Mesoporous silica nanoparticles with chiral pattern topological structure function as“antiskid tires”on the intestinal mucosa to facilitate oral drugs delivery

The weak adhesion between nanocarriers and the intestinal mucosa was one of the main reasons caused the failure in oral delivery.Inspired by the“antiskid tires”with complex chiral patterns,mesoporous silica nanoparticles AT-R@CMSN exhibiting geometrical chiral structure were designed to improve the surface/interface roughness in nanoscale,and employed as the hosting system for insoluble drugs nimesulide(NMS)and ibuprofen(IBU).Once performing the delivery tasks,AT-R@CMSN with rigid skeleton protected the loaded drug and reduced the irritation of drug on gastrointestinal tract(GIT),while their porous structure deprived drug crystal and improved drug release.More importantly,AT-R@CMSN functioned as“antiskid tire”to produce higher friction on intestinal mucosa and substantively influencedmultiple biological processes,including“contact”,“adhesion”,“retention”,“permeation”and“uptake”,compared to the achiral S@MSN,thereby improving the oral adsorption effectiveness of such drug delivery systems.By engineering AT-R@CMSN to overcome the stability,solubility and permeability bottlenecks of drugs,orally administered NMS or IBU loaded AT-R@CMSN could achieve higher relative bioavailability(705.95%and 444.42%,respectively)and stronger anti-inflammation effect.In addition,AT-R@CMSN displayed favorable biocompatibility and biodegradability.Undoubtedly,the present finding helped to understand the oral adsorption process of nanocarriers,and provided novel insights into the rational design of nanocarriers.

Hypertonic saline resuscitation reduces apoptosis of intestinal mucosa in a rat model of hemorrhagic shock

Objective: To investigate the early effects of hypertonic and isotonic saline solutions on apoptosis of intestinal mucosa in rats with hemorrhagic shock. Methods: A model of rat with severe hemorrhagic shock was established in 21 Sprague-Dawley (SD) rats. The rats were randomly divided into the sham group, normal saline resuscitation (NS) group, and hypertonic saline resuscitation (HTS) group, with 7 in each group. We detected and compared the apoptosis in small intestinal mucosa of rats after hemorrhagic shock and resuscitation by terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL), FITC (fluo- rescein-iso-thiocyanate)-Annexin V/PI (propidium iodide) double staining method, and flow cytometry. Results: In the early stage of hemorrhagic shock and resuscitation, marked apoptosis of small intestinal mucosa in the rats of both NS and HTS groups was observed. The numbers of apoptotic cells in these two groups were significantly greater than that in the sham group (P<0.01). In the HTS group, the apoptic cells significantly decreased, compared with the NS group (P<0.01). Conclusion: In this rat model of severe hemorrhagic shock, the HTS resuscitation of small volume is more effective than the NS resuscitation in reducing apoptosis of intestinal mucosa in rats, which may improve the prognosis of trauma.

Mucin 1 and interleukin-11 protein expression and inflammatory reactions in the intestinal mucosa of necrotizing enterocolitis children after surgery

