• The Korean Journal of Physiology and Pharmacology
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• 제22권3호
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• pp.269-275
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• 2018

$Na^+/H^+$ exchangers (NHEs) have been shown to be involved in regulating cell volume and maintaining fluid and electrolyte homeostasis. Pooled evidences have suggested that loss of $Na^+/H^+$ exchanger isoform 8 (NHE8) impairs intestinal mucosa. Whether NHE8 participates in the pathology of infectious colitis is still unknown. Our previous study demonstrated that somatostatin (SST) could stimulate the expression of intestinal NHE8 so as to facilitate $Na^+$ absorption under normal condition. This study further explored whether NHE8 participates in the pathological processes of infectious colitis and the effects of SST on intestinal NHE8 expression in the setting of infectious colitis. Our data showed that NHE8 expression was reduced in Citrobacter rodentium (CR) infected mice. Up-regulation of NHE8 improved diarrhea symptom and mucosal damage induced by CR. In vitro, a similar observation was also seen in Enteropathogenic E. coli (EPEC) infected Caco-2 cells. Seglitide, a SST receptor (SSTR) 2 agonist, partly reversed the inhibiting action of EPEC on NHE8 expression, but SSTR5 agonist (L-817,818) had no effect on the expression of NHE8. Moreover, SST blocked the phosphorylation of p38 in EPEC-infected Caco-2 cells. Taken together, these results suggest that enhancement of intestinal NHE8 expression by SST could ameliorate the symptoms of mice with infectious colitis.

• Molecules and Cells
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• 제38권12호
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• pp.1079-1085
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• 2015

Originally, activins were identified as stimulators of FSH release in reproduction. Other activities, including secondary axis formation in development, have since been revealed. Here, we investigated the influence of activin ${\beta}_A$ on the body, including the gastro-intestinal (GI) tract. Initially, the activin ${\beta}_A$ protein was detected in the serum proportional to the amount of pCMV-rAct plasmid injected. The induced level of activin ${\beta}_A$ in muscle was higher in female than male mice. Subsequent results revealed that stomach and intestine were severely damaged in pCMV-rAct-injected mice. At the cellular level, loss of parietal cells was observed, resulting in increased pH within the stomach. This phenomenon was more severe in male than female mice. Consistent with damage of the stomach and intestine, activin ${\beta}_A$ often led to necrosis in the tip of the tail or foot, and loss of body weight was observed in pCMV-rAct-injected male but not female mice. Finally, in pCMV-rAct-injected mice, circulating activin ${\beta}_A$ led to death at supraphysiological doses, and this was dependent on the strain of mice used. Taken together, these results indicate that activin ${\beta}_A$ has an important role outside of reproduction and development, specifically in digestion. These data also indicate that activin ${\beta}_A$ must be controlled within a narrow range because of latent lethal activity. In addition, our approach can be used effectively for functional analysis of secreted proteins.

• Gut and Liver
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• 제12권6호
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• pp.682-693
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• 2018

Background/Aims: Intestinal barrier dysfunction is a hallmark of inflammatory bowel diseases (IBDs) such as ulcerative colitis. This dysfunction is caused by increased permeability and the loss of tight junctions in intestinal epithelial cells. The aim of this study was to investigate whether estradiol treatment reduces colonic permeability, tight junction disruption, and inflammation in an azoxymethane (AOM)/dextran sodium sulfate (DSS) colon cancer mouse model. Methods: The effects of $17{\beta}$-estradiol (E2) were evaluated in ICR male mice 4 weeks after AOM/DSS treatment. Histological damage was scored by hematoxylin and eosin staining and the levels of the colonic mucosal cytokine myeloperoxidase (MPO) were assessed by enzyme-linked immunosorbent assay (ELISA). To evaluate the effects of E2 on intestinal permeability, tight junctions, and inflammation, we performed quantitative real-time polymerase chain reaction and Western blot analysis. Furthermore, the expression levels of mucin 2 (MUC2) and mucin 4 (MUC4) were measured as target genes for intestinal permeability, whereas zonula occludens 1 (ZO-1), occludin (OCLN), and claudin 4 (CLDN4) served as target genes for the tight junctions. Results: The colitis-mediated induced damage score and MPO activity were reduced by E2 treatment (p<0.05). In addition, the mRNA expression levels of intestinal barrier-related molecules (i.e., MUC2, ZO-1, OCLN, and CLDN4) were decreased by AOM/DSS-treatment; furthermore, this inhibition was rescued by E2 supplementation. The mRNA and protein expression of inflammation-related genes (i.e., KLF4, NF-${\kappa}B$, iNOS, and COX-2) was increased by AOM/DSS-treatment and ameliorated by E2. Conclusions: E2 acts through the estrogen receptor ${\beta}$ signaling pathway to elicit anti-inflammatory effects on intestinal barrier by inducing the expression of MUC2 and tight junction molecules and inhibiting pro-inflammatory cytokines.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• 제7권2호
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• pp.239-242
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• 2004

저자들은 만성적이고 반복적인 복통을 호소하는 13세 여아에서 호산구성 위장관염 1례를 경험하여 보고하는 바이다.

