• Journal of Gastric Cancer
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• 제15권1호
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• pp.64-67
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• 2015

Inflammatory myofibroblastic tumors (IMTs) of the stomach are extremely rare in adults, and their oncologic prognosis is not well understood. We present a 28-year-old man with a proximal gastric IMT. The patient visited the emergency department of Yeouido St. Mary's Hospital with syncope and hematemesis. Hemoglobin levels were <5.5 g/dl. Gastric fibroscopy showed a protruding mass $4{\times}4cm$ in size, with central ulceration on the posterior wall of the fundus and diffuse wall thickening throughout the cardia and anterior wall of the upper body. Endoscopic biopsy revealed indeterminate spindle cells, along with inflammation. Given the risk of rebleeding, an operation was performed despite the uncertain diagnosis. Because the mass was circumferential, laparoscopic proximal gastrectomy and double-tract anastomosis were performed to ensure a safe resection margin. The pathological diagnosis was consistent with an IMT originating from the stomach, although the tumor was negative for anaplastic lymphoma kinase gene mutation.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.269.2-269.2
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• 2003

An extract of Alnus japonica (Betulaceae) cortex has been traditionally used for purifying blood, and curing feces containing blood, enteritis, diarrhea, alcoholism and cut wounds. In the preliminary test was carried out for determining whether it has the novel pharmacological activity, the butanol fraction showed significant inhibitory effect on carrageenan-induced paw edema as an acute inflammation, HCI.ethanol-induced gastric lesion and aspirin-ligation gastric ulcer. (omitted)

• 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.

• Asian Pacific Journal of Cancer Prevention
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• 제16권17호
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• pp.7393-7400
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• 2015

Matrix metalloproteinase (MMP) 9, a key member of multifunctional family of zinc dependent endopeptidases has been found to be upregulated during inflammation and in some cancers. MMPs cleave extracellular matrix (ECM) proteins and play critical roles in cellular apoptosis, angiogenesis, tumor growth and metastasis. Several genetic polymorphisms have been identified that show allele specific effects on MMP9 regulation and are associated with gastric cancer, the fourth most common malignancy in the world. Besides Helicobacter pylori infection, genetic predisposition is another documented risk factor for gastric carcinoma. The single nucleotide polymorphism (SNP) at position -1562C/T of MMP9 results in the modulation for binding of transcription factors to the MMP9 gene promoter and thereby causes differences in protein expression and enzymatic activity. MMP9 transcriptional regulation during gastric cancer development remains poorly known although several studies have demonstrated associations between MMP9 -1562 C/T polymorphism with different diseases. Knowledge on mechanisms of MMP9 upregulation during gastric cancer may provide new paradigm in diagnostics and therapeutics.

• 대한한의학회지
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• 제25권3호
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• pp.111-122
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• 2004

Objectives : This study was carried out to investigate the effects of Jaeumgeonbi-tang extract on indomethacin-induced gastric mucosal lesions of mice. Methods : Experimental groups were classified into non-treatment group (CON group), non-administered group (GE group), misoprostol administered group (MA group) and Jaeumgeonbi-tang extract administered group (JG group). This study examined the morphological change, distribution of mast cells, mucous secreted cells and apoptotic cells, BrdU, COX-1, Hsp70, NF-κB p50, PKC, COX-2 and TNF-α of gastric mucosa. Results : 1. The hemorrhagic erosion of gastric mucosa and infiltrated mast cells were reduced in the MA and JG groups. 2. PNA reaction and mucous secreted cells were increased in the MA and JG groups. 3. The distribution of apoptotic cells, Hsp70, NF-κB p50, PKC, COX-2 and TNF-α were increased in the gastro­inflammation elicitated group, but decreased in the MA and JG groups. 4. The MA and JG groups showed increase on COX-1, BrdU. Conclusions : Jaeumgeonbi-tang extract had excellent effects on indomethacin-induced gastric mucosal lesions.