BACKGROUND Necrotizing enterocolitis(NEC)of the newborn is a frequently occurring clinical disease in infants.The mortality rate of NEC in premature infants is as high as 50%,and the morbidity rate is on the rise.NEC has already caused serious impacts on newborn survival and poses serious threats to both children and families.AIM To investigate the expression and significance of mucin 1(MUC1)and interleukin-11(IL-11)in the intestinal mucosa of infants with neonatal NEC after surgery.METHODS Forty-eight postoperative intestinal mucosal specimens from children with NEC(NEC group)and twenty-two intestinal mucosal specimens from children with congenital intestinal atresia(control group)were collected in our hospital.Immunohistochemical staining and Western blot analysis were used to examine the protein expression of MUC-1 and IL-11 in the two groups.The serum levels of tumor necrosis factor-α(TNF-α)and IL-1βin the two groups were measured by enzyme-linked immunosorbent assay,and the relationship between MUC-1 and IL-11 protein expression and serum TNF-αand IL-1βlevels was analyzed by the linear correlation method.RESULTS The protein expression of MUC-1 and IL-11 in the NEC group was significantly lower than that in the control group,and the difference was statistically significant(P<0.05).The levels of serum TNF-αand IL-1βin the NEC group were significantly higher than those in the control group(P<0.05).The protein expression of MUC-1 and IL-11 in the NEC group negatively correlated with serum TNF-αand IL-1βlevels(P<0.05).There was a significant negative correlation between the protein expression of MUC-1 and IL-11 and the levels of serum TNF-αand IL-1βin the NEC group.CONCLUSION The protein expression of MUC1 and IL-11 in the intestinal mucosa of children with NEC is significantly downregulated after surgery.This downregulation may be involved in the pathogenesis of this disease and has a certain correlation with inflammatory response factors in children with NEC.

Emodin alleviates intestinal mucosal injury in rats with severe acute pancreatitis via the caspase-1 inhibition

BACKGROUND: Emodin, a traditional Chinese medicine, has a therapeutic effect on severe acute pancreatitis (SAP), whereas the underlying mechanism is still unclear. Studies showed that the intestinal mucosa impairment, and subsequent release of endotoxin and proinflammatory cytokines such as IL-1 beta, which further leads to the dysfunction of multiple organs, is the potentially lethal mechanism of SAP. Caspase-1, an IL-1 beta converting enzyme, plays an important role in this cytokine cascade process. Investigation of the effect of emodin on regulating the caspase-1 expression and the release proinflammatory cytokines will help to reveal mechanism of emodin in treating SAP. METHODS: Eighty Sprague-Dawley rats were randomly divided into four groups (n=20 each group): SAP, sham-operated (SO), emodin-treated (EM) and caspase-1 inhibitor-treated (ICE-I) groups. SAP was induced by retrograde infusion of 3.5% sodium taurocholate into the pancreatic duct. Emodin and caspase-1 inhibitor were given 30 minutes before and 12 hours after SAP induction. Serum levels of IL-1 beta, IL-18 and endotoxin, histopathological alteration of pancreas tissues, intestinal mucosa, and the intestinal caspase-1 mRNA and protein expressions were assessed 24 hours after SAP induction. RESULTS: Rats in the SAP group had higher serum levels of IL-1 beta and IL-18 (P<0.05), pancreatic and gut pathological scores (P<0.05), and caspase-1 mRNA and protein expressions (P<0.05) compared with the SO group. Compared with the SAP group, rats in the EM and ICE-I groups had lower IL-1 beta and IL-18 levels (P<0.05), lower pancreatic and gut pathological scores (P<0.05), and decreased expression of intestine caspase-1 mRNA (P<0.05). Ultrastructural analysis by transmission electron microscopy found that rats in the SAP group had vaguer epithelial junctions, more disappeared intercellular joints, and more damaged intracellular organelles compared with those in the SO group or the EM and ICE-I groups. CONCLUSIONS: Emodin alleviated pancreatic and intestinal mucosa injury in experimental SAP. Its mechanism may partly be mediated by the inhibition of caspase-1 and its downstream inflammatory cytokines, including IL-1 beta and IL-18. Our animal data may be applicable in clinical practice.

Elevated basal intestinal mucosal cytokine levels in asymptomatic first-degree relatives of patients with Crohn's disease

