A wide variety of drugs and endogenous bioactive amines are organic cations (OCs). Approximately 40% of all conventional drugs on the market are OCs. Thus, the transport of xenobiotics or endogenous OCs in the body has been a subject of considerable interest, since the discovery and cloning of a family of OC transporters, referred to as organic cation transporter (OCTs), and a new subfamily of OCTs, OCTNs, leading to the functional characterization of these transporters in various systems including oocytes and some cell lines. Organic cation transporters are critical in drug absorption, targeting, and disposition of a drug. In this review, the recent advances in the characterization of organic cation transporters and their distribution in the small intestine are discussed. The results of the in vitro transport studies of various OCs in the small intestine using techniques such as isolated brush-border membrane vesicles, Ussing chamber systems and Caco-2 cells are discussed, and in vivo knock-out animal studies are summarized. Such information is essential for predicting pharmacokinetics and pharmacodynamics and in the design and development of new cationic drugs. An understanding of the mechanisms that control the intestinal transport of OCs will clearly aid achieving desirable clinical outcomes.
Yousef, Amany I;El-Masry, Omar S;Abdel Mohsen, Mohamed A
Asian Pacific Journal of Cancer Prevention
/
v.17
no.2
/
pp.743-748
/
2016
Background: $K^-Ras$ activation is an early event in colorectal carcinogenesis and associated mutations have been reported in about 40% of colorectal cancer patients. These mutations have always been responsible for enhancing malignancy and silencing them is associated with attenuation of tumorigenicity. Among downstream effectors are the RAF/MEK/ERK and the PI3K/Akt signaling pathways. PI3K/Akt signaling leads to reduction of apoptosis, stimulated cell growth and enhanced proliferation. Ellagic acid (EA), a naturally occurring antioxidant, has recently emerged as a promising anti-cancer agent. Purpose: To evaluate the impact of cellular genetic makeup of two colon cancer cell lines with different genetic backgrounds, HCT-116 ($K^-Ras^-/p53^+$) and Caco-2 ($K^-Ras^+/p53^-$), on response to potential anti-tumour effects of EA. In addition, the influence of $K^-Ras$ silencing in HCT-116 cells was investigated. Materials and Methods: Cellular proliferation, morphology and cell cycle analysis were carried out in addition to Western blotting for detecting total Akt and p-Akt (at Thr308 and Ser473) in the presence and absence of different concentrations of EA. Cell proliferation was also assessed in cells transfected with different concentrations of $K^-Ras$ siRNA or incubated with ellagic acid following transfection. Results: The results of the present study revealed that EA exerts anti-proliferative and dose-dependent pro-apoptotic effects. Cytostatic and cytotoxic effects were also observed. p-Akt (at Thr308 and Ser473) was downregulated. Moreover, EA treatment was found to (i) reduce $K^-Ras$ protein expression; (ii) in cells transfected with siRNA and co-treated with EA, pronounced anti-proliferative effects as well as depletion of p-Akt (at Thr308) were detected. Conclusions: Cellular genetic makeup ($K^-Ras^-/p53^-$) was not likely to impose limitations on targeting EA in treatment of colon cancer. EA had a multi-disciplinary pro-apoptotic anti-proliferative approach, having inhibited Akt phosphorylation, induced cell cycle arrest and showed an anti-proliferative potential in HCT-116 cells (expressing mutant $K^-Ras$).
