Butyrate Research Articles

Characteristics of acidification fermentation and biogas production for co-digestion of Spartina alterniflora and potato

Influences of anaerobic co-digestion of Spartina alterniflora, a lignocellulosic material, and potato on acidification fermentation of S. alterniflora and its biogas production were investigated by anaerobic batch digestion experiments conducted at S. alterniflora to potato ratio of 6:1, 7:1 and 9:1 at 35°C. The results indicated that acidification fermentation for co-digestions was butyrate type compared with that of propionate type for mono-digestion of pure S. alterniflora, and the total volatile fatty acids (TVFA) concentrations for co-digestion increased more than twice compared with that of mono-digestion of pure S. alterniflora. The results also indicated that the cumulative biogas yields for co-digestion at SC:P ratios of 6:1, 7:1 and 9:1, respectively amounted to 460, 431 and 415 mL/g VS, increased by 27.4%, 19.3% and 15.0% than the 361 mL/g VS obtained in mono-digestion of pure S. alterniflora. In addition, the average methane contents of biogas produced in co-digestion at SC:P ratios of 6:1, 7:1 and 9:1 were 60.3%, 62.4% and 62.7%, respectively, about 3%-5% higher than 57.4% in mono-digestion of pure S. alterniflora. It was concluded that great changes of VFAs were obtained for co-digestion compared with mono-digestion of pure S. alterniflora, and in general, these changes were beneficial to improve biogas production and biogas quality of S. alterniflora digestion.

Plasma ghrelin concentration is decreased by short chain fatty acids in wethers

To examine the effects of short chain fatty acids (SCFAs) on plasma ghrelin concentration, 4 wethers were injected intravenously with SCFA solutions [acetate (ACE), propionate (PRO), and butyrate (BUT) (0.8 mmol/kg BW)] and saline. The experiment was conducted after a 4 × 4 Latin square design. Each solution was injected into the jugular vein catheter with blood samples taken at −10, 0, 5, 10, 15, 20, 25, 30, 40, 50, and 60 min relative to the injection time also from this catheter. Plasma ghrelin concentrations decreased after injection with ACE, PRO, and BUT. Although plasma glucose concentrations increased after injection with PRO and BUT ( P < 0.05), the increment areas were greater with BUT than with PRO. Plasma insulin concentrations increased after injection with PRO and BUT ( P < 0.05). The decrement areas in plasma ghrelin concentrations were equal in ACE, PRO, and BUT. These data suggest that SCFAs inhibit ghrelin secretion in wethers and not through increased circulating glucose and insulin as previously proposed.

Epstein-Barr virus and lymphoma

More and more studies have found that EBV infection is closely related to the occurrence, development, treatment and prognosis of lymphoma. The treatment of EBV-positive lymphoma bases mainly on combined chemo-radiotherapy together with ganciclovir, acyclovir and other antiviral drugs. Also there are novel ways to treat EBV positive- lymphoma including CD70 monoclonal antibody, butyrate, etc. The only way to prevent EBV infection is to inoculate anti-viral vaccine. The criterion of treating EBV positive-lymphoma remains to be further investigated. Key words: Epstein-Barr virus; Lymphoma; Therapy

Characterization of Butyrate Uptake by Nontransformed Intestinal Epithelial Cell Lines

