Alkaline sphingomyelinase deficiency impairs intestinal mucosal barrier integrity and reduces antioxidant capacity in dextran sulfate sodium-induced colitis

BACKGROUND Ulcerative colitis is a chronic inflammatory disease of the colon with an unknown etiology.Alkaline sphingomyelinase(alk-SMase)is specifically expressed by intestinal epithelial cells,and has been reported to play an anti-inflammatory role.However,the underlying mechanism is still unclear.AIM To explore the mechanism of alk-SMase anti-inflammatory effects on intestinal barrier function and oxidative stress in dextran sulfate sodium(DSS)-induced colitis.METHODS Mice were administered 3%DSS drinking water,and disease activity index was determined to evaluate the status of colitis.Intestinal permeability was evaluated by gavage administration of fluorescein isothiocyanate dextran,and bacterial translocation was evaluated by measuring serum lipopolysaccharide.Intestinal epithelial cell ultrastructure was observed by electron microscopy.Western blotting and quantitative real-time reverse transcription-polymerase chain reaction were used to detect the expression of intestinal barrier proteins and mRNA,respectively.Serum oxidant and antioxidant marker levels were analyzed using commercial kits to assess oxidative stress levels.RESULTS Compared to wild-type(WT)mice,inflammation and intestinal permeability in alk-SMase knockout(KO)mice were more severe beginning 4 d after DSS induction.The mRNA and protein levels of intestinal barrier proteins,including zonula occludens-1,occludin,claudin-3,claudin-5,claudin-8,mucin 2,and secretory immunoglobulin A,were significantly reduced on 4 d after DSS treatment.Ultrastructural observations revealed progressive damage to the tight junctions of intestinal epithelial cells.Furthermore,by day 4,mitochondria appeared swollen and degenerated.Additionally,compared to WT mice,serum malondialdehyde levels in KO mice were higher,and the antioxidant capacity was significantly lower.The expression of the transcription factor nuclear factor erythroid 2-related factor 2(Nrf2)in the colonic mucosal tissue of KO mice was significantly decreased after DSS treatment.mRNA levels of Nrf2-regulated downstream antioxidant enzymes were also decreased.Finally,colitis in KO mice could be effectively relieved by the injection of tertiary butylhydroquinone,which is an Nrf2 activator.CONCLUSION Alk-SMase regulates the stability of the intestinal mucosal barrier and enhances antioxidant activity through the Nrf2 signaling pathway.

Interplay between intestinal alkaline phosphatase, diet, gut microbes and immunity

Intestinal alkaline phosphatase (IAP) plays an essential role in intestinal homeostasis and health through interactions with the resident microbiota, diet and the gut. IAP’s role in the intestine is to dephosphorylate toxic microbial ligands such as lipopolysaccharides, unmethylated cytosine-guanosine dinucleotides and flagellin as well as extracellular nucleotides such as uridine diphosphate. IAP’s ability to detoxify these ligands is essential in protecting the host from sepsis during acute inflammation and chronic inflammatory conditions such as inflammatory bowel disease. Also important in these complications is IAP’s ability to regulate the microbial ecosystem by forming a complex relationship between microbiota, diet and the intestinal mucosal surface. Evidence reveals that diet alters IAP expression and activity and this in turn can influence the gut microbiota and homeostasis. IAP’s ability to maintain a healthy gastrointestinal tract has accelerated research on its potential use as a therapeutic agent against a multitude of diseases. Exogenous IAP has been shown to have beneficial effects when administered during ulcerative colitis, coronary bypass surgery and sepsis. There are currently a handful of human clinical trials underway investigating the effects of exogenous IAP during sepsis, rheumatoid arthritis and heart surgery. In light of these findings IAP has been marked as a novel agent to help treat a variety of other inflammatory and infectious diseases. The purpose of this review is to highlight the essential characteristics of IAP in protection and maintenance of intestinal homeostasis while addressing the intricate interplay between IAP, diet, microbiota and the intestinal epithelium.