• 대한핵의학회지
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• 제30권1호
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• pp.118-125
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• 1996

Scrub typhus의 발현증상에는 저알부민혈증, 단백뇨, 전신 부종 등을 들 수 있다. 그러나, 저알부민혈증에 비해 단백뇨와 부종 등은 심하지 않은 경우가 많다. 본 연구에서는 저알부민혈증이 장내에서의 단백질 소실에 의한 것인지를 확인하고자 하였다. Scrub typhus가 의심되는 25명의 환자를 대상으로 (1) 저알부민혈증의 원인 장내 단백질 소실에 의한 것인지 여부와 (2) $^{99m}Tc$-HSA 신티그램의 진단적 유용성을 알아보고자 하였다. 신티그램은 혈청학적 검사상 Scrub typhus로 확인된 18명의 환자에서 (13예는 항생제 치료 개시후 1일에서 8일 사이에, 5예는 치료 전에 시행하였으며, 11예에서는 대변에서 alpha-1- antitrypsin (${\alpha}AT$)배설 여부를 확인하였다. 촬영방법은 $^{99m}Tc$-HSA 30mCi를 정맥 주사한 후, 2, 4, 6, 24시간에 복부 전면상을 얻었다. 판정은 소장과 대장의 주행 위치에서의 혈관외 방사능 소견을 장내 단백질 소실로 간주하였다. 13예에서 양성으로 판정하였는데, 이중 8예는 대변에서의 ${\alpha}AT$치도 높게 나왔다. 신티그램상 음성을 보인 5예중 2예에서는 대변중 ${\alpha}AT$치가 매우 높게 나왔는데 그 이유는 신티그램 검사는 치료 도중에 하였고, 대변 검사는 치료 전에 하였기 때문인 것으로 간주하였다. 결론적으로 전체 18예중 15예에서 신티그램이나 대변검사로 Scrub typhus로 진단하였다. 한편, 13예 (72%)에서 저알부민혈증을 보였는데 이중 4예는 장내단백질 소실과 단백뇨를, 5예는 장내단백질 소실만을, 3예에서는 단백뇨만을 보였고, 1예는 아무 소견이 없었다. 요약하면, 장내단백질 소실 소견은 Scrub typhus환자의 83%에서 보여, 혈중 알부민치가 저하되는 원인으로 추정된다. 따라서 $^{99m}Tc$-HSA 신티그램은 장내단백질 소실의 진단에 매우 유용한 검사방법이다. 또한, 검사방법이 다소 어렵지만 대변에서의 ${\alpha}AT$측정도 동위원소 검사상 음성 소견을 보이는 환자에게는 어느 정도 진단에 도움을 주리라 보여진다.

• Asian Pacific Journal of Cancer Prevention
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• 제15권7호
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• pp.2987-2991
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• 2014

Connexin 43 is an important gap junction protein in vertebrates and is known for its tumor suppressive properties. Cx43 is abundantly expressed in the human intestinal epithelial cells and muscularis mucosae. To explore the role of Cx43 in the genesis of human colon cancer, we performed the expression analysis of Cx43 in 80 cases of histopathologically confirmed and clinically diagnosed human colon cancer samples and adjacent control tissue and assessed correlations with clinicopathological variables. Western blotting using anti-Cx43 antibody indicated that the expression of Cx43 was significantly down regulated (75%) in the cancer samples as compared to the adjacent control samples. Moreover, immunohistochemical analysis of the tissue samples confirmed the down regulation of the Cx43 in the intestinal epithelial cells. Cx43 down regulation showed significant association (p<0.05) with the histological type and tumor invasion properties of the cancer. Our data demonstrated that loss of Cx43 may be an important event in colon carcinogenesis and tumor progression, providing significant insights about the tumor suppressive properties of the Cx43 and its potential as a diagnostic marker for colon cancer.

