• 고신대학교 의과대학 학술지
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• 제33권3호
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• pp.463-467
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• 2018

The hepatic artery can have numerous variations. However, a common hepatic artery originating from the left gastric artery and the entire hepatic blood supply furnished by the left gastric artery is an extremely rare anomaly. We encountered this anomaly in a patient with advanced gastric cancer. A surgeon should recognize this image appearance and identify the anomaly. Without knowledge of this anomaly and given the strategy for extensive lesser sac dissection generally employed during gastric cancer surgery, a surgeon could easily inadvertently divide this vessel, resulting in critical liver damage. We report a case of common hepatic artery originating from left gastric artery and review of the literatures.

• 사상체질의학회지
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• 제12권2호
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• pp.171-183
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• 2000

1. Back ground and purpose An experimental study has done to examine the effect of defense and cure gastric mucasal damage of Mokdan-pijihwang-tang. 2. Methods Mice had intragastric injected with MJ extract before indomethacin treatment which induces homorrhage infarct and erosion artificially. Degree of lipid peroxidation, general morphology, change of mucous cell, the distribution of PNA, ICAM and distribution of apoptotic cell were objected. (Abbreviation) MJ : Mokdanpijihwang-tang, PNA : Peanut Agglutinin, ICAM : Intercellular Adhesion Molecule 3 Results 1) The degree of lipid peroxidation in INDO-group had increased conspicuously than control group. But the degree of lipid peroxidation in MJ-group had decreased than INDO-group and these decline had probability. 2) After indomethacin treatment, hemorrhage infarct and erosion had increased in stomach body. But in MJ-group, the configuration is normal, except the group intragastric injected with MJ extract at hour 24 before indomethacin treatment. 3) Surface mucous cell and neck mucous had disappeared in INDO-group. But in MJ-group tormal distribution had shown like control group except the group intragastric injected with MJ extract at hour 24 before indomethacin treatment. 4) PNA positive reaction had not shown in INDO-group. But medium PNA positive reaction had shown In Mj-group. 5) ICAM positive reacted cell had shown in INDO-group. The decrease of ICAM positive cell were shown than INDO-group. 6) A number of apoptotic cell was distributed in hemorrhagic erosion. A few number of apoptotic cell was distributed in MJ-group except some surface mucous. 4. Conclusion These results suggest that MJ has an effect on cure of gastric mucosal damage.

• 동의생리병리학회지
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• 제30권4호
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• pp.257-265
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• 2016

The aim of this study was to investigate the effects of Ulmi Pumilae cortex extracts on acute reflux esophagitis rats induced by pylorus and forestomach ligation operation. 40 rats were divided into five groups; Normal group, Sham group, Control group, T1 group and T2 group. 4 groups has a laparotomy after controled 2weeks and sham group, T1 group, T2 group has ligation in stomach. After laparotomy, all group`s body weight, gastric volume, gastric juice PH, SOD activities, catalase activities, lipid peroxidation, total glutathione, the effects on esophageal and stomach mucosa damage were checked. There was significant statistical differences between control group and Ulmi Pumilae cortex extracts adminitration groups(T1 and T2 group) in terms of gastric volume decreasing. Also, adminitration groups has significant effect than control group in decreasing mucosa damage. SOD(superoxide dismutase) and catalase activities has a significant statistical differences between control group and T2 group not in T1 group. These results suggest that the medication of Ulmi Pumilae cortex extracts is effective for the treatment of acute reflux esophagitis in terms of decerasing gastric volume and mucosa damage. Especially, the results were shown to be more positive in High-dose administration group (T2 group) than in Low-dose administration group (T1 group) in SOD and catalase activities.

• 한국임상수의학회지
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• 제30권1호
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• pp.5-11
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• 2013

급성 위궤양은 위점막에서 세포증식과 세포사멸의 불균형으로 발병되어진다. 현재 Platycodin D (PD)는 항산화 및 항염증 등의 다양한 약리효능을 가진다고 보고되고 있다. 본 실험은 ibuprofen에 의해 유발된 급성 위궤양이 전처치한 PD에 의해 위궤양 보호효과를 가지는 가를 알아보기 위해 실시하였다. PD의 효능은 위점막에서의 COX-2의 발현과 더불어 위점막상피세포의 증생과 세포사멸정도에 의해서 평가하였다. 실험군은 정상대조군, ibuprofen 유발 위궤양군, 2.5 mg/kg PD 전처치군, 5 mg/kg PD 전처치군으로 분류하였다. 급성위궤양은 200 mg/kg의 ibuprofen을 하루에 3번 8시간 간격으로 경구 투여하여 유발하였다. PD는 5일간 경구로 하루에 한 번씩 전처치하였다. PD의 전처치가 ibuprofen에 의해 유발된 위궤양 병변을 유의적으로 감소시켰으며 과도한 위점액 분비로 인한 점액질의 소실을 억제하였다. 또한 PD 전처치가 위점막의 상피세포증식층에서 Ki-67 양성세포의 감소 및 세포사멸을 억제하였다. 추가적으로 PD의 전처치가 위궤양에 의해 증가된 COX-2 발현을 감소시켰다. 이상의 연구결과는 PD의 전처치가 ibuprofen에 의해 유발된 위점막손상에 있어 COX-2의 발현조절을 통하여 위점막세포의 증식과 사멸에 관여할 것으로 보여진다.

