Crypt-JDBC模型:洋葱加密算法的优化改进

CryptDB是一种典型的密文存储技术,它根据运算操作语义使用洋葱加密算法将SQL语句改写到不同的洋葱密文列,从而仅暴露数据的部分属性即可执行查询任务。针对洋葱加密算法的不足之处提出了一种名为Crypt-JDBC的改进模型:(1)鉴于洋葱层数多,且相邻层功能差异大,新模型把洋葱列分为主列与辅助列,并压缩洋葱层的改进方法(主列使用双向算法可还原明文,辅助列使用单向算法提供属性,保证安全性);(2)鉴于等值连接算法复杂低效,新模型通过简化一个关键模块(差异性转换)来降低复杂度;(3)鉴于列名的明文、密文名称对应性弱,新模型重新设计了明密文列名称的对应关系,减少了上下文信息,加强了密钥整体性。实现了Crypt-JDBC模型,用JDBC替换中间件软件MySQL-Proxy。实验结果表明,该模型具有较高的执行效率。

CryptDB密文数据库系统并行方案研究

加密数据库对隐私数据的加密存储保护是解决当前互联网中用户隐私数据泄露的一种可行方案。鉴于互联网中每日产生的用户隐私数据规模巨大,传统的串行计算会导致隐私数据的加密存储时间消耗较长。为提高加密存储等数据处理的速度,将MapReduce并行框架与Crypt DB密文数据库系统进行有机结合,设计并实现了Crypt DB密文数据库系统并行加密和分布式存储的方案。并行方案采用任务调度算法、文件分割算法来提高其并行性和可控性,通过重写MapReduce框架中的Map方法来实现Crypt DB密文数据库系统的并行加密和分布式存储。基于由1个Master节点、3个Crypt DB节点和3个My SQL服务器构成的实验平台,进行了并行方案的实验验证及其性能分析。实验结果表明,所构建的并行方案在3个Crypt DB节点集群中的加速比可达到2.51,加密和存储时间节省了60.2%,可用于大规模关系数据的加密存储。

Linux加密文件系统:Crypt-FS

随着便携式计算设备的普及，保存数据的存储设备失窃或遗失的可能性增大。在这种情况下，能够保证敏感数据不被泄露的唯一方案是使用数据加密技术。相对于其它加密方式，使用加密文件系统对用户透明、可靠，有着不容忽视的优势。文章在Linux 2.4操作系统上设计和实现了一个加密文件系统——Crypt-FS，并对其进行了介绍。

Cancer and age related colonic crypt deficiencies in cytochrome c oxidase Ⅰ

AIM: To investigate whether defi ciency of expressionof cytochrome c oxidase I (CcOI) in colonic crypts is associated with colon cancer.METHODS: The pattern and level of expression of CcOI in non-neoplastic colonic crypts,and in dysplastic tissues,was assessed using standard immunohis-tochemical methods.Biopsies were obtained from individuals undergoing colonoscopies for screening purposes or for a medically indicated reason.Tissue samples were also obtained from surgical colonic resections.Samples from resections were taken from colonic mucosa 1 and 10 cm from tumors and from the tumors themselves.Samples were evaluated for frequency of crypts with reduced or absent expression of CcOI.In most crypts the loss was apparent throughout the entire crypt,while in a small minority the loss was segmental.The strong immunoreactivity using this monoclonal antibody makes the scoring unambiguous.The percent of crypts with reduced or absent expression of CcOI or (infrequent) segmented loss of expression was then calculated.Data analyses were performed using SPSS statistical package 17.0.RESULTS: The average frequency of CcOI deficient crypts (CcOI-DC) is low in individuals between 20 and 39 years of age,with 0.48% ± 0.40% CcOI-DC for women and 1.80% ± 0.35% for men.CcOI-DC increases after age 40 years,so that between the ages of 40 and 44 years the average frequency of CcOI- DC goes up to 5.89% ± 0.84% in women and 2.15% ± 1.27% in men.By 80-84 years of age,the average frequency of CcOI-DC goes up in women to 15.77% ± 0.97% and in men to 22.6% ± 0.65%.The increases in CcOI-DC from ages 40-44 years compared to 80-84 years in women and men are significantly different with P < 0.01.For women over age 60 years,deficiency of CcOI expression is greater in those women who have had a cancer in their colon.The frequency of CcOI-DC,measured in men,increased in tissues adjacent to colon cancer,being 4.03% ± 0.27% in individuals free of neoplasia in the age range 55-64 yearsand 14.13% ± 0.35% in resected histologically normal tissue of men with cancer in the same age range,P < 0.001.Similar signifi cant differences were noted in older age ranges.The frequency of CcOI-DC crypts in the cecum and sigmoid colon of an individual are signifi cantly correlated,with an R2 = 0.414 for women and R2 = 0.528 for men,P < 0.001.This suggests that the factors determining the level of CcOI deficiency act throughout the colon.Most defective crypts are in clusters of two or more,a likely consequence of crypt fission.In the non-neoplastic margins of cancers,crypts are frequently defi cient for CcOI,and such crypts may appear in large clusters,some containing more than 100 defi cient crypts.CcOI defi ciency is also apparent in colon cancers and sometimes involves a large section of the tumor.Overall,CcOI deficient cells can be visualized in segments of crypts,in whole crypts that increase in frequency with age,in crypts undergoing f ission,in clusters of crypts where the clusters increase in size with age,in increased frequency near tumors,in large clusters in the intimate margins of tumors,and in the tumors themselves.There is no clear dividing line between early stages that can be considered aspects of aging and later stages that can be considered aspects of the progression to cancer.This ambiguity may re ect a rather general situation leading to adult cancer where the early stages of cellular change appear to be relatively innocuous features of the aging process but over decades may evolve into malignancy.CONCLUSION: CcOI defi cient crypts increase in frequency with age,and clusters of defi cient crypts are associated with,and may give rise to,colon cancer.