AIM To determine levels of cytokines incolonic mucosa of asymptomatic first degreerelatives of Crohn’s disease patients.METHODS Cytokines(Interleukin(IL)1-Beta,IL-2,IL-5 and IL-8)were measured using ELISAin biopsy samples of normal looking colonicmucosa of first degree relatives of Crohn’sdisease patients(n = 9)and from normalcontrols(n = 10)with no family history ofCrohn’s disease.RESULTS Asymptomatic first degree relativesof patients with Crohn’s disease had significantlyhigher levels of basal intestinal mucosalcytokines(IL-2,IL-5 and IL-8)than normalcontrols.Whether these increased cytokinelevels serve as phenotypic markers for a geneticpredisposition to developing Crohns diseaselater on,or whether they indicate early(pre-clinical)damage has yet to be further defined.CONCLUSION Asymptomatic first degreerelatives of Crohn’s disease patients have higherlevels of cytokines in their normal-lookingintestinal mucosa compared to normal controls,This supports the hypothesis that increasedcytokines may be a cause or an early event inthe inflammatory cascade of Crohns disease andare not merely a result of the inflammatoryprocess.

Changes in intestinal mucosal immune barrier in rats with endotoxemia

AIM： To investigate the dysfunction of the immunological barrier of the intestinal mucosa during endotoxemia and to elucidate the potential mechanism of this dysfunction. METHODS： Male Wistar rats were randomly distributed into two groups： control group and lipopolysaccharide （LPS） group. Endotoxemia was induced by a single caudal venous injection of LPS. Animals were sacrificed in batches 2, 6, 12 and 24 h after LPS infusion. The number of microfold （M）-cells, dendritic cells （DCs）, CD4＋ T cells, CD8＋ T cells, regulatory T （Tr） cells and IgA＋ B cells in the intestinal mucosa were counted after immunohistochemical staining. Apoptotic lymphocytes were counted after TUNEL staining. The levels of interleukin （IL）-4, interferon （IFN）-γ, and forkhead box P3 （Foxp3） in mucosal homogenates were measured by ELISA. The secretory IgA （sIgA） content in the total protein of one milligram of small intestinal mucus was detected using a radioimmunological assay.RESULTS： This research demonstrated that LPS-induced endotoxemia results in small intestinal mucosa injury. The number of M-cells, DCs, CD8~ T cells, and IgA~ B cells were decreased while Tr cell and apoptotic lymphocyte numbers were increased significantly. The number of CD4＋ T cells increased in the early stages and then slightly decreased by 24 h. The level of IL-4 significantly increased in the early stages and then reversed by the end of the study period. The level of IFN-T increased slightly in the early stages and then decreased markedly by the 24 h time point. Level of Foxp3 increased whereas sIgA level decreased.CONCLUSION： Mucosal immune dysfunction forms part of the intestinal barrier injury during endotoxemia. The increased number and function of Tr cells as well as lymphocyte apoptosis result in mucosal immunode- ficiency.

Review:Mechanism of acute pancreatitis complicated with injury of intestinal mucosa barrier

Acute pancreatitis (AP) is a common acute abdomen in clinic with a rapid onset and dangerous pathogenetic condition. AP can cause an injury of intestinal mucosa barrier, leading to translocation of bacteria or endotoxin through multiple routes, bacterial translocation (BT), gutorigin endotoxaemia, and secondary infection of pancreatic tissue, and then cause systemic in- flammatory response syndrome (SIRS) or multiple organ dysfunction syndrome (MODS), which are important factors influencing AP’s severity and mortality. Meanwhile, the injury of intestinal mucosa barrier plays a key role in AP’s process. Therefore, it is clinically important to study the relationship between the injury of intestinal mucosa barrier and AP. In addition, many factors such as microcirculation disturbance, ischemical reperfusion injury, excessive release of inflammatory mediators and apoptosis may also play important roles in the damage of intestinal mucosa barrier. In this review, we summarize studies on mechanisms of AP.

