦趋于恢复正常细胞网络分布模式。结论 当肠壁内ICCs及其网络损伤后 。

新鲜分离小鼠胃Cajal间质细胞样细胞的鉴定及其电生理学特性

将免疫荧光及传统全细胞膜片钳技术应用于新鲜分离的小鼠胃Cajal间质细胞样细胞上,探讨了小鼠胃Cajal间质细胞样细胞形态和电生理学特性。经胶原酶消化得到的Cajal间质细胞样细胞胞体呈短梭形,且自胞体发出多个较短的毛刺状突起。免疫细胞化学结果表明,Cajal间质细胞样细胞胞体和突起酪氨酸激酶受体c-kit表达呈阳性。在传统全细胞记录模式、膜电位钳制在-60mV的条件下,可以记录到自发、节律性内向电流,即起搏电流。钙调蛋白抑制剂W-7(50μmol/L)明显增强了起搏电流幅度并引发明显的内向钳制电流。当电极内液中EGTA的浓度由0.1mmol/L增加到10mmol/L时,也明显增强了起搏电流幅度并引发明显的内向钳制电流。实验结果提示,新鲜分离的小鼠胃Cajal间质细胞样细胞可以产生自发、自律性内向电流,而这种电流对胞内低钙或钙调蛋白抑制剂敏感。这种具有自发性电活动的Cajal间质细胞样细胞可能就是胃Cajal间质细胞。

胃肠道神经-Cajal间质细胞-平滑肌网络研究进展

Cajal间质细胞是胃肠起搏细胞,并具有传导神经递质的作用。近年来的研究表明胃肠神经-ICC-平滑肌网络间存在密切的联系。此文就近期胃肠神经-ICC-平滑肌网络的研究进展作一综述。

双重染色显示Cajal细胞和NOS神经在胎儿小肠肌间神经丛的分布

目的 研究Cajal细胞与NOS神经在胎儿小肠肌间神经丛的分布模式。方法 采用 18～ 2 6周龄胎儿小肠全层铺片和冰冻切片的NADPH 黄递酶 (NADPH d)组织化学法和c kit免疫细胞化学双重染色。结果 胎儿肌间神经丛周围Cajal细胞体为梭形或卵圆形 ,核周胞质较少 ,常见 2～ 3个细长的突起 ,彼此间形成完整的独立细胞网络。NOS阳性神经广泛分布于小肠的肌间神经丛和环肌内 ,其中 ,以肌间神经丛最为丰富 ,构成神经节、节间束及三级神经纤维网的主要神经成分。肌间神经节内的NOS阳性神经元轮廓较清晰 ,多数为DogielⅠ型神经元 ,成簇密集分布 ,每个神经节内含有数个至数 10个NOS阳性神经元。NADPH d和c kit免疫细胞化学双重染色未发现NOS阳性神经和Cajal细胞有共存现象 ,但NOS阳性神经纤维的走行与Cajal细胞及突起间的距离较近。结论 本研究结果提示在胚胎发育中晚期 。

胎儿肠道Cajal间质细胞的发育

目的:研究胎儿肠道Cajal间质细胞(interstitial cells of Cajal,ICC)分布及发育情况. 方法: 搜集中止妊娠3～8 mo胎儿标本12份,采用酪氨酸激酶受体(c-kit)抗体免疫组织化学方法标记胎儿肠道ICC. 结果: ①ICC分布于肠肌间神经丛、纵肌和环肌层面;②不同胎龄胎儿标本,不同层面ICC分布存在差异,随胎龄增加,ICC数目增多;③ICC的呈现按一定时间顺序,肠肌间神经丛,ICC呈现最早,肌内次之,深肌丛较晚;④ICC胞体逐渐增大,足突延长并互相连接,形成细胞间网络结构. 结论: 胎儿肠道ICC主要分布肠肌间神经丛周围,不同胎龄ICC分布及发育存在差异,不同层面ICC分布不同,随着胎龄增加,ICC数目增多,逐渐形成网络结构.