Intestinal alkaline phosphatase in the colonic mucosa of children with inflammatory bowel disease

AIM： To investigate intestinal alkaline phosphatase （iAP） in the intestinal mucosa of children with inflammatory bowel disease （IBD）. METHODS： Colonic biopsy samples were taken from 15 newly diagnosed IBD patients and from 10 healthy controls. In IBD patients, specimens were obtainedboth from inflamed and non-inflamed areas. The lAP mRNA and protein expression was determined by reverse transcription-polymerase chain reaction and Western blotting analysis, respectively. Tissue localiza- tion of lAP and Toll-like receptor （TLR） 4 was investi- gated by immunofluorescent staining. RESULTS： The lAP protein level in the inflamed muco- sa of children with Crohn＇s disease （CD） and ulcerative colitis （UC） was significantly decreased when compared with controls （both P 〈 0.05）. Similarly, we found a significantly decreased level of lAP protein in the in- flamed mucosa in CD compared with non-inflamed mucosa in CD （P 〈 0.05）. In addition, the iAP protein level in inflamed colonic mucosa in patients with UC was decreased compared with non-inflamed mucosa in patients with CD （P 〈 0.05）. lAP protein levels in the non-inflamed mucosa of patients with CD were similar to controls, lAP mRNA expression in inflamed colonic mucosa of children with CD and UC was not significant- ly different from that in non-inflamed colonic mucosa with CD. Expression of lAP mRNA in patients with non- inflamed mucosa and in controls were similar. Co-local- ization of lAP with TLR4 showed intense staining with a dotted-like pattern, lAP was present in the inflamed and non-inflamed mucosa of patients with CD, UC, and in control biopsy specimens, irrespective of whether it was present in the terminal ileum or in the colon. However, the fluorescent signal of TLR4 was more pro- nounced in the colon compared with the terminal ileum in all groups studied. CONCLUSION： Lower than normal lAP protein levels in inflamed mucosa of IBD patients may indicate a role for lAP in inflammatory lesions in IBD. Based on our results, administration of exogenous lAP enzyme to pa- tients with the active form of IBD may be a therapeutic option.

EFFECTSOFVASOACTIVEINTESTINALPEPTIDEONACTIVITIESOFSUCCINICDEHYDROGENASEANDALKALINEPHOSPHATASEINRATHEPATOMACELLS

Using cytochemical method,microspectrophotometry and image analysis,effects of va-soactive intestinal peptide(VIP)on activities of succinic dehydrogenase(SDH)and alkalinephosphatase(ALP)in rat hepatoma cells were studied in vitro.The results showed that thehepatoma cell expressed potent positive reactions of SDH and ALP,the positive positionswere located at the cell membranes and/or cytoplasm.Having been treated with VIP,ALPdecreased obviously in activity(P【0. 01,compared with hepatoma cells untreated by VIP).The sites of ALP activty were chiefly located at the cell membranes,particularly at the cell-cell contacts.Cultured rat hepatoma cells had intensive SDH activity in their cytoplasm.Compared with untreated eclls,there was no marked difference in the intensity of SDH activ-ity in VIP-treated hepatoma cells(P】0.05).

Development of a Detection Method for Assaying Calf Intestine Alkaline Phosphatase Activity

[ Objective] This study was to develop a detection method for assaying calf intestine alkaline phasphatase activity in scientific research. [ Method ] By simulating the conditions and buffers for assaying calf intestine alkaline phosphatase used in the scientific research, the parameters influencing substmte concentration, reaction duration, eoloration time and buffer pH were optimized. [ Result] The activity of alkaline phosphatase detected varied hugely among different buffers, and potassium ferricyanide solution added with boracic acid achieved the stable coloration. The optimal water bath time was determined as 10 rain, and the substrate concentration was optimized as 0.04 moL/L. The increasing temperature did not have a large influence on low temperature enzymatic activity while did on high coneentration enzymatic activity. When the buffer pH was 7.0 - 8.0, the detection stability of alkaline phosphatase could be maintained well The ion intensity of buff- er had little effects on alkaline phasphatase activity. [ Conclusion] A detection method for assaying calf intestine alkaline phosphatase activity in scientific research was successfully developed in this study.