Effects of intestinal mucosal blood flow and motility on intestinal mucosa

AIM： To investigate the role of intestinal mucosal blood flow （IMBF） and motility in the damage of intestinal mucosal barrier in rats with traumatic brain injury. METHODS： Sixty-four healthy male Wistar rats were divided randomly into two groups： traumatic brain injury （TBI） group （n = 32）, rats with traumatic brain injury; and control group （n = 32）, rats with sham-operation. Each group was divided into four subgroups （n = 8） as 6, 12, 24 and 48 h after operation. Intestinal motility was measured by the propulsion ratio of a semi-solid colored marker （carbon-ink）. IMBF was measured with the laser-Doppler technique. Endotoxin and D-xylose levels in plasma were measured to evaluate the change of intestinal mucosal barrier function following TBI. RESULTS： The level of endotoxin was significantly higher in TBI group than in the control group at each time point （0.382 ± 0.014 EU/mL vs 0.102 ± 0.007 EU/mL, 0.466 ± 0.018 EU/mL vs 0.114 ± 0.021 EU/mL, 0.478± 0.029 EU/mL vs 0.112 ±- 0.018 EU/mL and 0.412± 0.036 EU/mL vs 0.108 ±0.011 EU/mL, P 〈 0.05）. D-xylose concentrations in plasma in TBI group were significantly higher than in the control group （6.68 ± 2.37 mmol/L vs 3.66 ±1.07 retool/L, 8.51 ± 2.69 mmol/L vs 3.15 ＋ 0.95 mmol/L, 11.68 ±3.24 mmol/L vs 3.78 ± 1.12 mmol/L and 10.23 ± 2.83 mmol/L vs 3.34 ± 1.23 mmol/L, P 〈 0.05）. The IMBF in TBI group was significantly lower than that in the control group （38.5 ± 2.8 PU vs 45.6 ± 4.6 PU, 25.2 ± 3.1 PU vs 48.2 ± 5.3 PU, 21.5 ± 2.7 PU vs 44.9 ± 2.8 PU, 29. 4 ± 3.8 PU vs 46.7 ± 3.2 PU） （P 〈 0.05）. Significant decelerations of intestinal propulsion ratio in T8I groups were found compared with the control group （0.48% ± 0.06% vs 0.62%± 0.03%, 0.37% ±0.05% vs 0.64% ± 0.01%, 0.39% ± 0.07% vs 0.63% =1= 0.05% and 0.46% ± 0.03% vs 0.65% ± 0.02%） （P 〈 0.05）. CONCLUSION： The intestinal mucosal permeability is increased obviously in TBI rats. Decrease of intestinal motility and IMBF occur early in TBI, both are important pathogenic factors for stress-related damage of the intestinal mucosal barrier in TBI.

Protective effect of rhubarb on barrier of intestinal mucosa

AIM To investigate the mechanism of the rhubarb on gut barrier protection. METHODS The models of gut barrier damage caused by hemorrhagic shock and intraperitoneal endotoxin were used to study the protective effect of rhubarb on the barrier of intestinal mucosa. They were randomly divided into four groups: treatment (rhubarb) group; positive control group; negative control group; placebo treatment group. The concentration of plasma endotoxin, tissue superoxide dismutase and lipoperoxide were measured. The histological analysis was also used. The effect of rhubarb on gut protection was observed. RESULTS The rhubarb could decrease intestinal permeability, attenuate endotoxin absorption within the gut, (the content of endotoxin in serum: shock group 0 557EU/ml±0 069EU/ml vs rhubarb group 0 345EU/ml±0 055EU/ml), obviously decrease the consumption of tissue SOD and the formation of tissue LPO (the content of SOD in serum, intestine and liver: endotoxin group 122 92NU/ml±43 19NU/ml, 292 24NU/ml±88 76NU/ml, 272 70NU/ml±85 79NU/ml vs rhubarb group 312 23NU/ml±54 93NU/ml, 391 09NU/mg±98 16NU/mg, 542 86NU/mg±119 93NU/mg; The content of LPO in intestine and liver: endotoxin group 8 57μmol/L±2 58μmol/L, 86 97μmol/L±46 54μmol/L vs rhubarb group 3 05μmol/L±1 13μmol/L, 13 18μmol/L±19 64μmol/L). Gut histopathology revealed that rhubarb could promote proliferation of gut goblet cells, increase secretion of mucus and protect intestinal mucosa in hemorrhagic shock model. CONCLUSION The mechanism of the rhubarb on gut barrier protection might involve in decreasing intestinal permeability, scavenging oxygen free radicals, promoting proliferation of goblet cells within intestinal mucosa.

