• Title/Summary/Keyword: 점막 손상

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Protective Effect of Nicotine on Gastrin-induced Gastric Mucosal Damage in Rats (Gastrin 유발 위점막 손상에 대한 Nicotine의 보호 효과)

  • Piao, Shi-Hao;Kim, Dong-Goo;Jin, De-Nan;Wu, Zhen-Jiu;Hong, Chun-Lan;Kim, Kyung-Hwan
    • The Korean Journal of Pharmacology
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    • v.31 no.3
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    • pp.313-321
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    • 1995
  • Conflicting data have been reported on the effect of nicotine on gastric mucosal damage. To elucidate the effect of chronic intermittent nicotine on gastric mucosal damage, intragastric nicotine (5 mg/kg, 10 mg/kg) was administered twice per day for 9 days. Gastric mucosal damage was created by s.c. injection of a large dose (1.2 mg/kg) of pentagastrin followed by pylorus ligation for 6 hours. Nicotine treated rats showed reduced gastric mucosal damage about 50% of the control. To examine the mechanism of the protective effect of nicotine, gastric perfusion experiments were done. Basal acid secretion was not affected by intragastric or intravenous nicotine. However, pentagastrin-stimulated acid secretion markedly inhibited by a bolus injection of nicotine, and this response was dose-related. These data indicates that chronic intermittent administration of nicotine protects gastric mucosa against gastrin-induced gastric mucosal damage, and nicotine-induced inhibition of gastrin-stimulated acid secretion has an important role for the protective effect of nicotine. Considering reports concerning nicotine's aggravating effect on the gastric mucosal damage, it is suggested that the methods of administration of nicotine may be an important decisive factor of the divergent action of nicotine on the gastric mucosa.

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후두 및 기관협착증의 유발인자로서의 위산 및 펩신의 역할에 대한 실험적 연구

  • Cho, Jae-Sik;Kim, Pan-Soo;Cho, Won; Lee, Jong-Won
    • Proceedings of the KOR-BRONCHOESO Conference
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    • 1995.04a
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    • pp.93.2-93
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    • 1995
  • 후두 및 기관지 협착증은 대개가 기도확보를 목적으로 후두 및 기관내에 삽관을 시행하였을 때 삽관튜브에 부착된 cuff내에 압력이 높게 되면 점막에 혈류장애가 초래되고 궤양등의 점막손상이 뒤따르며 여기에 2차감염이 초래되어 육아종과 반흔이 생기면서 결국은 협착이 초래되는 것으로 알려져 있다. 이와 같이 손상된 후두및 기관의 점막에 산도가 강하고 소화효소가 함유된 위액이 역류되어 접촉될 경우 협착이 더욱 조장되리라고 가정할 수 있다. 따라서 위액이 과연 후두 및 기관지 협착증에 관여 한 것인지를 실험적으로 규명해 보고자 하였다. 실험동물은 가토를 대상으로 하여 Urethan마취를 시행하고, 삽관한 다음 합성위액 pH 1.5, 3, 5 짜리 용액을 기관 내에 1시간정도 관류시킨 다음 후두 및 기관을 적출하여 점막상태의 변화를 현미경으로 관찰하였다. 그 결과 산도가 강하고 펩신이 첨가된 합성위액으로 관류한 군에서는 성모의 파괴점막의 궤양, 부종과 염증소견 등이 심하게 관찰되었다. 그러나 산도가 약할수록, 그리고 펩신이 첨가되지 않은 합성위액으로 관류한 군에서는 섬모 및 점막의 손상이나 염증 및 부종등의 소견이 경미하게 관찰되었다. 이러한 결과로 미루어 강한 산도의 위액이 후두 및 기관으로 역류될 경우 협착증의 발생에 깊이 관여하리라고 추측되었다.