血清肠脂肪酸结合蛋白、碱性磷酸酶、D-二聚体在肠梗阻患者中的表达变化及临床价值研究

目的:探讨血清肠脂肪酸结合蛋白(IFABP)、碱性磷酸酶(ALP)、D-二聚体(D-D)在肠梗阻患者中表达变化及临床价值。方法:选取肠梗阻患者201例,根据是否行手术治疗分为手术组(105例)和保守治疗组(96例)。根据肠道血运情况将手术组分为单纯性肠梗阻组(46例)、无肠壁坏死组(34例)和肠壁坏死组(25例)。另选同期体检健康者40例为健康对照组。比较肠梗阻患者与健康对照组及不同肠道血运患者血清IFABP、ALP、D-D水平。分析绞窄性肠梗阻患者血清IFABP、ALP、D-D间的相关性。绘制受试者工作特征(ROC)曲线,分析血清IFABP、ALP、D-D水平对绞窄性肠梗阻的诊断价值。结果:手术组患者血清IFABP、ALP、D-D水平高于保守治疗组和健康对照组(均P<0.05)。保守治疗组血清IFABP水平高于健康对照组(P<0.05)。肠壁坏死组血清IFABP、ALP、D-D水平高于无肠壁坏死组及单纯性肠梗阻组,且无肠壁坏死组高于单纯性肠梗阻组(均P<0.05)。血清IFABP、ALP、D-D三者间均呈正相关(均P<0.05)。血清IFABP、ALP、D-D水平对绞窄性肠梗阻均有诊断价值,且三者联合检测的诊断价值更高。结论:肠梗阻患者血清IFABP、ALP、D-D水平升高,且与肠绞窄严重程度有关,三者联合检测对绞窄性肠梗阻均具有较高的诊断价值。

炎症相关指标对儿童炎症性肠病的诊断价值及列线图预测模型构建

目的分析炎症相关性指标对儿童炎症性肠病(inflammatory bowel disease,IBD)的诊断价值并构建IBD列线图预测模型。方法选择2020年1月至2023年8月无锡市儿童医院消化内科的炎症性肠病和非炎症性肠病的患儿。比较两组患儿的一般临床资料,采用相关性分析各指标与儿童发生炎症性肠病的关联性。受试者工作特征曲线(receiver operating characteristic curve,ROC)分析单个指标和联合指标的诊断价值。通过Lasso和逐步回归法筛选出最终变量,并构建列线图预测模型。结果本研究共纳入387例样本,其中炎症性肠病组163例,非炎症性肠病组224例。组间比较结果显示两组患者的家族史、肠道碱性磷酸酶(intestinal alkaline phosphatase,IAP)、中性粒细胞计数、C反应蛋白(C-reactive protein,CRP)、红细胞沉降率、中性粒细胞与淋巴细胞比值(neutrophil-lymphocyte count ratio,NLR)、血小板与淋巴细胞比值(platelet to lymphocyte ratio,PLR)、血小板与白蛋白比值(platelet to albumin ratio,PAR)、系统性免疫炎症指数(systemic immune-inflammation index,SII)、淋巴细胞计数、血小板计数、白蛋白比较差异均有统计学意义(P<0.05)。相关性分析结果表明家族史(r=0.199,P<0.001)、中性粒细胞计数(r=0.915,P<0.001)、红细胞沉降率(r=0.608,P<0.001)、SII(r=0.464,P<0.001)、碱性磷酸酶(r=0.491,P<0.001)、C反应蛋白(r=0.423,P<0.001)、NLR(r=0.480,P<0.001)、PLR(r=0.353,P<0.001)、PAR(r=0.371,P<0.001)与炎症性肠病的发生呈正相关;淋巴细胞计数(r=-0.711,P<0.001)、血小板计数(r=-0.136,P=0.007)、白蛋白(r=-0.638,P<0.001)与炎症性肠病的发生呈负相关(P均<0.05)。进一步ROC分析结果显示,肠道碱性磷酸酶(AUC=0.741,95%CI 0.689~0.793),C反应蛋白(AUC=0.747,95%CI 0.690~0.804),NLR(AUC=0.781,95%CI 0.734~0.828),PLR(AUC=0.706,95%CI 0.653~0.759),PAR(AUC=0.717,95%CI 0.666~0.768),SII(AUC=0.756,95%CI 0.706~0.806)具有一定的诊断价值,各指标联合明显提高对于IBD的诊断效能(AUC=0.964,95%CI 0.946~0.982)。通过碱性磷酸酶、C反应蛋白、NLR、PAR、SII、家族史、红细胞沉降率、白蛋白变量建立IBD列线图预测模型,结果显示模型C-index为0.988,提示模型具有较好的区分度,Bootstrap抽样内验证表明模型具有较高的一致性,进一步临床决策曲线分析表明该模型具有显著的临床净收益。结论基于肠道碱性磷酸酶、C反应蛋白、NLR、PLR、PAR、SII的炎症相关指标对儿童炎症性肠病具有一定的诊断价值,各指标联合诊断价值更高。本研究构建的儿童炎症性肠病的Nomogram预测模型具有一定的临床应用价值,有利于疾病的早期筛查诊断,为临床必要的干预提供指导。