Azoxymethane-induced rat aberrant crypt foci:Relevance in studying chemoprevention of colon cancer

The pathogenesis of colon cancer involves sequential and multistep progression of epithelial cells initiated to a cancerous state with defined precancerous intermediaries. Aberrant crypt foci （ACF） represent the earliest identifiable intermediate precancerous lesions during colon carcinogenesis in both laboratory animals and humans. ACF are easily induced by colon-specific carcinogens in rodents and can be used to learn more about the process of colon carcinogenesis. For over two decades, since its first discovery, azoxymethane （AOM）-induced rodent ACF have served as surrogate biomarkers in the screening of various anticarcinogens and carcinogens. Several dietary constituents and phytochemicals have been tested for their colon cancer chemopreventive efficacy using the ACF system. There has been substantial effort in defining and refining ACF in terms of understanding their molecular make-up, and extensive research in this field is currently in progress. In chemoprevention studies, AOM-induced rat ACF have been very successful as biomarkers, and have provided several standardized analyses of data. There have been several studies that have reported that ACF data do not correlate to actual colon tumor outcome, however, and hence there has been an ambiguity about their role as biomarkers. The scope of this mini-review is to provide valuable insights and limitations of AOM-induced rat ACF as biomarkers in colon cancer chemoprevention studies. The role of the dynamics and biological heterogeneity of ACF is critical in understanding them as biomarkers in chemoprevention studies.

Aberrant crypt focus and fragile histidine triad protein in sporadic colorectal carcinoma

AIM:To characterize aberrant crypt focus (ACF) in adjoining mucosa in sporadic colorectal carcinoma and to evaluate fragile histidine triad (Fhit) protein and Ki67. METHODS:ACF was identified grossly and classified histologically in 75 resected specimens. ACF was typed into hyperplastic ACF (HACF) and dysplastic ACF (DACF). Sections of ACF, carcinoma and normal colonic mucosa as control were studied for Fhit and Ki67 expressions by immunohistochemistry and were grouped according to staining intensity and the number of positive stained cells observed in different histological groups. Comparison was done between the different groups by Pearson's χ 2 test and γ test for the ordinal data. P value < 0.05 was considered as significant.RESULTS:Age range was 40 to 86 years in males (mean = 43.36) and 45 to 70 years in females (mean = 56). HACF was identified in all cases studied in the non-tumorous colonic mucosa; ACF was observed as non-contiguous scattered foci, which supports the hypothesis of acquisition of single focus monoclonality by colonic epithelial cells in tumor generation. Twenty-four (32%) had DACF and were observed as closure to carcinoma foci. Intensity of Fhit expression:(1) HACF 40% exhibited strong intensity, similar to normal, moderate in 36% and weak in 24%; (2) DACF strong in 25%, moderate in 37.5% and weak in 37.5%; and (3) carcinoma negative in 16%, strong in 43% and moderate and weak in 28.5% each. Significant difference was observed in intensity of the Fhit protein expressions by HACF and DACF (P < 0.05). Tumor in older patients showed a stronger Fhit intensity compared to younger patients (P = 0.036). Vegetarian diet intake and nonsmokers showed stronger Fhit intensities. Advanced stage tumor, non-vegetarian diet and younger age was associated with loss of Fhit protein. Ki67 positivity was an extended crypt pattern in HACF and DACF showed extension up to the neck region of the crypts and surface epithelium. Carcinomas showed a marked increase in Ki67 expression (P < 0.05). Fhit protein had an inverse association with Ki67 expression. CONCLUSION:Weaker Fhit intensity was associated with smoking, non-vegetarian diet intake and increasing Ki67 expression. Loss of Fhit protein expression is possibly influenced by environmental factors like smoking and non-vegetarian diet intake.

