• Biomolecules & Therapeutics
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• v.27 no.2
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• pp.222-230
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• 2019

Intestinal barrier dysfunction always accompanies cirrhosis in patients with advanced liver disease and is an important contributor facilitating bacterial translocation (BT), which has been involved in the pathogenesis of cirrhosis and its complications. Several studies have demonstrated the protective effect of Vitamin D on intestinal barrier function. However, severe cholestasis leads to vitamin D depletion. This study was designed to test whether vitamin D therapy improves intestinal dysfunction in cirrhosis. Rats were subcutaneously injected with 50% sterile $CCl_4$ (a mixture of pure $CCl_4$ and olive oil, 0.3 mL/100 g) twice a week for 6 weeks. Next, $1,25(OH)_2D_3$ ($0.5{\mu}g/100g$) and the vehicle were administered simultaneously with $CCl_4$ to compare the extent of intestinal histologic damage, tight junction protein expression, intestinal barrier function, BT, intestinal proliferation, apoptosis, and enterocyte turnover. Intestinal heme oxygenase-1 (HO-1) expression and oxidative stress were also assessed. We found that vitamin D could maintain intestinal epithelial proliferation and turnover, inhibit intestinal epithelial apoptosis, alleviate structural damage, and prevent BT and intestinal barrier dysfunction. These were achieved partly through restoration of HO-1 and inhibition of oxidative stress. Taken together, our results suggest that vitamin D ameliorated intestinal epithelial turnover and improved the integrity and function of intestinal barrier in $CCl_4$-induced liver cirrhotic rats. HO-1 signaling activation was involved in these above beneficial effects.

• Journal of Animal Reproduction and Biotechnology
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• v.39 no.1
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• pp.2-11
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• 2024

Background: The small intestine plays a crucial role in animals in maintaining homeostasis as well as a series of physiological events such as nutrient uptake and immune function to improve productivity. Research on intestinal organoids has recently garnered interest, aiming to study various functions of the intestinal epithelium as a potential alternative to an in vivo system. These technologies have created new possibilities and opportunities for substituting animals for testing with an in vitro model. Methods: Here, we report the establishment and characterisation of intestinal organoids derived from jejunum tissues of adult pigs. Intestinal crypts, including intestinal stem cells from the jejunum tissue of adult pigs (10 months old), were sequentially isolated and cultivated over several passages without losing their proliferation and differentiation using the scaffold-based and three-dimensional method, which indicated the recapitulating capacity. Results: Porcine jejunum-derived intestinal organoids showed the specific expression of several genes related to intestinal stem cells and the epithelium. Furthermore, they showed high permeability when exposed to FITC-dextran 4 kDa, representing a barrier function similar to that of in vivo tissues. Collectively, these results demonstrate the efficient cultivation and characteristics of porcine jejunum-derived intestinal organoids. Conclusions: In this study, using a 3D culture system, we successfully established porcine jejunum-derived intestinal organoids. They show potential for various applications, such as for nutrient absorption as an in vitro model of the intestinal epithelium fused with organ-on-a-chip technology to improve productivity in animal biotechnology in future studies.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.4
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• pp.375-383
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• 2021

The intestinal barrier function disrupted in sepsis, while little is known about the variation in different phases of sepsis. In this study, mouse models of sepsis were established by caecal ligation and puncture (CLP). The H&E staining of sections and serum diamine oxidase concentration were evaluated at different timepoint after CLP. TUNEL assay and EdU staining were performed to evaluate the apoptosis and proliferation of intestinal epithelium. Relative protein expression was assessed by Western blotting and serum concentrations of pro-inflammatory cytokines was measured by ELISA. The disruption of intestinal barrier worsened in the first 24 h after the onset of sepsis and gradually recovered over the next 24 h. The percentage of apoptotic cell increased in the first 24 h and dropped at 48 h, accompanied with the proliferative rate of intestinal epithelium inhibited in the first 6 h and regained in the later period. Furthermore, the activity of nuclear factor kappa B (NF-κB) presented similar trend with the intestinal barrier function, shared positive correction with apoptosis of intestinal epithelium. These findings reveal the conversion process of intestinal barrier function in sepsis and this process is closely correlated with the activity of NF-κB signaling.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.24
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• pp.10971-10975
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• 2015

Objective: To investigate bladder and intestinal function recovery and quality of sexual life after laparoscopic nerve-sparing radical hysterectomy (LNRH) for treatment of early invasive cervical carcinoma. Methods: Subjects included patients who underwent radical hysterectomy by laparotomy who were randomly assigned to 2 groups: 30 patients who underwent LNRH and 35 classical laparoscopic radical hysterectomy (LRH). We assessed the patients general clinical information, surgical characteristics, pathological findings, and adjuvant therapies. A urodynamic study was used to assess bladder function. Intestinal function recovery and quality of sexual life were evaluated by questionnaire. Results: No significant differences were found in age, surgery characteristics, pathological findings, adjuvant therapies, and main adverse effects between the 2 groups. The mean duration of the postoperative catheterization (DPC) in group LNRH was shorter than that in group LRH (P < 0.001). The maximum flow rate, maximum cystometric capacity, maximum detrusor pressure and urinary complications in group LNRH were better than those in group LRH. The quality of sexual life evaluated according to the female sexual function index (FSFI) was better in group LNRH than in those who underwent LRH. The intestinal function of patients in group LNRH also recovered better compared with patients in group LRH.