胰岛素和酶解配方奶粉对初生仔猪小肠生长发育的影响

为研究胰岛素和酶（胰蛋白酶和糜蛋白酶）解配方奶粉是否促进初生仔猪小肠的组织生长和功能成熟，本试验比较了饲喂配方奶粉与饲喂配方奶粉补加胰岛素（６０ｍ Ｉ Ｕ／ｍ ｌ）或酶解配方奶粉３ｄ 后仔猪小肠的重量和长度，组织形态学结构，粘膜 Ｄ Ｎ Ａ、 Ｒ Ｎ Ａ 和蛋白质含量，及小肠内容物中乳糖酶、麦芽糖酶和碱性磷酸酶活性。饲喂配方奶粉补加胰岛素或酶解配方奶粉的仔猪，与饲喂配方奶粉的仔猪相比，小肠的重量、长度、组织形态学结构及粘膜 Ｄ Ｎ Ａ 和 Ｒ Ｎ Ａ 含量均无显著变化（ Ｐ＞ ００５）。但饲喂配方奶粉补加胰岛素的仔猪小肠粘膜尤其是回肠后段粘膜的重量和蛋白质含量显著高于饲喂配方奶粉的仔猪（ Ｐ＜ ００５ 或 Ｐ＜ ００１）。与仅喂配方奶粉的仔猪相比，饲喂配方奶粉补加胰岛素的仔猪小肠内容物中乳糖酶、麦芽糖酶和碱性磷酸酶总活性显著升高；饲喂酶解配方奶粉的仔猪小肠内容物中乳糖酶和碱性磷酸酶总活性显著升高（ Ｐ＜ ００１）。结果表明，口饲胰岛素刺激小肠粘膜尤其是回肠后段粘膜重量和蛋白质含量的增加及小肠内容物中乳糖酶、麦芽糖酶和碱性磷酸酶总活性的升高；酶解配方奶粉中含有能刺激初生仔猪小肠发育的活性物质。