Crypt abscess-associated microbiota in inflammatory bowel disease and acute self-limited colitis

AIM:To evaluate whether crypt abscesses frominflammatory bowel disease(IBD)patients containbacteria and to establish their nature.METHODS:We studied 17 ulcerative colitis patients,11 Crohn's disease patients,7 patients with acute selflimited colitis(ASLC)and normal colonic biopsies from5 subjects who underwent colonoscopy for colon cancer screening.A fluorescent in situ hybridization techniquewas applied to colonic biopsies to assess the microbiotacomposition of the crypts and crypt abscesses.RESULTS:Crypts colonized by bacteria were observedin 42.9%and 3.6%of ASLC and IBD patients,respectively(P=0.019).Crypt abscesses colonized bybacteria were observed in 28.6%and 0.0%of ASLCand IBD patients,respectively(P=0.035).CONCLUSION:These results do not support thehypothesis that crypt abscesses in IBD are the resultof localized dysbiosis arising from persistence of livingbacteria colonizing the crypts.

Relationship of human rectal aberrant crypt foci and formation of colorectal polyp:One-year following up after polypectomy

AIM:To clarify the relationship of human rectal aberrant crypt foci and formation of colorectal polyp.METHODS:Eighty-nine subjects were recruited from the population of Japanese individuals who underwent polypectomy at Yokohama City University Hospital.All patients had baseline adenomas removed at year 0 colonoscopy.Aberrant crypt foci(ACF) were defined as lesions in which the crypts were more darkly stained with methylene blue than normal crypts and had larger diameters,often with oval or slit-like lumens and a thicker epithelial lining.RESULTS:A total of 366 ACFs were identified in 89 patients;all had baseline adenomas removed at the first examination(year 0) colonoscopy and returned for the second(year 1).ACF in the lower rectum were assessed at year 0 and study group were divided into two groups depend on ACF numbers,0-3 or over 3.All participants were examined in the number and maximum size of adenoma.There was no statistical difference in number and maximum size of ACF at year 0,however,maximum size of adenoma was larger in over 3 group than 0-3 group at year 1.CONCLUSION:The number of ACF may be a predictive factor of relatively large adenoma incidence in the pilot phase study.

INHIBITORY EFFECT OF FERMENTED MILK ON DMH-INDUCED MICRO-NUCLEI AND APOPTOSIS IN THE COLON CRYPT CELLS OF MICE

The effect of fermented milk on micronuclei andapoptosis induced by DimethyIhydraziine(DMH)in thecolon crypt cells of mouse was studied.Fermented milk,milk and tap water were fed to three groups of C57BL mice.The animals were given DMH i.p.at a dosage of 20mg/kg onthe 7th day.The animals were sacrificed 24 hours

Crypt region localization of intestinal stem cells in adults

The intestinal epithelial lining plays a central role in the digestion and absorption of nutrients,but exists in a harsh luminal environment that necessitates continual renewal.This renewal process involves epithelial cell proliferation in the crypt base and later cell migration from the crypt base to the luminal surface.This process is dependent on multi-potent progenitor cells,or stem cells,located in each crypt.There are about 4 to 6 stem cells per crypt,and these stem cells are believed to generate distinct end-differentiated epithelial cell types,including absorptive cells,goblet cells,enteroendocrine cells and Paneth cells,while also maintaining their own progenitor cell state.Earlier studies suggested that intestinal stem cells were located either in the crypt base interspersed between the Paneth cells [i.e.crypt base columnar(CBC) cell model] or at an average position of 4 cells from the crypt base [i.e.label-retaining cells(LRC +4) model].Recent studies have employed biomarkers in the in vivo mammalian state to more precisely evaluate the location of these progenitor cells in the intestinal crypt.Most notable of these novel markers are Lgr5,a gene that encodes a G-protein-coupled receptor with expression restricted to CBC cells,and Bmi 1,which encodes a chromatin remodeling protein expressed by LRC.These studies raise the possibility that there may be separate stem cell lines or different states of stem cell activation involved in the renewal of normal mammalian intestinal tract.