Lansoprazole ameliorates intestinal mucosal damage induced by ischemia-reperfusion in rats

AIM: To investigate the protective effect of lansoprazoleon ischemia and reperfusion (I/R)-induced rat intestinalmucosal injury in vivo.METHODS: Intestinal damage was induced by clampingboth the superior mesenteric artery and the celiac trunkfor 30 rain followed by reperfusion in male Sprague-Dawleyrats. lansoprazole was given to rats intraperitoneally 1 hbefore vascular clamping.RESULTS: Both the intraluminal hemoglobin and proteinlevels, as indices of mucosal damage, significantlyincreased in I/R-groups comparion with those of sham-operation groups. These increases in intraluminal hemoglobinand protein levels were significantly inhibited by the treatmentwith lansoprazole at a dose of 1 mg/kg. Small intestineexposed to I/R resulted in mucosal inflammation that wascharacterized by significant increases in thiobarbituric acid-reactive substances (TBARS), tissue-associatedmyeloperoxidase activity (MPO), and mucosal content of ratcytokine-induced neutrophil chemoattractant-1 (CINC-1).These increases in TBARS, MPO activities and CINC-1 contentin the intestinal mucosa after I/R were all inhibited bypretreatment with lansoprazole at a dose of 1 mg/kg.Furthermore, the CINC-1 mRNA expression was increasedduring intestinal I/R, and this increase in mRNA expressionwas inhibited by treatment with lansoprazole.CONCLUSION: Lansoprazole inhibits lipid peroxidation andreduces development of intestinal mucosal inflammationinduced by I/R in rats, suggesting that lansoprazole mayhave a therapeutic potential for I/R injury.

Effect of Danshen on apoptosis and NF-кB protein expression of the intestinal mucosa of rats with severe acute pancreatitis or obstructive jaundice

BACKGROUND:Intestinal mucosa injury in cases of severe acute pancreatitis(SAP) or obstructive jaundice(OJ) is one of the main reasons for the accelerated aggravation of these diseases.Besides being an organ to digest and absorb nutrients,the intestine is also a unique immune organ.When SAP and OJ develop,the destruction of the intestinal mucosa barrier is an important contributing factor for the development of bacterial translocation,systemic inflammatory response syndrome,and multiple organ dysfunction syndrome.It is important to protect the intestinal mucosa in the therapy for SAP and OJ.In this study,we determined the effect of Radix Salviae Miltiorrhizae(Danshen) injection on apoptosis and NF-κB P65 protein expression in the intestinal mucosa of rats with SAP or OJ,and explored the protective mechanism of Danshen in their mucosa.METHODS:Sprague-Dawley rats were used in the SAP and OJ experiments.These rats were randomly divided into shamoperated,model control,and treated groups.At various times after operation,the mortality rates were calculated.Subsequently,the rats were killed to assess the pathological changes,the expression levels of Bax and NF-κB proteins,and the apoptosis indices in the intestinal mucosa.RESULTS:Compared to the corresponding model control group,the number of SAP or OJ rats that died in the treated group decreased but showed no statistically significant difference.At all time points after operation,there was no significant difference between the treated and model control groups in the staining intensity as well as the product of staining intensity and positive staining rate of Bax protein in the intestinal mucosa of SAP and OJ rats.At 3 hours after operation,the apoptosis index of the intestinal mucosa of SAP rats in the treated group was lower than that in the model control group(P【0.01).At 12 hours after operation in SAP rats and 28 days after operation in OJ rats,the staining intensity as well as the product of staining intensity and positive staining rate of NF-κB protein of the intestinal mucosa in the treated group were lower than those in the model control group(P【0.01).CONCLUSION:Danshen exerts protective effects on the intestinal mucosa of SAP and OJ rats perhaps by inhibiting apoptosis and down-regulating NF-κB protein.