• Journal of Korean Medical classics
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• v.37 no.1
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• pp.25-39
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• 2024

Objectives : This paper focuses on recent research related to the relationship between 'Pizhuweiwei(脾主爲衛)' and intestinal flora, and suggests Korean Medical treatment methods that can treat and prevent diseases related to Spleen Deficiency(脾虛) such as ulcerative colitis, atrophic gastritis, diabetes, and obesity that is prevalent today. Methods : This study summarizes recent research results based on various literature on the relationship between the spleen and intestinal flora. Results : Polysaccharides contained in Jianpi herbs(健脾藥) have the effect of increasing beneficial bacteria and maintaining the diversity of intestinal microorganisms to improve intestinal function, managing intestinal metabolites to improve the body's immune function, and regulating the intestinal immune defense system. Therefore, based on the theory of 'Pizhuweiwei(脾主爲衛)', if the symptoms are treated through the spleen with Spleen-strengthening herbal medicinals, it could provide a substantial starting point for improving immunity. Conclusions : Polysaccharides contained in Jianpi herbs(健脾藥) could be considered as potential probiotics based on research findings which show that polysaccharides can regulate the intestinal flora and strengthen weak spleen, playing an important role.

• Asian-Australasian Journal of Animal Sciences
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• v.14 no.1
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• pp.54-60
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• 2001

A study was conducted to assess the nutritive value of two diets based on a low-energy variety of wheat, RAC C1 and their effects on intestinal mucosal structure and function in broiler chickens. The diets were fed with or without microbial enzyme supplement to male and female broiler chickens. The digesta viscosity was reduced (p<0.001) through supplementation with a microbial enzyme in male and female chicks. Enzyme supplementation also improved the dietary apparent metabolizable energy content (p<0.001) and had slight but non-significant positive effects on chick growth and feed conversion ratio. Intestinal mucosal structure and enzyme function were not affected by microbial enzyme supplement. Male chicks consumed more feeds (p<0.001), attained higher final body weight (p<0.001) and were more efficient at feed utilization (p<0.01) than the female chicks. Except for duodenal villus surface area and ileal protein content, intestinal mucosal structure and enzyme activities were similar between the two sexes and dietary treatment groups. The study showed an improvement in the nutritive value of the diets in the presence of the microbial enzyme supplement.

• Korean Journal of Pharmacognosy
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• v.50 no.1
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• pp.37-45
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• 2019

Portulaca oleracea L. (PL) has been used in traditional medicine herb for treatment of various diseases, such as diarrhea, dysentery, and skin inflammation. Previous studies have shown that the PL regulates the inflammation by inhibition of pro-inflammatory cytokines. Although PL might have improvement effects of intestinal function and bioactive effects, there are not enough studies to demonstrate. This study investigated the effects of KDC16-2 on the improvement of intestinal function and anti-inflammatory effects in vivo and in vitro. The improvement effect of intestinal function was measured fecal amount, water content and intestinal transit rate in KDC16-2 treated ICR mice. As results, compared with the control group, the KDC16-2 group showed a significant increase in wet fecal weight, dry fecal weight and fecal water content. The intestinal transit rate of KDC16-2 group was significantly increased. Based on the results, KDC16-2 is considered to have effects on improving intestinal function. The effect of anti-inflammatory demonstrated by using dextran sulfate sodium (DSS)-induced colitis mice. The mice were administered 3% DSS along with KDC16-2 (100, 300 mg/kg) for 14 days. DSS-induced colitis mice were significantly ameliorated in KDC16-2 treated group, including body weight loss, colon length shortening, tight junction protein of colon and histological colon injury. The levels of inflammatory mediators (IgG2a, IgA, C-reactive protein and Myeloperoxidase) and pro-inflammatory cytokines (tumor necrosis factor (TNF)-${\alpha}$, Interleukin (IL)-6) which are involved in inflammatory responses were increased in the DSS-treated group as compared to those in the control group, and the levels were significantly decreased in the KDC16-2 groups. In addition, we investigated the impact of KDC16-2 on lipopolysaccharide (LPS)-induced inflammatory responses in J774A.1 cells. KDC16-2 inhibited production of prostaglandin E2 (PGE2) and reactive oxygen species (ROS). These results suggested that the KDC16-2 could effectively alleviate the dysfunction of intestinal and inflammatory mediators. Thus, these KDC16-2 can be potentially used as health functional food of intestinal.

• IMMUNE NETWORK
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• v.22 no.6
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• pp.46.1-46.25
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• 2022

T-helper-17 (Th17) cells and related IL-17-producing (type17) lymphocytes are abundant at the epithelial barrier. In response to bacterial and fungal infection, the signature cytokines IL-17A/F and IL-22 mediate the antimicrobial immune response and contribute to wound healing of injured tissues. Despite their protective function, type17 lymphocytes are also responsible for various chronic inflammatory disorders, including inflammatory bowel disease (IBD) and colitis associated cancer (CAC). A deeper understanding of type17 regulatory mechanisms could ultimately lead to the discovery of therapeutic strategies for the treatment of chronic inflammatory disorders and the prevention of cancer. In this review, we discuss the current understanding of the development and function of type17 immune cells at the intestinal barrier, focusing on the impact of microbiota-immune interactions on intestinal barrier homeostasis and disease etiology.

• CELLMED
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• v.13 no.5
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• pp.21.1-21.4
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• 2023

Objective: A case report on the improvement of patients with intestinal metaplasia by Ortho-Cellular Nutrition Therapy (OCNT). Methods: A 55-year-old Korean male suffering from the symptoms of the reduced digestive function, bloating, and hypoacidity. Results: The severity of the symptoms improved after Ortho-Cellular Nutrition Therapy (OCNT), and the patient was finally cured of intestinal metaplasia. Conclusion: Ortho-Cellular Nutrition Therapy (OCNT) is effective in relieving the symptoms of patients with intestinal metaplasia.

• Biomolecules & Therapeutics
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• v.29 no.2
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• pp.175-183
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• 2021

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.