Ventricular Septal Crypts:Remnants of Spontaneous Interventricular Defect Closure?

Background:Ventricular crypts are quite a common finding during cardiac imaging,but their etiology is unclear.A possible final result of a spontaneous ventricular septal defect closure has been supposed but never investigated in earlier studies.Method:From January 1997 to December 2020,all newborns diagnosed to have a ventricular septal defect were prospectively entered in our database and those with an isolated defect were included in the study.Ventricular septal defects were classified into four types:perimembranous,trabecular muscular,inlet and outlet.A long-term follow up was performed in order to visualize the possible residual formation of a septal myocardial crypt.Results:A total of 376 isolated ventricular septal defects(314 muscular and 54 perimembranous,4 inlet,4 outlet)were detected.Follow up ranged from 1 to 23 years and showed that,among muscular type,a spontaneous closure occurred in 284(91%),26 did not close(8,28%),2 required surgical intervention(0,63%),3 were lost at follow up(0,95%).During this period,after spontaneous defect closure closure,20 crypts were found(6,4%).Conclusion:This study shows that a muscular ventricular septal defect may evolve in the 6.4%of cases in a residual septal crypt.Although septal crypts occur more frequently in patients affected by hypertrophic and hypertensive cardiomyopathy,they may also represent the evolution of a spontaneous closure of a muscular interventricular defect.

EPITHELIAL CELL NECROSES IN MOUSE INTESTINAL CRYPTS AFTER CONTINUE IRRADIATION WITH βRAYS FROM TRIATED WATER

In this paper epithelial cell necroses(apoptosis)of mouse intestinal crypts induced by βRays fromtritiated water(HTO)was reported.The resultsshowed that the number of apoptotic cells perintestinal crypt 20 hrs after injection of

APC and K-ras gene mutation in aberrant crypt foci of human colon

AIM:To study the genetic alteration in ACF and to define the possibility that ACF may be a very early morphological lesion with molecular changes,and to explore the relationship between ACF and colorectal adenoma even carcinoma. METHODS: DNA from 35 CRC, 15 adenomas, 34 ACF and 10 normal mucus was isolated by means of microdissection. Direct gene sequencing of K-ras gene including codon 12, 13 and 61 as well as the mutation cluster region (MCR) of APC gene was performed. RESULTS: K-ras gene mutation frequency in ACF, adenoma and carcinoma was 17.6% (6/34), 13.3% (2/15), and 14.3% (5/35) respectively, showing no difference (P 】 0.05) in K-ras gene mutation among three pathologic procedures. The K-ras gene mutation in adenoma, carcinoma and 4 ACF restricted in codon 12 (GGT GAT), but the other 2 mutations from ACF located in codon 13 (GGC GAC). K-ras gene mutation was found more frequently in older patients and patients with polypoid cancer. No mutation in codon 61 was found in the three tissue types. Mutation rate of APC gene in adenoma and carcinoma was 22.9% (8/35) and 26.7% (4/15), which was higher than ACF (2.9%) (P 【0.05). APC gene mutation in carcinoma was not correlated with age of patients, location, size and differentiation of tumor. CONCLUSION: ACF might be a very early morphological lesion in the tumorogenesis of colorectal tumor. The morphological feature and gene mutation status was different in ACF and adenoma. ACF is possibly putative microadenoma that might be the precursor of adenoma. In addition, the development of a subgroup of colorectal carcinomas might undergo a way of normal epithelium ACF carcinomas .