盐碱环境下青海湖裸鲤肠道HCO3-分泌相关基因表达差异

以青海湖裸鲤(Gymnocypris przewalskii)为研究对象,采用半定量和定量PCR法研究HCO-3分泌相关基因SLC4(solute carrier family 4)和SLC26(solute carrier family 26)家族slc4a1、slc4a2、slc4a4和slc26a6基因组织分布情况,并对不同盐碱环境下肠道中SLC基因家族的表达情况进行定量分析,揭示青海湖裸鲤适应盐碱环境的肠道调节机制。结果表明,slc4a1、slc4a2、slc4a4和slc26a6基因在青海湖祼鲤鳃、肝脏、肾脏和肠道等多个组织中均有表达,且在肠道中的表达量较高,其中slc26a6在肠道中高表达,而在鳃中表达量极低,表现出组织特异性;在碱度组[盐度1.31±0.02,碳酸盐碱度(30.66±0.08)mmol·L-1]、盐度组[盐度15.02±0.02,碳酸盐碱度(2.12±0.05)mmol·L-1]和湖水组[盐度14.84±0.03,碳酸盐碱度(29.57±0.11)mmol·L-1]青海湖裸鲤肠slc4a1、slc4a2、slc4a4和slc26a6基因的表达量在胁迫4 d过程中均呈现出先升高后回落的现象,其中湖水组裸鲤肠SLC4、SLC26家族基因表达量上调最为明显,尤其是slc26a6基因表达量最高上升为对照组的4.9倍,同时,湖水组裸鲤直肠排泄HCO-3浓度也最高,说明盐碱环境下青海湖裸鲤通过肠道Cl–/HCO-3交换子(slc4a1、slc4a2、slc26a6)、Na+–HCO-3联合转运子(slc4a4)分泌和排泄机体内积累的碱,这一调节途径有助于青海湖裸鲤补偿因水环境中盐碱度升高而造成的渗透及酸碱失衡。

小鼠成长过程中小肠碱性磷酸酶活性的变化及组织细胞定位

目的:研究小鼠成长过程中小肠碱性磷酸酶(Alkaline phosphatase,AKP)的活性变化及其组织细胞定位。方法:利用比色法对AKP活性进行定量分析;用酶的原位复性电泳分析小肠中AKP的种类和活性变化;用组织化学、电镜细胞化学方法研究酶定位。结果:在小鼠成长过程中,AKP活性呈先上升后下降的趋势,D14活性最强,Da活性最弱;共出现2条AKP同工酶带,各同工酶的活性随小鼠的生长发育发生不同的变化;AKP活性主要出现在小肠上皮细胞的细胞质、细胞膜、微绒毛和微绒毛表面的糖衣上。结论:小肠AKP可能参与某些物质的消化吸收及运输,其活性的变化可能与小肠的机能分化有关。

肠碱性磷酸酶在肠屏障中作用的研究进展

肠碱性磷酸酶(IAP)是一种经糖基磷脂酰肌醇键锚定于肠上皮细胞顶膜上的糖蛋白,在肠黏膜屏障的维护中发挥着重要作用,包括调节十二指肠表面p H值、解除脂多糖(LPS)和游离核苷酸的毒性、抑制肠道炎性反应、调节肠道菌群等。以下就近年来IAP在肠屏障中的作用研究进展作一综述。

饲料中添加水解鱼蛋白对半滑舌鳎稚鱼生长及生理生化指标的影响

试验研究了饲料中添加不同水平(0%、20%、40%和60%)的水解鱼蛋白(Fish potein hdrolysate,FPH)对半滑舌鳎(Cynoglossus semilaevis Günther)稚鱼生长及生理生化指标的影响。28d饲养实验结束后,对试验鱼生长指标、鱼体消化酶活性、碱性磷酸酶(AKP)及肠道发育情况进行分析。结果显示:实验鱼的存活率为64.44%—78.88%,其中20%与40%添加组存活率显著高于其他两组(P<0.05);实验鱼的特定生长率(SGR)随饲料中FPH添加水平升高呈下降趋势,20%添加组特定生长率最高,显著高于其他3组(P<0.05),且60%添加组与对照组(FM)之间无显著差异(P>0.05);各试验组鱼体消化酶(脂肪酶、淀粉酶、胃蛋白酶和胰蛋白酶)的比活力在14d与28d时的强弱关系不一致。鱼体碱性磷酸酶比活力大小依次为:20%组>40%组>对照组>60%组,各组间差异均显著(P<0.05);半滑舌鳎肠道微绒毛长度和黏膜厚度均以20%添加组为最优,显著优于其他3组(P<0.05)。以上结果表明,在实验条件下,饲料中FPH的添加水平为20%时,能提高半滑舌鳎稚鱼的存活率及生长性能,并增强其对营养物质的吸收能力。