• Journal of Microbiology and Biotechnology
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• 제26권5호
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• pp.823-828
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• 2016

The present study investigated the protective effect of naturally purified 4-(3,4-dihydroxyphenyl)-3-buten-2-one (DHP) from Phellinus linteus against naproxen-induced gastric antral ulcers in rats. To verify the protective effect of DHP on naproxen-induced gastric antral ulcers, various doses (1, 5, and 10 μg/kg) of DHP were pretreated for 3 days, and then gastric damage was caused by 80 mg/kg naproxen applied for 3 days. DHP prevented naproxen-induced gastric antral ulcers in a dose-dependent manner. In particular, 10 μg/kg DHP showed the best protective effect against naproxen-induced gastric antral ulcers. Moreover, DHP significantly attenuated the naproxen-induced lipid peroxide level in gastric mucosa and increased the activities of radical scavenging enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase, in a dose-dependent manner. A histological examination clearly demonstrated that the gastric antral ulcer induced by naproxen nearly disappeared after the pretreatment of DHP. These results suggest that DHP can inhibit naproxen-induced gastric antral ulcers through prevention of lipid peroxidation and activation of radical scavenging enzymes.

• Anatomy and Cell Biology
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• 제57권1호
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• pp.105-118
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• 2024

The world has witnessed tremendous advancements in nano-base applications. Zinc oxide nanoparticles (ZON) are widely used in food industry and medicine. Although their application is of important value, they may cause toxicity to body tissues. Peripheral blood mononuclear cells (PBMCs) proved its efficacy in tissue regeneration especially when it is preconditioned by activated platelet supernatant (APS). The aim of this study is to evaluate the effect of ZON on the gastric mucosa and the therapeutic role of the PBMCs preconditioned by APS in rats. Ten rats were donors and fifty rats were recipients. The recipients were divided into; control group, ZON group (10 mg/kg/day orally for five days) and preconditioned PBMCs group (1×10⁷ once intravenously 24 hours after ZON). Gastric specimens were processed for histological, immunohistochemical, biochemical and quantitative real-time polymerase chain reaction studies. ZON group showed marked structural changes in the gastric mucosa. There was desquamation or deep ulceration of the epithelium. Cytoplasmic vacuoles and pyknotic nuclei were in glandular cells. Reduced proliferating cell nuclear antigen and increased tumor necrosis factor-α were in epithelial cells. There were significant elevation in malondialdahyde and reduction in glutathione, superoxide dismutase, and catalase. Enhancement in mRNA expression of nuclear factor kappa-B and cyclooxygenase-2 was detected. The preconditioned PBMCs group showed significant improvement of all parameters. So, ZON had cytotoxic effects on the gastric mucosa and the preconditioned PBMCs had a therapeutic effect on gastric mucosal damage after ZON.

• Journal of Ginseng Research
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• 제25권4호
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• pp.141-149
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• 2001

The effect of ginseng on gastric ulcer and gastric acid secretion was investigated in pylorus-ligated rats. Methods: Sprague-Dawley strain rats were used after 24 hours fast. Pylorus-ligation was performed under light ether anaesthesia, then gastric mucosal damage was evoked in conscious pylorus-ligated rats by the administration of subcutaneous (s.c.) indomethancin (20mg/kg), s.c. histamine (150mg/kg) or by pylorus-ligation (Shay ulcer). Ginseng was given by intragastric (i.g.) or intraperitoneal (i.p.) route simultaneously with the ulcerogens. Rats were killed after 3h (indomethacin) and histamine models) or after 18h (Shay ulcer), when the gastric secretory responses, the number and severity of gastric mucosal lesions and mucosal mucus content deetermined. the effect of i.p. ginseng on basal gastric acid secretion and on gastric acide secretion in indomethacin (20mg/kg, s.c.)-treated rats was also investigated in urethane anesthetized rats. Gastric acid secretion was measured by flushing of the gastric lumen with saline every 15min through an oesophageal cannula. Results: In conscious pylorus-ligated rats, i.g. ginseng(12.5-50mg/$m\ell$; 50-200mg/kg) protected against gastric mucosal lesions evoked by s.c. indomethacin or s.c. histanmine in the d3-h pylorus-lighted rat, withoutmodifying gastric acid secretory responses. Ginseng given i.p. (150 or 200mg/kg) did not reduce the gastric lesions produced by histamine or by ligating the pylorus (Shay ulcer) Ginseng given orally in 50mg/$m\ell$ (200mg/kg) increased gastric mucus secretion in saline- and indomethacin-treated conscious pylorus-ligated rats. In anaesthetized rats ginseng (50 or 200mg/kg) did not modify basal gastric acid secretion or gastric acid secretion in the indomethacin-treated rats. Conclusions: ginseng given orally exerts gastroprotective effects in the rat stomach. Such anti-ulcer effect does not involve changes in gastric acid secretory responses. In addition, ginseng possesses stimulatory effect on gastric mucus secretion, which could be one mechanism by which the compound exerts its antiulcer effect. Our data are in favor for a beneficial effect for topically applied ginseng on the gastric mucosa.