The effects of PAF antagonist on intestinal mucosal microcirculation after burn in rats

INTRODUCTIONGut originated infection(GOI)has been recognizedas a potential factor for postburn irreversible shock,early sepsis and multiple system organ failure.The intestinal mucosal barrier injury has beenimplicated as the cause of postburn GOI.However,pathogenesis of the lesion is not

Effects of psychological stress on small intestinal motility and bacteria and mucosa in mice

AIM: To investigate the effects of psychological stress on small intestinal motility and bacteria and mucosa in mice, and to explore the relationship between small intestinal dysfunction and small intestinal motility and bacteria and mucosa under psychological stress. METHODS: Sixty mice were randomly divided into psychological stress group and control group. Each group were subdivided into small intestinal motility group (n= 10), bacteria group (n = 10), and D-xylose administered to stomach group (n= 10). An animal model with psychological stress was established housing the mice with a hungry cat in separate layers of a two-layer cage. A semi-solid colored marker (carbon-ink) was used for monitoring small intestinal transit. The proximal small intestine was harvested under sterile condition and processed for quantitation for aerobes (Escherichia coli) and anaerobes (Lactobacilli). The quantitation of bacteria was expressed as Iog10(colony forming units/g). D-xylose levels in plasma were measured for estimating trie damage of small intestinal mucosa. RESULTS: Small intestinal transit was inhibited (39.80±9.50% vs 58.79±11.47%,P<0.01) in mice after psychological stress, compared with the controls. Psychological stress resulted in quantitative alterations in the aerobes (E.coli). There was an increase in the number of E coli in the proximal small intestinal flora (1.78±0.30 log10(CFU/g) vs 1.37±0.21 log10(CFU/g), P<0.01), and there was decrease in relative proportion of Lactobacilli and E.coli of stressed mice (0.53±0.63 vs 1.14±1.07,P<0.05), while there was no significant difference in the anaerobes (Lactobacilli) between the two groups (2.31±0.70 log10 (CFU/g) vs 2.44±0.37 log10(CFU/g), P>0.05). D-xylose concentrations in plasma in psychological stress mice were significantly higher than those in the control group (2.90±0.89 mmol/L vs 0.97±0.33 mmol/L, P<0.01). CONCLUSION: Small intestinal dysfunction under psychological stress may be related to the small intestinal motility disorder and dysbacteriosis and the damage of mucosa probably caused by psychological stress.

Intestinal mucosal atrophy and adaptation

Mucosal adaptation is an essential process in gut ho- meostasis. The intestinal mucosa adapts to a range of pathological conditions including starvation, short-gut syndrome, obesity, and bariatric surgery. Broadly, these adaptive functions can be grouped into proliferation and differentiation. These are influenced by diverse interactions with hormonal, immune, dietary, nervous, and mechanical stimuli. It seems likely that clinical out- comes can be improved by manipulating the physiol- ogy of adaptation. This review will summarize current understanding of the basic science surrounding adapta- tion, delineate the wide range of potential targets for therapeutic intervention, and discuss how these might be incorporated into an overall treatment plan. Deeper insight into the physiologic basis of adaptation will identify further targets for intervention to improve clini- cal outcomes.

Intestinal Transport and Biotransformation of Resibufogenin and Cinobufagin in Chan Su via HPLC/APCI-MS^n

In vitro models of human colon carcinoma cell line(Caco-2 cell monolayer) and human intestinal bacteria were used to investigate the intestinal transport and biotransformation of resibufogenin and cinobufagin in Chan Su by HPLC/APCI-MSn. The experimental results of Caco-2 cell monolayer demonstrate that the apparent permeability coefficients(Papp) of resibufogenin and cinobufagin are higher than 10–6 cm/s, which indicates that both resibufogenin and cinobufagin have a good absorption in the small intestine. And the biotransformation result of human intestinal bacteria shows that resibufogenin has been transformed to 3-epiresibufogenin and cinobufagin has been transformed to 3-epicinobufagin, deacetylcinobufagin and 3-epideacetycinobufagin, respectively.