番鸭小肠碱性磷酸酶的分离纯化及部分性质研究

分离纯化番鸭小肠中碱性磷酸酶,并对其酶促动力学性质进行研究.结果表明:该酶催化磷酸苯二钠水解反应时最适温度为45℃,最适pH为9.72,米氏常数(Km)为4.76 mmol.L-1.Mg2+对碱性磷酸酶活性有明显激活作用;Cd2+浓度小于0.4 mg.L-1时对碱性磷酸酶有激活作用,而浓度高于0.4 mg.L-1时则有抑制作用;Cu2+对碱性磷酸酶活性有明显抑制作用.

再议肠道屏障功能分子机制的研究进展

肠屏障功能受损与临床多种疾病的发生发展有密切的关系.近几年来国内外对益生菌的研究表明,在发挥其益生作用时,其表面蛋白的黏附结构域起着核心作用.肠上皮细胞间紧密连接蛋白的作用及地位已得到了充分的肯定,肠上皮细胞绒毛刷状缘的碱性磷酸酶(IAP),胞质内蛋白磷酸酶2A(PP2A)的保护作用及肠上皮细胞内淋巴细胞(IEL)免疫调节作用备受关注.此外,小肠干细胞(ISC)所起的作用也备受研究者的重视.

金属离子对牛小肠碱性磷酸酶的影响

经Tris-HCl缓冲液抽提,硫酸铵分级分离沉淀,2次DEAE-32柱层析和SephadexG-150凝胶过滤,从牛小肠中得到碱性磷酸酶(ALP),提纯倍数为50.69倍,比活为48.87U/mg,酶液经十二烷基硫酸钠-聚丙烯酰胺凝胶电泳(SDS-PAGE)检测呈现单一条带。该酶催化底物对硝基苯磷酸二钠(pNPP)水解反应的最适pH值为9.7,最适温度为45℃。研究了多种金属离子对牛小肠碱性磷酸酶活性的影响,结果表明:一价金属离子Na+、K+对酶活力没有影响;不同的二价金属离子对酶的影响不同,过渡态金属离子中,Ni2+、Co2+对酶的活力影响不大,Mg2+、Ca2+、Mn2+对酶有不同程度的激活作用,Zn2+、Cu2+对酶有抑制作用;重金属离子Pb2+、Cd2+对酶的活力起抑制作用。

早期肠内营养对腹部手术后患者T淋巴细胞亚群的影响

腹部手术后早期肠内营养作为一种新的临床营养支持方法,其营养及代谢效果已得到肯定.但是,对机体免疫功能影响如何,目前研究较少.本研究旨在探讨腹部手术后早期肠内营养对机体 T 淋巴细胞免疫功能的影响.

热应激对蛋鸡肠道菌群结构、碱性磷酸酶活性及氨基酸转运载体mRNA表达丰度的影响

【目的】揭示热应激环境下蛋鸡肠道菌群结构、肠黏膜碱性磷酸酶活性和氨基酸转运载体mRNA表达量的变化机理。【方法】试验选择16周龄济宁百日鸡96只,随机分成对照组((24±1)℃;Ⅰ)和热应激((38±1)℃)组,各组设6个重复,每个重复8只,试验持续14 d。采用16S rDNA的PCR-DGGE技术和实时荧光定量PCR等手段,分析热应激2(Ⅱ)、7(Ⅲ)、14 d(Ⅳ)时,对十二指肠、空肠及回肠内容物菌群多样性和肠黏膜碱性磷酸酶活性以及氨基酸转运载体rBAT、y+LAT1、CATl mRNA基因表达的相对丰度变化规律。【结果】热应激7 d开始各肠段菌群多样性较为丰富,热应激7、14 d时空肠和回肠部位敏感乳杆菌(Lactobacillus agilis),回肠部位约氏乳杆菌(Lactobacillus johnsonii)、不可培养细菌(uncultured bacterium)和不可培养的拟杆菌属(uncultured Bacteroidales bacterium)均末检测到;而热应激不同时间段空肠和回肠部位可检测到不可培养细菌、溃疡拟杆菌(Bacteroides helcogenes)、卵形拟杆菌(Bacteroides ovatus)、索氏志贺氏菌(Shigella sonnei);空肠和回肠部位黏膜上皮细胞表面的碱性磷酸酶活性与Ⅰ组比较显著下降(P<0.05);而空肠和回肠Ⅲ组的rBAT、y+LAT1mRNA表达丰度均最低,空肠在各热应激时段表达丰度变化幅度最大(P<0.05),回肠的CAT1mRNA表达丰度在Ⅲ、Ⅳ组与Ⅰ组比较影响更明显(P<0.01)。【结论】热应激对空肠和回肠部位微生物菌群影响较为明显,肠道微生物群落改变可导致肠道的消化吸收功能发生改变。