Butyrate (BT) is one of the main end products of anaerobic bacterial fermentation of dietary fiber within the human colon. Among its recognized effects, BT inhibits colon carcinogenesis. Our aim was to characterize uptake of BT by two nontransformed intestinal epithelial cell lines: rat small intestinal epithelial (IEC-6) and fetal human colonic epithelial (FHC) cells. Uptake of ¹⁴C-BT by IEC-6 cells was (1) time- and concentration-dependent; (2) pH-dependent; (3) Na+-, Cl⁻- and energy-dependent; (4) inhibited by BT structural analogues; (5) sensitive to monocarboxylate transporter 1 (MCT1) inhibitors; and (6) insensitive to DIDS and amiloride. IEC-6 cells express both MCT1 and Na+-coupled monocarboxylate transporter 1 (SMCT1) mRNA. We conclude that ¹⁴C-BT uptake by IEC-6 cells mainly involves MCT1, with a small contribution of SMCT1. Acute exposure to ethanol, acetaldehyde, indomethacin, resveratrol and quercetin reduced ¹⁴C-BT uptake. Chronic exposure to resveratrol and quercetin reduced ¹⁴C-BT uptake but had no effect on either MCT1 or SMCT1 mRNA levels. Uptake of ¹⁴C-BT by FHC cells was time- and concentration-dependent but pH-, Na+-, Cl⁻- and energy-independent and insensitive to BT structural analogues and MCT1 inhibitors. Although MCT1 (but not SMCT1) mRNA expression was found in FHC cells, the characteristics of ¹⁴C-BT uptake by FHC cells did not support either MCT1 or SMCT1 involvement. In conclusion, uptake characteristics of ¹⁴C-BT differ between IEC-6 and FHC cells. IEC-6 cells demonstrate MCT1- and SMCT1-mediated transport, while FHC cells do not.

The research of tumor necrosis factor-related apoptosis-inducing ligand in combination with sodium butyrate on hepatoma cell HepG2

Objective To investigate the inhibitory effects of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) combined with sodium butyrate (NaB) on hepatic carcinoma cell line HepG-2.Methods different concentrations of NaB( 1.0,2.5,5.0 mmol/L)and TRAIL ( 10,100,500,1000ng/ml) solely or combined with both added to the culture plates including HepG-2 suspension,inhibitory action of NaB and TRAIL on HepG-2 were Measured by MTT assays; The apoptotic rate of HepG-2 cells and the mRNA expressions of DR4 ,DR5 in HepG-2 cells were respectively detected by flow cytometry analysis and Real-time RT-PCR.Results By using different concentrations of TRAIL,the inhibitory rate of HepG-2 growth and HepG-2 apoptotic rate were ( 4.5 ± 1.3 ) % and 3.2 ± 0.7 ) % respectively,compared with control group,the differences were not significant statistically ( P ＞ 0.05 ).There was a dose-dependent inhibition of cell growth of HepG-2 by NaB ( P ＜ 0.05 ).The combination of the NaB and TRAIL can significantly increase the inhibitory rate of HepG-2 growth and HepG-2 apoptotic rate ( P ＜ 0.05 ).Expression level of DR5 mRNA of HepG-2 deal with NaB were higher than control group.Conclusion HepG-2 cells were resistant to apoptosis induced by TRAIL,NaB could enhance the sensitivity of Hep-2 cells to TRAIL by up-regulating the mRNA expressions of DR5 in HepG-2 cells. Key words: Apoptosis; TRAIL; Hepatoma; Sodium butyrate

Effects of sodium butyrate on proliferation of human oral squamous carcinoma cell line and expression of p27Kip1

To investigate the effect of sodium butyrate (NaB) on inhibition of human oral squamous carcinoma cell line. Human oral squamous carcinoma cell line Tca8113 was treated with different concentration of NaB. Light microscope was used to observe the morphological changes of the carcinoma cells. The cell cycle was analyzed by flow cytometry. Expression of p27(Kip1) was determined with immunocytochemical assay. NaB significantly inhibited the proliferation of Tca8113 in a time- and dose-dependent manner. Tca8113 cells treated with NaB was arrested in G(0)-G(1) phase. The fraction of cells in G(0)-G(1) were (63.2 ± 2.4)% and (77.2 ± 3.8)% after treated with NaB at the concentration of 2 and 4 mmol/L alternatively, whereas (48.1 ± 2.4)% in G(0)-G(1) phase were observed in control group (P < 0.05). The expression of p27(Kip1) was markedly up-regulated after being treated with NaB. NaB treatment can inhibit the growth of oral squamous carcinoma cell line in vitro and induce cell cycle arrest, which might be associated with the increased expression of p27(Kip1) protein.