Early weaning leads to the remodeling of lipid profile in piglet jejunal crypt cells during post-weaning days

Reportedly,proteins involved in lipid metabolism change significantly in the jejunal crypt cells of earlyweaned piglets,but the exact lipid profile change remains uncertain.In the present study,32 piglets weaned at 21 d of age were randomly divided into 4 groups with 8 replicates.The jejunal crypt cells of a group of piglets on the post-weaning day(PWD)1,3,7,and 14 were isolated per time point.Crypt cell lipid profiles were analyzed using ultra-high-performance liquid chromatography coupled with hybrid quadrupole time-of-flight mass spectrometry.This study showed that piglets suffered the greatest weaning stress on PWD 3 in terms of the lowest relative weight of the small intestine,the highest relative weight of the spleen,and the highest levels of malondialdehyde,cholesterol,and low-density lipoprotein cholesterol.The lipid profile of jejunal crypt cells including carnitine,sulfatide,sphingomyelin,hexosylceramide,and ceramide greatly changed after weaning,especially between PWD3 and 14(P<0.05).The differential lipid species between these 2 d were mainly involved in the glycerophospholipid metabolism pathway.In addition,potential lipid biomarkers for weaning stress in crypt cells such as phosphatidylcholine(PC)(9:0/26:1),PC(17:0/18:2),carnitine(24:0),carnitine(22:0),sphingomyelin(d14:1/22:0),PC(P-18:0/18:4),phosphatidylethanolamine(P-16:0/20:4),phosphatidylinositol(15:1/24:4),and dihexosylceramide(d14:1/26:1)were identified.The changes in lipid profile might be related to the inflammation caused by early weaning.These findings might provide new therapeutical targets for intestinal dysfunctions caused by weaning stress.

Modeling colorectal tumorigenesis using the organoids derived from conditionally immortalized mouse intestinal crypt cells (ciMICs)

Intestinal cancers are developed from intestinal epithelial stem cells(ISCs)in intestinal crypts through a multi-step process involved in genetic mutations of oncogenes and tumor suppressor genes.ISCs play a key role in maintaining the homeostasis of gut epithelium.In 2009,Sato et al established a three-dimensional culture system,which mimicked the niche microenvironment by employing the niche factors,and successfully grew crypt ISCs into organoids or Mini-guts in vitro.Since then,the intestinal organoid technology has been used to delineate cellular signaling in ISC biology.However,the cultured organoids consist of heterogeneous cell populations,and it was technically challenging to introduce genomic changes into three-dimensional organoids.Thus,there was a technical necessity to develop a twodimensional ISC culture system for effective genomic manipulations.In this study,we established a conditionally immortalized mouse intestinal crypt(ciMIC)cell line by using a piggyBac transposon-based SV40 T antigen expression system.We showed that the ciMICs maintained long-term proliferative activity under two-dimensional niche factor-containing culture condition,retained the biological characteristics of intestinal epithelial stem cells,and could form intestinal organoids in three-dimensional culture.While in vivo cell implantation tests indicated that the ciMICs were non-tumorigenic,the ciMICs overexpressing oncogenic b-catenin and/or KRAS exhibited high proliferative activity and developed intestinal adenoma-like pathological features in vivo.Collectively,these findings strongly suggested that the engineered ciMICs should be used as a valuable tool cell line to dissect the genetic and/or epigenetic underpinnings of intestinal tumorigenesis.

Successful microsurgical vasoepididymostomy for a case of cryptozoospermia

Dear Editor,Cryptozoospermia is defined as the apparent absence of spermatozoa from fresh semen samples,but they can.be found in centrifuged pellets.1 It is usually caused by a spermatogenic disorder,while cryptozoospermia associated with seminal duct obstruction is less common.2 Because of the extremely low sperm counts in semen samples,men with cryptozoospermia are often reliant on intracytoplasmic sperm injection(ICSI)for paternity.