小鼠成长过程中肾、肝、小肠碱性磷酸酶活性变化及组织细胞定位

利用比色、酶的原位复性电泳、组织化学和电镜酶化学等方法,观察了小鼠出生后的成长过程中肝、肾和小肠内碱性磷酸酶(AKP)的活性变化及组织细胞定位。结果表明,在小鼠成长过程中,3种器官内的AKP活性依次为小肠>肾>肝,小肠和肝AKP活性先上升后下降,肾内酶活性呈上升趋势。AKP活性在小肠主要分布在小肠绒毛上皮细胞的细胞膜、细胞浆、微绒毛和微绒毛表面的糖衣上,在肝主要分布在胆小管,在肾主要分布在皮质肾小管,尤以近曲小管的刷状缘、近曲小管上皮细胞膜和各种管状结构之间的腔隙内分布较多。小鼠成长过程中肝内共出现3条AKP同工酶带,小肠内出现2条,肾内出现3条,各同工酶活性随着小鼠的生长发育发生不同的变化。

人参养荣汤改善老龄鼠小肠粘膜上皮纹状缘吸收功能作用的研究

目的:观察中药人参养荣汤对老龄鼠小肠粘膜纹状缘吸收功能的影响。方法:将ICR系70周龄雌性小鼠分为老龄对照与人参养荣汤用药组,每组20只。灌胃4周,取空肠组织进行碱性磷酸酶(ALP),亮氨酸氨肽酶(LAP),腺苷三磷酸酶(ATPase)染色。利用图象处理系统测量ALP、LAP、ATPase着色面积,计算消化酶活性率。采用冰冻蚀刻法复制微绒毛膜膜内粒子形态。透射电镜下观察二糖类分解酶活性部位的变化。通过计测微绒毛及表面糖衣吸附feritin的个数、微绒毛糖衣层钌红电子染色,观察糖衣吸附功能及荷电位。结果:人参养荣汤用药组可显著提高ALP、LAP,ATPase活性率。结论:人参养荣汤能促进二糖酶合成,并显著提高糖衣吸附蛋白能力和增强糖锁阴性荷电位。

早期断奶对仔猪小肠碱性磷酸酯酶活力的影响

本试验旨在研究早期断奶对仔猪小肠碱性磷酸酯酶(AKP)活力的影响。选取10日龄、体重[(4.48±0.26)kg]相近的"杜×长×大"三元杂交仔猪40头(分别由40头母猪生产),随机分为2组,每组20个重复,每个重复1头仔猪,2组仔猪分别以随母猪哺乳和早期断奶方式饲养。试验期10 d。饲养结束后,屠宰取小肠,测定小肠AKP活力及含量。结果表明:早期断奶显著降低了仔猪各肠段及整个小肠AKP的亲和力、最大酶活力和消化能力(P<0.05),显著降低了空肠细胞内质和细胞顶膜AKP的亲和力和消化能力(P<0.05),显著降低了空肠细胞顶膜AKP的最大酶活力(P<0.05),同时显著降低了空肠组织匀浆、细胞内质和细胞顶膜中分子质量为60 ku的AKP的相对含量(P<0.05)。结果提示,早期断奶可降低小肠AKP活力、亲和力、消化能力及含量。