Butyrate uptake and effect on proliferation, differentiation, viability and apoptosis of Caco‐2 cells: influence of polyphenols

The short‐chain fatty acid butyrate (BT) is one of the main end‐products of anaerobic bacterial fermentation of dietary fibre within the human colon. Among its recognized effects, BT is known to inhibit colon carcinogenesis. Polyphenols have several properties, including anti‐oxidant, anti‐carcinogenic and anti‐inflammatory activity. The aim of this study was to investigate the influence of some polyphenols upon the apical uptake of BT into human colonic adenocarcinoma Caco‐2 cells, and to evaluate their influence upon the effect of BT on proliferation, differentiation, viability and apoptosis.In the first part of the study, we demonstrated that MCT1‐mediated apical uptake of 14C‐BT in Caco‐2 cells is modulated by either acute or chronic exposure to some polyphenols, and that resveratrol acts as a competitive inhibitor of 14C‐BT uptake. In the second part of the study, we evaluated the effect of those polyphenols that chronically increased the apical uptake of 14C‐BT, alone or together with BT, on cell viability, cell proliferation, differentiation and apoptosis. In general, combination of polyphenols with BT did not significantly modify the changes in proliferation, differentiation, viability and apoptosis induced by BT alone. In conclusion, changes in uptake of BT induced by polyphenols do not correlate with changes on cell viability, cell proliferation, differentiation and apoptosis.

Deacetylase Inhibitor Cocktails Provide Striking Synergistic Interactions in Human Leukemia Cells.

Abstract 4404Cancer cells almost invariably exhibit aberrant histone deacetylase (HDAC) activity leading to changes in chromatine structure, altered gene expression, poor differentiation, impaired apoptosis and increased proliferation. Accordingly, virtually all the HDAC inhibitors currently available show some degree of antitumor activity in preclinical cancer models and several of these compounds are currently under investigation or already approved for the treatment of human malignancies. Such is the case of the hydroxamic acid derivative suberoylanilide hydroxamic acid (Vorinostat, Zolinza), approved for the treatment of cutaneous T cell lymphomas. Sirtuins are a large family of deacetylases characterized by a unique, NAD+-dependent enzymatic mechanism. In addition to their established role in metabolism and longevity, recent evidence points to an emerging role for sirtuins in carcinogenesis. In the attempt to identify drug combinations that would increase the activity of traditional HDAC inhibitors we have explored the combination of valproic acid (VA) and butyrate (BU) with the sirtuin inhibitors cambinol and sirtinol in primary B-cell chronic lymphocytic leukemia (B-CLL) cells (n=35), acute myelogenous leukemia (AML) cells (n=10) and leukemia cell lines. Cell viability was assessed by propidium iodide staining and flow cytometry. Combination indices were determined using the median-effect method. In leukemia cells, exposure to sirtuin inhibitors synergistically increased VA and BU mediated cytotoxicity. Conversely, these drugs were poorly active and failed to show any cooperation in healthy cells, including peripheral blood mononuclear cells and fibroblasts, suggesting a cancer-specific mode of action. Similar results were obtained by combining VA or BU with the Nampt inhibitor APO866, which reduces intracellular NAD+ levels and thereby prevents sirtuin activity. Remarkably, SIRT1 and SIRT6 inhibition per se did not seem to account for cell demise upon HDAC inhibition since expression of a dominant negative SIRT1 isoform or RNA interference-mediated SIRT6 silencing failed to increase VA and BU activity. Our data indicate a specific requirement by leukemia cells for sustained sirtuin activity when classical HDACs are inhibited. This feature is suitable to be therapeutically exploited by combining sirtuin inhibitors or APO866 with classical HDAC inhibitors especially for the treatment of hematological malignancies. Disclosures:No relevant conflicts of interest to declare.