Effects of Intestinal Trefoil Factor on Colonic Mucosa in Experimental Colitis of Rats

In order to investigate the protective effects of intestinal trefoil factor (ITF) on colonic mucosa in experimental colitis of rats, ITF was detected by RT-PCR and immunohistochemistry at different time points. Three days after colitis induction, rats were treated with either 0.9 % saline solution or rhITF. Pathological changes and the expression of iNOS mRNA, NO, MDA and SOD were measured respectively. It was found that ITF was mainly located in goblet cells, significantly higher in model group than in normal group (P<0.05). rhITF could increase the iNOS mRNA expression and NO contents, and there was statistically significant difference between rhITF group and model group (P<0.05). rhITF also caused an increase of MDA and a decrease of SOD, but there was no significant difference between two groups. These results indicated that ITF has apparent therapeutic effects in ulcerative colitis, which may be associated with iNOS and NO.

Protection effect of Emodin pretreatment on intestinal I-RI damage of intestinal mucosa in ratsa

Objective:To linvestigate the protective effect and mechanism of emodin pretreatment on intestinal mucosa of rats with intestinal ischemia-reperfusion injury.Methods:A total of 50SD rats were randomly divided into control group,model group,emodin groups of low,medium and high dose,with 10 in each group.Ischemia-reperfusion injury(I-RI)mode was established by using noninvasive clamp on superior mesentericartery(SMA).Control group and model group were pretreated with 0.5%sodium carboxymethyl cellulose solution lavage 2 h before operation,emodin groups of low,medium and high dose were given emodin lavage with 20,40,60 mg/kg pretreatment,femoral venous blood before the lavage pretreatment(TO)and 1 h ischemia(Tl),and inferior vena venous blood after 1 h of reperfusion(T2)were extracted from each group of rats for detection of serun level of intestinal fatty acid binding protein(I-FABP),tumor necrosis factor(TNF-α),endotoxin,interleukin 6(IL-6),and die content of diamine oxidase(DAO);Mter model establishment,the rats were sacrificed,intestine homogenate was prepared by using blind intestinal tissue to detect intestinal tissue myeloperoxidase(MPO],malondialdehyde(MDA)and superoxide dismutase(SOD)levels.And upper small intestine tissue was retrieved,followed by fixation and conventional HE staining to observe intestinal tissue morphology under light microscopy.Results:In emodin groups of low,medium and high dose at T1 and T2,I-FABP,TNF-α,endotoxin.IL,-6 and DAO level were significandy lower than that of model group(P<0.05);in emodin group of low,medium and high dose,MPO and MDA content in intestinal tissue homogenate was significantly lower than that in model group(P<0.05),SOD level was significantly higher than that of model group(P<0.05).Intestinal damage of emodin low,medium and high dose groups were significandy lighter than model group.Conclusions:Emodin pretreatment has certain protective effect on intestinal mucosa in ischemia reperfusion injury.

Effects of dietary tributyrin on intestinal mucosa development,mitochondrial function and AMPK-mTOR pathway in weaned pigs