• Journal of Gastric Cancer
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• 제14권3호
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• pp.147-155
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• 2014

Homeostatic imbalance between cell proliferation and death in gastric mucosal epithelia may lead to gastritis and gastric cancer. Despite abundant gastrokine 1 (GKN1) expression in the normal stomach, the loss of GKN1 expression is frequently detected in gastric mucosa infected with Helicobacter pylori, as well as in intestinal metaplasia and gastric cancer tissues, suggesting that GKN1 plays an important role in gastric mucosal defense, and the gene functions as a gastric tumor suppressor. In the stomach, GKN1 is involved in gastric mucosal inflammation by regulating cytokine production, the nuclear factor-${\kappa}B$ signaling pathway, and cyclooxygenase-2 expression. GKN1 also inhibits the carcinogenic potential of H. pylori protein CagA by binding to it, and up-regulates antioxidant enzymes. In addition, GKN1 reduces cell viability, proliferation, and colony formation by inhibiting cell cycle progression and epigenetic modification by down-regulating the expression levels of DNMT1 and EZH2, and DNMT1 activity, and inducing apoptosis through the death receptor-dependent pathway. Furthermore, GKN1 also inhibits gastric cancer cell invasion and metastasis via coordinated regulation of epithelial mesenchymal transition-related protein expression, reactive oxygen species production, and PI3K/Akt signaling pathway activation. Although the modes of action of GKN1 have not been clearly described, recent limited evidence suggests that GKN1 acts as a gastricspecific tumor suppressor. This review aims to discuss, comment, and summarize the recent progress in the understanding of the role of GKN1 in gastric cancer development and progression.

• Clinical and Experimental Pediatrics
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• 제46권3호
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• pp.308-311
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• 2003

저자들은 복부 팽만과 체중감소를 주소로 내원한 신생아에서 복부 팽만이 심하여 기계적 장 폐색을 의심하여 시험적 개복술 시행하였으나, 폐색 소견 발견되지 않았고 이후 대변의 염소 이온 농도를 검사한 결과 CLD로 진단된 1례를 경험하였기에 문헌 고찰과 함께 보고하는 바이다.

• Korean Journal of Acupuncture
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• 제23권4호
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• pp.147-156
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• 2006

Objectives : The purpose of the present study is to evaluate the effects of herbal acupuncture with Ginseng Radix for the treatment to intestinal disease in the rat with 2, 4, 6-trinitrobenzenesulfonic acid (TNBS) induced colitis. Methods : All animals were subjected to the injection of saline $(300{\mu}{\ell},\;500{\mu}{\ell})$ for a study control or TNBS $(300{\mu}{\ell},\;500{\mu}{\ell})$ into the lumen of the colon, 8cm proximal to the anus through the intestine. Ginseng Radix herbal acupuncture ($20mg/m{\ell},\;0.4m{\ell}$) were injected to the both $Hapgok(LI_4)$ acupoints at 2nd injection of TNBS in rats. Thus, the body weight, RBC count, WBC count, total protein, IgG levels and IgM levels were observed to study the effects of Ginseng Radix herbal acupuncture. Results : Ginseng Radix herbal acupuncture on $Hapgok(LI_4)$ for TNBS-induced colitis inhibited the body weight loss rate but did not affect RBC and WBC counts. Furthermore, it inhibited the reduction of total protein concentration and serum IgG and IgM levels in TNBS induced colitis were recovered. Conclusions : Herbal acupuncture with Ginseng Radix helps recover the TNBS-induced colonic damage and may be an important method for treatment of the colitis.

• International Journal of Internet, Broadcasting and Communication
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• 제13권2호
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• pp.145-155
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• 2021

With the recent rapid improvement in the standards of life and westernization of dietary lifestyles, the consumption of high-calorie diets such as high-fat and high-protein red meat and instant foods has increased, while less vegetables containing dietary fiber are consumed. In addition to that, stress, erroneous dietary behaviors, and contaminated environments are linked to the risk of developing ulcerative colitis, which is on the rise. Another cause of ulcerative colitis is that involve laxative abuse, including repeated, frequent use of laxatives, and include such conditions as deteriorated bowel function, irritable bowel syndrome, diarrhea, intestinal inflammation, etc. The present study aimed to investigate the comparative evaluation of pharmacological efficacy between sulfasalazine alone and combination with herbal medicine on dextran sodium sulfate (DSS)-induced UC in mice. Balb/c mice received 5% DSS in drinking water for 7 days to induce colitis. Animals were divided into five groups (n = 9): group I-normal group, group II-DSS control group, group III-DSS + sulfasalazine (30 mg/kg), group IV-DSS + sulfasalazine (60 mg/kg), group V-DSS + sulfasalazine (30 mg/kg) + Radish Extract mixture (30 mg /kg) (SRE). DSS-treated mice developed symptoms similar to those of human UC, such as severe bloody diarrhea and weight loss. SRE supplementation, as well as sulfasalazine, suppressed colonic length and mucosal inflammatory infiltration. In addition, SRE treatment significantly reduced the expression of pro-inflammatory signaling molecules through suppression both mitogen-activated protein kinases (MAPK) and nuclear factor-kappa B (NF-κB) signaling pathways, and prevented the apoptosis of colon. Moreover, SRE administration significantly led to the up-regulation of antioxidant enzyme including SOD and Catalase. This is the first report that Radish extract mixture combined with sulfasalazine protects against experimental UC via the inhibition of both inflammation and apoptosis, very similar to the standard-of-care sulfasalazine.