The Influence of sodium butyrate on growth curve of bladder cancer cell and cell cycle

Objective To investigate the effect of sodium butyrate on growth of bladder cancer cells. Methods Make a comparison among the growth curve changes of BIU-87 cell and E-J cell of blad-der cancer after the interference of sodium butyrate with different concentrations by applying ~3H-TdR incor-poration test, and adopt flow cytometry to conduct a research on the influence of sodium butyrate on the cell cycle of bladder cancer. Results 1 mmol/L concentration group hasn't shown the restraint on BIU-87 cell and E-J cell in each observation time spots;the 5mmol/L and 10 mmol/L concentration groups have shown obvious growth restraint and the difference is significant (P<0.01); along with the rising sodium butyrate concentration,more and more BIU-87 cells and E-J cells are blocked in G_0/G_1 phrase. Conclu-sion The sodium butyrate restrain the growth of bladder cancer cells with concentration and time depend-ence,which is achieved through the cell cycle blockade in G_0/G_1 phrase. Key words: Bladder carcinoma; Sodium butyrate; Cell cycle

Transplantation of hepatocytes derived from mouse embryonic stem cells into liver-injured mouse liver

Objective To explore the feasibility of embryonic stem (ES) cells-derived hepatocyte transplantation into hver-injured mouse liver. Methods Mouse ES cells were induced to differentiate into hepatocytes using sodium butyrate and cholestatic serum. During the course of cell differentiation, cell mor-phological changes and hepatic-specific genes were detected. The resulting ES cells-derived hepatocytes were labelled with CFDA-SE followed by transplantation into liver-injured mouse liver. Then the recipient liver was removed,sliced,and immunofluorence staining of ALB was performed. The hver slice was examined u-sing confocal laser scanning microscopy. Results During the course of ES cell differentiation induced by so-chum butyate and cholestatic senun, numerous epithelial cells resembling hepatocytes were observed. Elec-tron micrographs revealed that the differentiated cells were rich in endoplasmic reticulum, ribosomes, mito-chondria,and glycogen,which were typical uhrastructural features of mature hepatocytes. RT-PCR analysis showed that these hepatocyte-like cells expressed hepatic-specific genes. Immunofluorence staining of ALB (red fluorence) showed that CFDA-SE labelled ES cells-derived hepatocytes (green fluorence) could settle down,proliferate in recipient liver,and no teratoma formation was found two weeks after transplantation.Conclusion In vivo transplantation of ES cells-derived hepatocytes into liver-injured mouse liver is feasible and safe,which may provide a new cell source for cell transplantation treatment in liver dieases. Key words: Embryonic stem cell; Hepatocyte; Differentiation; Transplantation

The role of IDO in T cell anergy of sodium butyrate-induced immature DC

Objective To investigate the role of indoleamine 2,3-dioxygense(IDO) in T cell an-ergy of the immature dendritic cells (DCs) induced by sodium butyrate. Methods Human monecyte-de-rived immature DCs were induced with granulocyte macrophage-colony stimulating factor (GM-CSF) and interleukin-4 (IL-4), and divided into 5 groups on the 6th day. Trizol was added to extract total RNA of each group after 24-h induction. IDO mRNA expression was detected by RT-PCR and real-time PCR. 1-methyl-tryptophan(1-MT) was also used to test mixed lymphocyte reaction in sodium butyrate-induced DCs. Cells were harvested after 96-h incubation and fluorescence intensity was detected by FCM. Results IDO mRNA expression in sodium butyrate group was significantly higher (0.84±0.01) than control group (0.55±0.01) and other mature groups (0.53±0.01) by RT-PCR. The result was further confirmed by real-time PCR. In comparison with the control group,the IDO mRNA expression of DCs was increased by (32.03±4.01) fold. The proliferation of lymphocytes was increased in sodium butyrate group with 1-MT by FCM,which suggested 1-MT may antagonize the inhibition of sodium butyrate-indueed lymphocyte pro-liferation. Conclusion Sodium butyrate may inhibit the lymphocyte proliferation by IDO that can degrada-te amino-indole propionic acid in microenvironment. Key words: Dendritic cell; Indoleamine 2,3-dioxygense; Immunotolerance