一株鸡源唾液乳杆菌的分离鉴定及其对育雏早期蛋鸡肠道健康的影响

旨在从健康海兰褐鸡肠道中分离鉴定乳酸菌,并研究其对育雏早期蛋鸡肠道健康的影响。本研究采用细菌培养技术、16S rRNA测序和牛津杯扩散法,分离、筛选、鉴定可产细菌素的乳酸菌菌株,检测其对高温、pH和胆盐的耐受性;动物试验选取240只1日龄健康、体重相近的海兰褐鸡,随机分为4组,每组60只鸡,包括对照组(C)、低剂量唾液乳杆菌CL09组(L)、中剂量唾液乳杆菌CL09组(M)和高剂量唾液乳杆菌CL09组(H),研究该乳酸菌菌株对育雏早期蛋鸡生长性能、免疫器官指数及肠道健康相关指标的影响。试验周期为21 d。结果表明:分离菌为可产细菌素的革兰阳性菌,结合16S rRNA鉴定结果将其命名为唾液乳杆菌CL09,该菌的无细胞上清液可抑制大肠杆菌、沙门菌、金黄色葡萄球菌和李斯特菌的生长。该菌的耐受温度为60℃,具有耐酸、耐胆盐的特性。动物试验结果显示:与对照组相比,灌服唾液乳杆菌CL09可以增加雏鸡体重和免疫器官重量;H组十二指肠、空肠的隐窝深度变化最为显著,L和M组十二指肠绒毛高度显著增加,且H组十二指肠绒毛呈“波浪形”;M和H组肠道干细胞标记基因Lgr 5和Bmi1表达水平升高极显著(P<0.001);H组的黏膜屏障基因Zo-1和Ocln的mRNA表达水平升高极显著(P<0.01);M组潘氏细胞标记性基因Lyz的mRNA表达水平最高。L、M和H组的杯状细胞标记基因Muc的mRNA表达水平均升高,且差异极显著(P<0.01)。综上所述,源自健康海兰褐鸡肠道的唾液乳杆菌CL09,通过促进雏鸡肠道干细胞分化为潘氏细胞和杯状细胞,增加绒毛高度,降低隐窝深度,从而增大肠道的黏膜面积。该菌具有调节育雏早期鸡肠道健康的良好特性,可作为益生菌的备选菌株。

从“玄府-隐窝”视域辨治溃疡性结肠炎肠屏障受损

“玄府”作为中医藏象理论的微观结构遍布于人体各部,急性溃疡性结肠炎微观病变表现为结肠隐窝脓肿甚至结构紊乱。其湿热蕴结大肠,肠道因实而闭的发病特点与“玄府”贵开忌阖、贵通忌闭的理念契合。肠道隐窝机械屏障与黏液屏障功能与“玄府”推陈出新、气液宣通的特点有共通之处,可为肠“玄府”理论提供形态学依据。清开玄府法能够抑制湿热郁腐之物蕴结、肠道郁闭不通导致的肠“玄府闭阖”状态,推动“玄府-隐窝”学说在治疗溃疡性结肠炎早期隐窝病变的指导作用和理论支撑。

小鼠小肠类器官炎症模型的构建

目的建立体外小肠类器官培养体系,探讨脂多糖(LPS)对小肠类器官生长和炎性因子分泌的影响。方法体外无菌分离并收集C57BL/6小鼠小肠隐窝细胞团,使用类器官基质胶进行包埋,并在完全培养基的支撑下,培养形成具有小肠上皮样结构的立体多叶结构的小肠类器官。小肠类器官培养5~7 d或类器官中央区域变黑时传代,传代后3 d将小肠类器官随机分为不同质量浓度LPS组(0、150、175、200、225、250、275、300 mg/L)。在LPS诱导24 h和48 h后观察小肠类器官生长和形态特征变化;用CCK-8法检测不同时间和质量浓度LPS对小肠类器官诱导炎症后增殖活力的影响;采用酶联免疫吸附试验检测4种不同质量浓度LPS(0、175、200、225 mg/L)在不同时间对类器官培养上清液中粒细胞-巨噬细胞集落刺激因子(GM-CSF)、白细胞介素(IL)-1α、IL-6、IL-10水平的影响。结果初步构建了小鼠小肠类器官培养体系。不同时间和质量浓度LPS作用小肠类器官诱导炎症后,通过形态学观察到小肠类器官会有不同程度的膨胀和内腔凋亡现象的发生,受损的肠上皮中隐窝或肠干细胞的增殖分化和出芽数量也受到不同程度的抑制。小肠类器官在175~225 mg/L的LPS诱导24 h和48 h后,其增殖活力呈现不同程度的降低(P<0.05),但细胞活力仍大于50%。200 mg/L和225 mg/L的LPS诱导24 h和48 h后,IL-1α、IL-6和GM-CSF水平部分升高(P<0.05);200 mg/L的LPS诱导24 h和48 h后,IL-10水平降低(P<0.05)。结论本研究初步构建了不同质量浓度和时间的LPS诱导小肠类器官体外肠道炎症损伤模型,为今后肠道疾病的机制研究和有效药物的筛选提供了更为可靠的研究平台。