Kim, Min Ju;Kim, Min Seo;Kang, Sung Tae;Kim, Ji Yeon
Journal of Applied Biological Chemistry
/
v.60
no.4
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pp.321-326
/
2017
We aimed to assess the potential growth-promoting effects of ginger and cinnamon mixtures (GCM) on intestinal bacteria and their anti-inflammatory effects in a cellular model of intestinal inflammation. Bifidobacterium longum, Lactobacillus sp., and Lactobacillus acidophilus served as intestinal bacteria. Further, in the inflammatory co-culture model, Caco-2 cells co-cultured with RAW264.7 cells were treated with GCM before the addition of lipopolysaccharide (LPS) to induce inflammation in RAW264.7 cells. Addition of GCM to modified Eggerth Gagnon media at a ginger:cinnamon ratio of 1:5 increased the growth of B. longum, Lactobacillus sp., and L. acidophilus compared to that of the control. In a cellular model, compared to LPS-treated groups, GCM-treated groups maintained high transepithelial electrical resistance at ginger:cinnamon ratios of 1:1, 1:3, 1:5, and 1:7 and decreased the tight junction permeability at 3:1, 1:1, 1:3, and 1:5 ratios, similar to that shown by the control groups. In addition, GCM-treated groups showed decreased levels of nitrite at 1:1, 1:5, and 1:7 ginger:cinnamon ratios. Based on these results, it can be concluded that among the various combinations of GCM, the ginger:cinnamon ratio of 1:5 is the optimal composite ratio that shows positive effects on the intestinal beneficial bacteria and in anti-inflammation.
To evaluate the effects of lactic acid bacteria (LAB) on Peyer's patch cells, mice were treated with a high dose of kanamycin to disturb the gut microbial environment. The overarching goal was to explore the potential of LAB for use as a dietary probiotic that buffers the negative consequences of antibiotic treatment. In vitro, LAB stimulated the production of immunoglobulin A (IgA) from isolated Peyer's patch cells. Inflammation-related genes (TNF-α, IL-1β, and IL-8) were up-regulated in Caco-2 cells stimulated with lipopolysaccharide (LPS), while tight-junction-related genes (ZO-1 and occludin) were down-regulated; the effects of LPS on inflammatory gene and tight-junction gene expression were reversed by treatment with LAB. Mice treated with a high dose of kanamycin showed increased serum IgE levels and decreases in serum IgA and fecal IgA levels; the number of Peyer's patch cells decreased with kanamycin treatment. However, subsequent LAB treatment was effective in reducing the serum IgE level and recovering the serum IgA and fecal IgA levels, as well as the number of Peyer's patch cells. In addition, ZO-1 and occludin mRNA levels were up-regulated in the ileum tissues of mice receiving LAB treatment. Lactic acid bacteria can enhance the intestinal immune system by improving the integrity of the intestinal barrier and increasing the production of IgA in Peyer's patches. Lactic acid bacteria should be considered a potential probiotic candidate for improving intestinal immunity, particularly in mitigating the negative consequences of antibiotic use.
Intestinal epithelial cell (IEC) apoptosis induced by hypoxia compromise intestinal epithelium barrier function. Both Akt and Hsp90 have cytoprotective function. However, the specific role of Akt and $Hsp90{\beta}$ in IEC apoptosis induced by hypoxia has not been explored. We confirmed that hypoxia-induced apoptosis was reduced by $Hsp90{\beta}$ overexpression but enhanced by decreasing $Hsp90{\beta}$ expression. $Hsp90{\beta}$ overexpression enhanced BAD phosphorylation and thus reduced mitochondrial release of cytochrome C. Reducing $Hsp90{\beta}$ expression had opposite effects. The protective effect of $Hsp90{\beta}$ against apoptosis was negated by LY294002, an Akt inhibitor. Further study showed that Akt phosphorylation was enhanced by $Hsp90{\beta}$, which was not due to the activation of upstream PI3K and PDK1 but because of stabilization of pAkt via direct interaction between $Hsp90{\beta}$ and pAkt. These results demonstrate that $Hsp90{\beta}$ may play a significant role in protecting IECs from hypoxia-induced apoptosis via stabilizing pAkt to phosphorylate BAD and reduce cytochrome C release.