Modulation of butyrate uptake by Caco‐2 cells

The aim of this study was to investigate the putative influence of some pharmacological agents and drugs of abuse upon the apical uptake of butyrate (BT) by Caco‐2 cells. Apical uptake of 14C‐BT by Caco‐2 cells seems to involve MCT1‐mediated transport (it was time‐, concentration‐, pH‐ and energy‐dependent, Na+‐independent, Cl− ‐dependent, inhibited by several BT structural analogues, insensitive to anion exchange inhibitors and inhibited by monocarboxylate transport (MCT) inhibitors). Acutely, uptake of 14C‐BT (10 µM) was reduced by acetaldehyde (ACA), acetylsalicylic acid (ASA), indomethacin, caffeine and theophylline, and increased by MDMA. Chronically, it was increased by caffeine and decreased by tetrahydrocannabinol (THC) and MDMA; qRT‐PCR analysis showed that these three compounds decreased the mRNA levels of MCT1. Acutely, ACA, indomethacin and MDMA reduced the uptake of 14C‐BT (20 mM), and ASA increased it. Chronically, none of the compounds affected uptake. ACA, indomethacin and propionate seem to be competitive inhibitors of 14C‐BT uptake. ASA simultaneously increased the Km and the Vmax of 14C‐BT uptake. In conclusion, MCT1‐mediated transport of 14C‐BT in Caco‐2 cells is modulated by either acute or chronic exposure to some pharmacological agents and drugs of abuse (ACA, ASA, indomethacin, caffeine, theophylline and the drugs of abuse THC and MDMA).Supported by FCT (PTDC/SAU‐FCF/67805/2006)

Sodium butyrate enhances the IDO expression in immature dendritic cells to induce T cells anergy in vitro

Objective To investigate the expression of IDO in immature dendritic cells (DCs) induced by sodium butyrate and its effects on T cells immune reaction in vitro. Methods Human mono-cyte-derived immature DCs were induced with GM-CSF and IL-4 for 6 days,then supplemented with sodi-um butyrate, LPS and cytokines cocktail (TNF-α, IL-6, IL-1β, PGE2) respectively. DCs were harvested af-ter incubation for 24 h. The phenotype of DCs was detected by FCM, IDO mRNA expression by RT-PCR and quantitative real-time PCR,and IL-12 production by ELISA. Mixed lymphocyte reactions (MLR) be-tween DCs and allogeneic lymphocytes were performed to analyze the proliferative response of T cells. Re-suits The DCs induced by sodium butyrate still kept on typical characteristics of immature DCs.lowly ex-pressing CD83, CD80 and HLA-DR, producing low levels of IL-12, and having fewer effects on T cells pro-liferation. In eomparion to the control group, the IDO mRNA expression of DCs was increased by ( 32.03± 4.02 ) fold and (1.01 ± 0.43 ) fold in sodium butyrate and LPS groups, and decreased by (3.31 ± 1.07 ) fold in cocktail group respectively (P <0.01 ). The sodium butyrate induced-DCs could stimulate T cells proliferation effectively in the presence of 1-MT, an inhibitor of IDO, but their stimulating capabilities were still lower than those of the mature DCs induced by LPS or cocktail. Conclusion Sodium butyrate could obviously enhance the IDO expression in immature DCs,which might be a significant mechanism for sodi-um butyrate inducing immature DCs to induce T cells anergy. Key words: Sodium butyrate; Dendritic cell; Immune tolerance

Optimization of multi-factors co-induce of K562 cell into erythroid differentiation and analysis of gene and membrane protein expression of erythroid cell