• Asian Pacific Journal of Cancer Prevention
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• 제13권10호
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• pp.5043-5046
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• 2012

The role of Helicobacter pylori status and serum zinc value in gastric disease patients and healthy controls were investigated. Cases used in this work were 45 gastric cancer patients, 44 with peptic ulcers, 52 suffering gastritis and 64 healthy controls, all diagnosed histologically with the controls undergoing medical checkups. Helicobacter pylori status and serum levels of Zn were determined by 13C-urea breath test and flame atomic absorption spectrophotometer, respectively. Our study showed that Helicobacter pylori infection has no change in gastritis, peptic ulcer and gastric cancer group, on the contrast, serum levels of Zn were significantly reduced in gastritis, peptic ulcer and gastric cancer group, compared with healthy controls, and the higher the Zn levels are, the more increased risk of gastric cancer. Helicobacter pylori infection is a cause of gastritis, peptic ulcers and even gastric cancer, while serum zinc level is an indicator of protection of gastric membranes against damage.

• Journal of Microbiology and Biotechnology
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• 제14권5호
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• pp.996-1003
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• 2004

Nonsteroidal anti-inflammatory drugs such as indomethacin induce severe gastric mucosal damage in humans and rodents. In the present study, the in vivo protective effect of astaxanthin on indomethacin-induced gastric lesions in rats was investigated. The test groups were injected with indomethacin (25 mg/kg) after the oral administration of astaxanthin (25 mg/kg) for 1, 2, and 3 days, while the control group was treated only with indomethacin. Thiobarbituric acid reactive substances in the gastric mucosa, as an index of lipid peroxidation, increased significantly after indomethacin administration and this increase was inhibited by oral administration of astaxanthin. In addition, pretreatment with astaxanthin resulted in a significant increase of the activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-px). Histologic examination clearly revealed acute gastric mucosal lesions induced by indomethacin in the stomach of the control group, but were not observed in that of the test group. These results indicate that astaxanthin activates SOD, catalase, and GSH-px, and removes the lipid peroxides and free radicals induced by indomethacin. It is evident that astaxanthin acts as a free radical quencher and antioxidant, and is an effective molecule in the remedy of gastric mucosal lesions.

• 한국자기공명학회논문지
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• 제15권1호
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• pp.54-68
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• 2011

$^1H$ nuclear magnetic resonance (NMR) spectroscopy of biological samples has been proven to be an effective and nondestructive approach to probe drug toxicity within an organism. In this study, ketoprofen toxicity was investigated using $^1H$-NMR spectroscopy coupled with multivariate statistical analysis. Histopathologic test of ketoprofen-induced acute gastrointestinal damage in rats demonstrated a significant dose-dependent effect. Furthermore, principal component analysis (PCA) derived from $^1H$-NMR spectra of urinary samples showed clear separation between the vehicle-treated control and ketoprofen-treated groups. Moreover, PCA derived from endogenous metabolite concentrations through targeted profiling revealed a dose-dependent metabolic shift between the vehicle-treated control, low-dose ketoprofen-treated (10 mg/kg body weight), and high-dose ketoprofen-treated (50 mg/kg) groups coinciding with their gastric damage scores after ketoprofen administration. The resultant metabolic profiles demonstrated that the ketoprofen-induced gastric damage exhibited energy metabolism perturbations that increased urinary levels of citrate, cis-aconitate, succinate, and phosphocreatine. In addition, ketoprofen administration induced an enhancement of xenobiotic activity in fatty oxidation, which caused increase levels of N-isovalerylglycine, adipate, phenylacetylglycine, dimethylamine, betaine, hippurate, 3-indoxylsulfate, N,N-dimethylglycine, trimethyl-N-oxide, and glycine. These findings demonstrate that $^1H$-NMR-based urinary metabolic profiling can be used for noninvasive and rapid way to diagnose adverse drug effects and is suitable for explaining the possible biological pathways perturbed by nonsteroidal anti-inflammatory drug toxicity.