The mitogen-activated protein kinase (MAPK) pathway controls intestinal epithelial barrier permeability by regulating tight junctions (TJs) and epithelial cells damage. Heme oxygenase-1 (HO-1) and carbon monoxide (CO) protect the intestinal epithelial barrier function, but the molecular mechanism is not yet clarified. MAPK activation and barrier permeability were studied using monolayers of Caco-2 cells treated with tissue necrosis factor α (TNF-α) transfected with FUGW-HO-1 or pLKO.1-sh-HO-1 plasmid. Intestinal mucosal barrier permeability and MAPK activation were also investigated using carbon tetrachloride (CCl4) administration with CoPP (a HO-1 inducer), ZnPP (a HO-1 inhibitor), CO releasing molecule 2 (CORM-2), or inactived-CORM-2-treated wild-type mice and mice with HO-1 deficiency in intestinal epithelial cells. TNF-α increased epithelial TJ disruption and cleaved caspase-3 expression, induced ERK, p38, and JNK phosphorylation. In addition, HO-1 blocked TNF-α-induced increase in epithelial TJs disruption, cleaved caspase-3 expression, as well as ERK, p38, and JNK phosphorylation in an HO-1-dependent manner. CoPP and CORM-2 directly ameliorated intestinal mucosal injury, attenuated TJ disruption and cleaved caspase-3 expression, and inhibited epithelial ERK, p38, and JNK phosphorylation after chronic CCl4 injection. Conversely, ZnPP completely reversed these effects. Furthermore, mice with intestinal epithelial HO-1 deficient exhibited a robust increase in mucosal TJs disruption, cleaved caspase-3 expression, and MAPKs activation as compared to the control group mice. These data demonstrated that HO-1-dependent MAPK signaling inhibition preserves the intestinal mucosal barrier integrity by abrogating TJ dysregulation and epithelial cell damage. The differential targeting of gut HO-1-MAPK axis leads to improved intestinal disease therapy.
Mechesso, Abraham F.;Quah, Yixian;Park, Seung-Chun
Journal of Ginseng Research
/
v.45
no.1
/
pp.75-85
/
2021
Background: Invasive infections due to foodborne pathogens, including Salmonella enterica serovar Typhimurium, are prevalent and life-threatening. This study aimed to evaluate the effects of ginsenoside Rg3 (Rg3) on the adhesion, invasion, and intracellular survival of S. Typhimurium. Methods: The impacts of Rg3 on bacterial growth and host cell viability were determined using the time kill and the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assays, respectively. Gentamicin assay and confocal microscopic examination were undertaken to determine the effects of Rg3 on the adhesive and invasive abilities of S. Typhimurium to Caco-2 and RAW 264.7 cells. Quantitative reverse transcription polymerase chain reaction was performed to assess the expression of genes correlated with the adhesion, invasion, and virulence of S. Typhimurium. Results: Subinhibitory concentrations of Rg3 significantly reduced (p < 0.05) the adhesion, invasion, and intracellular survival of S. Typhimurium. Rg3 considerably reduced (p < 0.05) the bacterial motility as well as the release of nitrite from infected macrophages in a concentration-dependent manner. The expression of genes related to the adhesion, invasion, quorum sensing, and virulence of S. Typhimurium including cheY, hilA, OmpD, PrgK, rsgE, SdiA, and SipB was significantly reduced after Rg3 treatment. Besides, the compound downregulated rac-1 and Cdc-42 that are essential for actin remodeling and membrane ruffling, thereby facilitating Salmonella entry into host cells. This report is the first to describe the effects of Rg3 on "trigger" entry mechanism and intracellular survival S. Typhimurium. Conclusion: Rg3 could be considered as a supplement agent to prevent S. Typhimurium infection.
Osman, Mohamed E.;El-nasr, Amany A. Abo;Hussein, Hagar M;Hamed, Moaz M
Microbiology and Biotechnology Letters
/
v.50
no.2
/
pp.255-269
/
2022
Actinomycetes isolated from marine habitats represent a promising source of bioactive substances. Here, we report on the isolation, identification, productivity enhancement and application of the bioactive compounds of Streptomyces qinglanensis H4. Eighteen marine actinomycetes were isolated and tested for resistance to seven bacterial diseases. Using 16S rRNA sequencing analysis (GenBank accession number MW563772), the most powerful isolate was identified as S. qinglanensis. Although the strain produced active compound(s) against a number of Gram-negative and Gram-positive bacteria, it failed to inhibit pathogenic fungi. The obtained inhibition zones were 22.0 ± 1.5, 20.0 ± 1, 16.0 ± 1, 12.0 ± 1, 22.0 ± 1 and 24.0 ± 1 mm against Bacillus subtilis ATCC 6633, Escherichia coli ATCC 19404, Enterococcus faecalis ATCC 29212, Pseudomonas aeruginosa ATCC 9027, Candida albicans ATCC 10231 and Staphylococcus aureus ATCC6538, respectively. To maximize bioactive compound synthesis, the Plackett-Burman design was used. The productivity increased up to 0.93-fold, when S. qinglanensis was grown in optimized medium composed of: (g/l) starch 30; KNO3 0.5; K2HPO4 0.25; MgSO4 0.25; FeSO4·7H2O, 0.01; sea water concentration (%) 100; pH 8.0, and an incubation period of 9 days. Moreover, the anticancer activity of S. qinglanensis was tested against two different cell lines: HepG2 and CACO. The inhibition activities were 42.96 and 57.14%, respectively. Our findings suggest that the marine S. qinglanensis strain, which grows well on tailored medium, might be a source of bioactive substances for healthcare companies.