Objective Optimization of the conditions to induce K562 cell into erythroid linage,and assessment of K562 cell erythroid differentiation potentiality by examining the expression of relevant gene and membrane protein.Method K562 cells were co-cultured with sodium butyrate,erythropoiehuman and hemin at the optimal concentrations.The morphology of the cells was observed by microscope and the hemoglobin content of K562 cells was monitored by benzidine staining.The abundance of P210 bcr/abl and eALAS mRNA,respectively representting granulocytic and erythroid lineages were used to evaluate the optimized induction.Further explore was performed by Reahime-PCR and flow cytometry to test 10 kinds of erythroid differentiation-related gene expression as well as some of erythroid membrane markers.Result The percentage of benzidine-positive cells induced by the optimized condition was up to 100%at 120 hours.Reahime-PCR showed the level of Spectrina,Spectrinβ,band3,eALAS,CD47,RhD,EPB4.2 was 14.52,22.87,26.53,8.05,14.58,2.71,3.48 fold respectively compared to the eontrol group,while that of the bcr/abl was 0.39 fold.The expression of three red cell membrane markers(CD47,band3 and RhD)were much higher than those of the controls(P<O.01)and the expression of GPA was negative.Conclusion K562 cells could stably differentiate into erythroid linage by the optimized cuhuration of multi-factors CO-induce.And all the cells were in good condition suitable for transgenic experiment in research on red blood cell disorders.Our findings also demonstrated that RhD expression was earlier than GPA at the stage of erythoid maturity so could be a reliably specific early-erythroid marker. Key words: K562 cells; erthyroid differentiation; the expression of gene and membrane protein

Modulation of butyrate transport in Caco-2 cells

The aim of this study was to investigate the putative influence of some pharmacological agents and drugs of abuse upon the apical uptake of butyrate (BT) into Caco-2 cells. The apical uptake of (14)C-BT by Caco-2 cells was (1) time and concentration dependent, (2) pH dependent, (3) Na(+) independent and Cl(-) dependent, (4) energy dependent, (5) inhibited by several BT structural analogues (acetate, propionate, alpha-ketobutyrate, pyruvate, lactate), (6) insensitive to the anion exchange inhibitors DIDS and SITS and (7) inhibited by the monocarboxylate transport (MCT) inhibitors NPPB and pCMB. These characteristics are compatible with an involvement of MCT1-mediated transport. Acutely, uptake of a low concentration of (14)C-BT (10 microM) was reduced by acetaldehyde, acetylsalicylic acid, indomethacin, caffeine and theophylline and increased by MDMA. Chronically, uptake was increased by caffeine and decreased by tetrahydrocannabinol and MDMA; reverse transcription quantitative real-time PCR analysis showed that these three compounds decreased the mRNA levels of MCT1. Acutely, acetaldehyde, indomethacin and MDMA reduced the uptake of a high concentration of (14)C-BT (20 mM), and acetylsalicylic acid increased it. Chronically, none of the compounds affected uptake. Acetaldehyde, indomethacin and propionate seem to be competitive inhibitors of (14)C-BT uptake. Acetylsalicylic acid simultaneously increased the K (m) and the V (max) of (14)C-BT uptake. In conclusion, MCT1-mediated transport of (14)C-BT in Caco-2 cells is modulated by either acute or chronic exposure to some pharmacological agents and drugs of abuse (acetaldehyde, acetylsalicylic acid, indomethacin, caffeine, theophylline and the drugs of abuse tetrahydrocannabinol and MDMA).