Background:The objective of this experiment was to investigate the influence of dietary tributyrin on intestinal mucosa development,oxidative stress,mitochondrial function and AMPK-mTOR signaling pathway.Methods:Seventy-two pigs were divided into two treatments and received either a basal diet or the same diet supplemented with 750 mg/kg tributyrin.Each treatment has six replicates of six pigs.After 14 days,6 pigs from each treatment were selected and the jejunal samples were collected.Results:Results showed that supplemental tributyrin increased(P<0.05)villus height and villus height:crypt depth of weaned pigs.Pigs fed tributyrin had greater(P<0.05)RNA/DNA and protein/DNA ratios than pigs on the control group.The mRNA levels of sodium glucose transport protein-1 and glucose transporter-2 in the jejunum were upregulated(P<0.05)in pigs fed the tributyrin diet.Dietary tributyrin supplementation lowered(P<0.05)the malondialdehyde and hydrogen peroxide(H2O2)content in jejunum,enhanced(P<0.05)the mitochondrial function,as demonstrated by decreased(P<0.05)reactive oxygen species level and increased(P<0.05)mitochondrial membrane potential.Furthermore,tributyrin increased(P<0.05)mitochondrial DNA content and the mRNA abundance of genes related to mitochondrial functions,including peroxisomal proliferator-activated receptor-γcoactivator-1α,mitochondrial transcription factor A,nuclear respiratory factor-1 in the jejunum.Supplementation with tributyrin elevated(P<0.05)the phosphorylation level of AMPK and inhibited(P<0.05)the phosphorylation level of mTOR in jejunum compared with the control group.Conclusions:These findings suggest that dietary supplementation with tributyrin promotes intestinal mucosa growth,extenuates oxidative stress,improves mitochondrial function and modulates the AMPK-mTOR signal pathway of weaned pigs.

The Influence of Chinese Medicinal Herb on Chicken Immune Organs and Small Intestinal Mucosa Immune Organization

[Objective] The aim was to explore the mechanism of Chinese medicinal herb to enhance the body＇s immune. [Method] The quantitative distribution of immunocytes in chicken small intestinal mucosa lymphoid tissue-secretory type immune globulin cell A were dynamic observed to research chicken immune organ growth with histology conventional slice technology and immunohistochemistry dye. 1 day age healthy roosters were divided into 3 groups： the group 3 was control group. 1% and 0.5% concentration of Chinese herbal medicine immunopotentiator drinking water were added in the group 1 and 2 in continuous 60 d. The immune organ index was determined every 12 d and the histotomy of chicken small intes- tine in group control and 1% were taken for histological observation on day 24, 36 and 48. [ Result] Treatment group immune organ index was significantly higher than that of the control group and 1% group of small intestinal villus inherent intraformational immune cells number significantly increased （P〈0.01） compared with controls. Day 36 age group and day 48 group immune cells were higher than day 24 group of cell number （P〈 0.01 ）. [ Conclusionl Chinese medicinal herb had obvious role in promoting chicken immune organ growth and obvious influence on the quantity change of the intestinal mucosal immune cells.

Pretreatment with intestinal trefoil factor alleviates stress-induced gastric mucosal damage via Akt signaling

BACKGROUND Stress-related gastric mucosal damage or ulcer remains an unsolved issue for critically ill patients.Stress ulcer prophylaxis has been part of routine intensive care,but uncertainty and controversy still exist.Co-secreted with mucins,intestinal trefoil factor(ITF)is reported to promote restitution and regeneration of intestinal mucosal epithelium,although the mechanism remains unknown.AIM To elucidate the protective effects of ITF on gastric mucosa and explore the possible mechanisms.METHODS We used a rat model of gastric mucosal damage induced by water immersion restraint stress and lipopolysaccharide-treated human gastric epithelial cell line to investigate the potential effects of ITF on damaged gastric mucosa both in vivo and in vitro.RESULTS ITF promoted the proliferation and migration and inhibited necrosis of gastric mucosal epithelia in vitro.It also preserved the integrity of gastric mucosa by upregulating expressions of occludin and zonula occludens-1.In the rat model,pretreatment with ITF ameliorated the gastric mucosal epithelial damage and facilitated mucosal repair.The protective effects of ITF were confirmed to be exerted via activation of Akt signaling,and the specific inhibitor of Akt signaling LY249002 reversed the protective effects.CONCLUSION ITF might be a promising candidate for prevention and treatment of stressinduced gastric mucosal damage,and further studies should be undertaken to verify its clinical feasibility.