• 대한의생명과학회지
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• 제28권2호
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• pp.92-100
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• 2022

Ginkgo biloba Leaf Extract (GBE) is an extract from leaves of the Ginkgo biloba tree, widely used as a health supplement. GBE can inhibit the proliferation of several types of tumor cell. Although it is known to have anti-cancer effects in breast cancer and skin cancer, research related to gastric cancer is still insufficient. Based on results showing anti-cancer effects on solid cancer, we aimed to determine whether GBE has similar effects on gastric cancer. In this study, the anti-cancer effect of GBE in gastric adenocarcinoma was investigated by confirming the cell proliferation inhibitory effect of AGS cells. We also evaluated whether GBE regulates expression of the tumor suppressor protein p53 and Rb. GBE has apoptotic effects on AGS cells that were confirmed by changes in anti-apoptosis protein Bcl-2, Bcl-xl and pro-apoptosis protein Bax levels. Wound healing and cell migration were also decreased by treatment with GBE. Furthermore, we verified the effects of GBE on mitogenic signaling by investigating AKT target gene expression levels and revealed downregulated Sod2 and Bcl6 expression. We also confirmed that expression of inflammation-related genes decreased in a time-dependent manner. These results indicate that GBE has an anti-cancer effect on human gastric cancer cell lines. Further research on the mechanism of the anti-cancer effect will serve as basic data for possible anti-cancer drug development.

• The Korean Journal of Physiology and Pharmacology
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• 제25권5호
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• pp.403-411
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• 2021

This study was designed to evaluate the gastroprotective activity of cirsilineol in hydrochloric acid (HCl)/ethanol-induced gastric ulcer model. Cirsilineol was administered at the doses of 20 and 40 mg/kg in HCl/ethanol-induced rats. The gastroprotective ability was verified by determining the ulcer score, total acidity, hemoglobin, inflammatory cytokines, lipid peroxides, and enzymatic antioxidants superoxide dismutase (SOD) and catalase (CAT) in gastric tissue and serum biochemical analysis. The results showed a favorable increase in the hemoglobin level, antioxidant enzymes (SOD and CAT), restored electrochemical balance (carbon dioxide & anion gap) while a noticeable decrease in ulcer index, total acidity, lipid peroxides, inflammatory cytokines (interleukin-1 beta [IL-1β], IL-6, and tumor necrosis factor alpha) in rats treated with the cirsilineol. The serum biochemical analysis on liver markers (alkaline phosphatases, alanine aminotransferase, and aspartate aminotransferase), kidney markers (urea, creatinine, albumin, globulin, total protein), and lipid profile (triglyceride, high-density lipoprotein, total cholesterol) were attenuated by cirsilineol treatment in rats. Histopathology showed enhanced gastric protection and preserved the integrity of gastric mucosa upon cirsilineol administration. These results ultimately suggest that cirsilineol has gastroprotective effects that prevent the development of gastric ulcer.

• Journal of Chest Surgery
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• 제38권12호
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• pp.807-814
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• 2005