Histone deacetylase inhibitors upregulate p57Kip2 level by enhancing its expression through Sp1 transcription factor

Histone deacetylase inhibitors (HDACIs) represent a new class of targeted anticancer agents. Here, we evaluate the effects of butyrate (BuA) and other HDACIs on p57(Kip2), a cyclin-dependent kinase inhibitor (cki). We observed that inhibitors of class I/II histone deacetylases (HDACs), but not of class III HDACs, induce a remarkable accumulation of p57(Kip2) in several cells. The cki upregulation is associated with an increased gene expression that was not prevented by cycloheximide, indicating that HDACIs affect directly p57(Kip2) transcription. The characterization of p57(Kip2) promoter indicates that the first 165 bp are mostly involved in the BuA effects. Chromatin immunoprecipitation studies demonstrated that the BuA treatment causes the recruitment of Sp1 transcription factor. The Sp1 importance was confirmed by the reduction of BuA effects by mithramycin A (an Sp1 antagonist) and, most stringently, by Sp1 downregulation due to Sp1 siRNA. Moreover, both the treatments reduce the p57(Kip2) transcription in untreated cells, suggesting that Sp1 is required for the constitutive cki expression. Studies employing plasmids containing parts of the 165 bp of p57(Kip2) promoter indicate that the promoter region between -87 and -113 bp, which includes two putative Sp1 consensus sequences, plays a critical role in the response to HDACIs. Since this p57(Kip2) promoter region also embraces the consensus sequence for the transcriptional repressor chicken ovalbumin upstream promoter transcription factor-interacting protein 2 (CTIP2), we evaluated whether this factor is involved into the BuA effect. When CTIP2 was downregulated by a specific siRNA, we observed the enhancement of BuA activity on p57(Kip2) expression suggesting that CTIP2 might also be involved in HDACIs effects.

Genetic networks involved in the process of the cell differentiation induced by sodium butyrate in colonic epithelial cells

Genetic networks involved in the process of the cell differentiation induced by sodium butyrate in colonic epithelial cells

The effect of polyethylene glycol and butyrate on anastomotic healing in the rat colon

The use of mechanical bowel preparation is much debated. We evaluated the effects of polyethylene glycol (PEG), with or without a single dose of 3.0 mmol butyrate (BUT), on the bursting pressure (BP) of an intact colon segment and a colon anastomosis in rats. Also, histopathologic damage was studied. In rats without colectomy, the mean BP was 159.2 mmHg (SD=18.9) after PEG treatment and 116.7 mmHg (SD=27.5) in controls (p=0.001). In rats with colectomy, the mean BP was 90.4 mmHg (SD=45.9) in the PEG group, 108.0 mmHg (SD=31.9) in the BUT group, and 102.7 mmHg (SD=44.7) in controls (p=0.44). No significant differences in histopathologic scores were observed between rats treated with PEG and controls. PEG does not interfere with anastomotic healing in rats as measured by BP. No benefit of a single dose of butyrate was observed.

Purification and characterization of butyrate-induced protein phosphatase involved in apoptosis of Ehrlich ascites tumor cells

Short chain fatty acids including butyrate exhibit wide variety of biological effects towards cell growth, morphology and gene expression. In this report, we study the mechanism by which butyrate (BuA) modulates the expression of protein phosphatase when treated to the cells. As a model system, we used Ehrlich Ascites Tumor (EAT) cells in which BuA-treatment induces expression of a protein phosphatase enzyme. Subsequently, BuA-induced protein phosphatase has been biochemically purified and characterized. Further, pretreatment of caspase-3 inhibitor abolished the activity of BuA-induced protein phosphatase indicating the involvement of caspase-3 in the activation of BuA-induced protein phosphatase. In addition, the relationship between BuA-induced protein phosphatase and apoptosis has been verified. Activation of endonuclease-II has been shown in BuA-treated EAT cells and that activity was completely inhibited by sodium orthovanadate, a tyrosine phosphatase inhibitor suggesting that endonuclease-II may serve as a possible down-stream target for BuA-induced protein phosphatase. Together, the data suggest that activation of protein phosphatase may be an early and essential step in BuA-mediated apoptotic signaling pathway in EAT cells.

Influence of carnitine on buty rate metabolism of colonocytes in a rat model of experimental colitis

Influence of carnitine on buty rate metabolism of colonocytes in a rat model of experimental colitis