Kim, Dong-Myung;Kim, Seong-Ho;Lee, Jin-Man;Kim, Ji-Eun;Kang, Sun-Chul
Applied Biological Chemistry
/
v.48
no.2
/
pp.132-139
/
2005
The major obstacle in the popularization of Chungkookjang is the short shelf-life of $2{\sim}3$ months and some problems concerning storage including the growth of molds even in the products even within shelf-life. To solve these problems we conducted a research to improve its storage by using the vacuumed packaging and sanitary method through seed culture, innoculation and sterilization. For the optimization of storage time, temperature and sterilization temperature, we measured viable cell numbers of bacteria and fungi, amount of gas outbreak and contents of amino type nitrogen and monitored these experimental results by response surface methodology of SAS program, so that we could observe the quality changes of Chungkookjang during shelf-life. Especially fungi, which are the biggest troublemaker in Chungkookjang shelf-life, couldn't be detected from the generally and vacuum-packed samples; also, viable cell numbers were highly influenced by sterilization temperature and in vacuum-packed samples. In the case of vacuum-packed samples, amount of gas outbreak was highly influenced by sterilization temperature of its storage conditions and it was higher in generally packed samples as compared to vacuum-packed samples even at any storage conditions. The changes of pH in generally and vacuum-packed samples were highly influenced by the storage temperature. As the temperatures of storage and sterilization were higher and the storage time was longer, so the amount of gas outbreak was accordingly lower. These results showed that amino type nitrogen contents in generally and vacuum-packed samples were systematically influenced by the temperature, storage time and sterilization temperature. Also the result showed that the change of amino type nitrogen contents during storage was less in vacuum-packed samples than in general ones. Based on the above results, we can produce Chungkookjang products with extended shelf-life of as far as 6 months without any quality change using sanitary manufacturing method, vacuumed packaging condition, sterilization in $70^{\circ}C$ for 60 minutes and storage under $10^{\circ}C$ during shelf-life. According to this research, we have the possibility to greatly increase the goods value of Chungkookjang by developing the manufacture processing and packaging.
Dextran-5-aminosalicylic acid conjugate (dextran-5-ASA) was in vitro-evaluated as a polymeric colon-spe-cific prodrug of 5-aminosalicylic acid (5-ASA). Chemical stability of dextran-5-ASA in the pH 1.2 or 6.8 buffer solutions was investigated at 37 for 6 hrs. The dextran backbone was not degraded and no 5-ASA release was detected. Moreover, dextran-5-ASA neither liberated 5-ASA in the homogenates of the small intestine of rats nor was transported across Caco-2 cell monolayers, suggesting no significant loss of dextran-5-ASA during transit through the upper intestine. Furthermore, incubation of dextran-5-ASA in 10% cecal contents of rats released about 37% and 55% of 5-ASA bound to dextran in 8 hr and 24 hr, respectively. While that with either esterase or dextranase failed to liberate 5-ASA from the polymeric prodrug, incubation of dextran-5-ASA with both esterases and dextranse released 5-ASA up to about 24% of 5-ASA bound to dextran. These results suggest that, after oral administration of dextran-5-ASA, the polymeric prodrug is delivered specifically to and releases 5-ASA in the large intestine, and reveal that the 5-ASA release by cleavage of the ester bond requires precedent depolymerization of the dextran backbone.
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