배경: 체외순환은 심정지를 필요로 하는 모든 심장 수술에서 정지된 심장의 기능을 대신하여 환자의 말초 장기의 혈액순환을 유지하기 위한 필수적인 과정이다. 그러나 체외순환은 필연적으로 인공도관을 관류하는 특성상 신체의 혈관계를 흐르는 혈류와 달리 혈액손상에 따른 전신성 염증반응을 피할 수 없으며, 이러한 전신성 염증반응과 함께 말초혈관의 미세혈관 순환장애가 체외순환동안에 원발장기의 손상을 초래하는 것으로 생각된다. 저자들은 전신성 염증반응을 일으키는 주된 혈액성분인 백혈구를 제거한 충진액을 사용하여 전신성 염증반응을 줄일 수 있는가를 확인하고, 체외순환도중 위점막의 산도를 측정함으로써 위점막의 미세혈류에 대한 백혈구 제거 충진액의 효과를 확인하기 위하여 실험을 진행하였다. 대상 및 방법: 실험군은 15마리의 한국산 잡견을 충진액의 성분에 따라 비혈액성 충진액군, 백혈구 제거 혈액성 충진액군, 백혈구 비제거 혈액성 충진액군으로 각각 5마리씩 세 군으로 나누었다. 세 군 모두에서 2시간의 체외순환 및 연속된 4시간의 마취유지를 시행하였으며, 체외순환 전과 체외순환 후 1시간, 2시간, 체외순환 종료 후 2시간 4시간에 위점막 이산화탄소 농도와 산도, 동맥혈 이산화탄소 분압 과 호기말 이산화탄소 분압을 측정하고, 염증반응의 지표검사를 위하여 동맥혈을 채혈하였다. 전신성 염증반응의 정도는 채취한 동맥혈에서 ELISA (enzyme linked immunosorbent assay)법을 이용하여 IL-8의 수준을 검사하였다. 결과: 1, 위점막의 이산화탄소 농도는 백혈구 제거 혈액성 충진액군이 백혈구 비제거 혈액성 충진액군과 비혈액성 충진액군에 비하여 유의하게 낮았다(p=0.02, 0.01). 2. 위점막의 산도는 백혈구 제거 혈액성 충진액군과 백혈구 비제거 혈액성 충진액군간에 유의한 차이를 보였다(p=0.01). 3. 전신성 염증반응의 정도를 확인하기 위하여 측정한 IL-8의 수준은 백혈구 제거 혈액성 충진액군과 비혈액성 충진액군이 백혈구 비제거 혈액성 충진액군에 비하여 유의하게 낮았다(p=0.01, 0.01). 결론: 백혈구를 제거한 혈액성 충진액을 사용하는 것이 체외순환중 위점막의 미세순환 장애를 방지하고 전신성 염증반응을 감소시킬 수 있음을 확인하였다.

• Journal of Microbiology and Biotechnology
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• 제26권8호
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• pp.1392-1397
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• 2016

Curcumin is a polyphenol derived from the plant Curcuma longa, which is used for the treatment of diseases associated with oxidative stress and inflammation. The present study was undertaken to determine the protective effect of curcumin against naproxen-induced gastric antral ulcerations in rats. Different doses (10, 50, and 100 mg/kg) of curcumin or vehicle (curcumin, 0 mg/kg) were pretreated for 3 days by oral gavage, and then gastric mucosal lesions were caused by 80 mg/kg naproxen applied for 3 days. Curcumin significantly inhibited the naproxen-induced gastric antral ulcer area and lipid peroxidation in a dose-dependent manner. In addition, curcumin markedly increased activities of radical scavenging enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase in a dose-dependent manner. Specifically, 100 mg/kg curcumin completely protected the gastric mucosa against the loss in the enzyme, resulting in a drastic increase of activities of radical scavenging enzymes up to more than the level of untreated normal rats. Histological examination obviously showed that curcumin prevents naproxen-induced gastric antral ulceration as a result of direct protection of the gastric mucosa. These results suggest that curcumin blocks naproxen-induced gastric antral ulcerations through prevention of lipid peroxidation and activation of radical scavenging enzymes, and it may offer a potential remedy of gastric antral ulcerations.

• 대한약침학회지
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• 제25권2호
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• pp.88-100
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• 2022

Gastric cancer (GC) is a significant cause of cancer mortality which has led to focused exploration of the pathology of GC. The advent of genome-wide analysis methods has made it possible to uncover genetic and epigenetic fluctuation such as abnormal DNA methylation in gene promoter regions that is expected to play a key role in GC. The study of gastric malignancies requires an etiological perspective, and Helicobacter pylori (H. pylori) was identified to play a role in GC. H. pylori infection causes chronic inflammation of the gastric epithelium causing abnormal polyclonal methylation, which might raise the risk of GC. In the last two decades, various pathogenic factors by which H. pylori infection causes GC have been discovered. Abnormal DNA methylation is triggered in several genes, rendering them inactive. In GC, methylation patterns are linked to certain subtypes including microsatellite instability. Multiple cancer-related processes are more usually changed by abnormal DNA methylation than through mutations, according to current general and combined investigations. Furthermore, the amount of acquired abnormal DNA methylation is heavily linked to the chances of developing GC. Therefore, we investigated abnormal DNA methylation in GC and the link between methylation and H. pylori infection.