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Gastric Mucosal Damage by Bile Acid (담즙산에 의한 위 점막 손상)

  • Cho, Hyun-Hong;Suh, Jeong-Ill;Lee, Keyong-Hee;Kim, Tae-Nyeun;Chung, Moon-Kwan;Lee, Hyun-Woo;Choi, Won-Hee;Yang, Chang-Heon
    • Journal of Yeungnam Medical Science
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    • v.9 no.2
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    • pp.342-350
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    • 1992
  • To investigate the effect of bile acid on gastric mucosa, we performed biologic test using Sprague-Dawley rat. Mixture solution of TDCA 15mM and HCl of pH 3 was given into stomach to one group and HCl of pH 3 was given into stomach to another group. The significant gastric mucosal change was vasodilatation and edema, that was disappeared progressively. These findings suggest the bile acid can damage gastric mucosa.

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Curcumin Induces Recovery from Indomethacin-Induced Gastric Mucosal Lesions in Rats (커규민의 인도메타신 유도 위점막 손상에 대한 치료 효과)

  • Kim, Jeong-Hwan;Kim, Byung-Woo;Kwon, Hyun-Ju;Kim, Yeon-Hee;Nam, Soo-Wan
    • Journal of Life Science
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    • v.24 no.1
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    • pp.20-25
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    • 2014
  • In the present study, the curative effect of curcumin on indomethacin-induced gastric mucosal lesions in rats was investigated. Indomethacin is a nonsteroidal anti-inflammatory drug (NSAID), with serious side effects, including erosion, ulcerative lesions, and petechial bleeding in the mucosa of the stomach. Gastric mucosal lesions were caused by oral administration of 25 mg/kg of indomethacin. Various doses (10, 50, and 100 mg/kg) of curcumin were treated for 3 days by oral gavage. Indomethacin clearly increased the gastric ulcer area in the stomach, and curcumin significantly decreased the gastric ulcer area in a dose-dependent manner. Curcumin also markedly inhibited lipid peroxidation in the gastric mucosa and activated radical scavenging enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, in a dose-dependent manner. These results suggest that curcumin can induce recovery from indomethacin-induced gastric mucosal lesions through inhibition of lipid peroxidation and activation of radical scavenging enzymes, such as SOD, catalase, and glutathione peroxidase. Curcumin appears to be a powerful free radical quencher, and it may offer an attractive strategy for healing gastric mucosal lesions in humans.

생쥐의 초기 미란성위궤양 상피세포의 미세구조 변화 및 분비면역계에 대한 연구

  • Ha, Mi-Hye;Choe, Eun-Sang;Ha, Jae-Cheong
    • The Korean Journal of Zoology
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    • v.35 no.1
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    • pp.45-57
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    • 1992
  • 생쥐를 48시간 동안 결식시킨 후 유문결찰하여 급성미란을 유발시키고 미란형성부의 점막 내위선을 구성하는 각 세포의 구조변화와 IgA 분비세포의 분포를 관찰하였다. 미란부 점액분포의 변화는 표면상피의 손상 정도가 심해질수록 경계부의 PAS양성반응은 감소되었으며 중심부에서는 표면상피의 소실로 인하여 PAS 양성반응이 관찰되지 않았다. Glycocalyx 관찰을 위한 ruthenium red 반응에서도 경계부의 상피세포 손상이 심해짐에 따라 정단세포막 상층에 나타나는 양성반응은 감소되었고 측면과 기저면의 양성반응은 관찰되지 않은 것으로 보아 세포 손상시 tight junction은 파괴되지 않음을 알 수 있었다. 미란경계부의 미세구조변화로서, 상피세포는 손상이 진행될수록 세포질이 용해되어 공포가 형성되고 핵응축 및 정 단세포질의 점액원과립의 소실이 관찰되었으나 tight junction은 유지되었다. 반면에 점액경세포는 점액원과립의 수가 증가되고 조면소포체가 종창되어 있었다. 미란의 경계부와 중심부에서 벽세포는 다수의 소포가 출현한 후 세포내세관이 종창되었으며 그 후에 mitochondria가 파괴되었고 주세포는 주변의 벽세포가 커지면서 가장자리로 밀려나 크기가 정상보다 작아지고 조면소포체와 mitochondria가 종창을 나타내었다. IgA분비세포는 점막이 파괴된 미란부 점막하조직의 혈관 주변에 다수 존재하는 형질세포에서 확인되었다.

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Protective effects of Gastrodia elata extract by steaming time on acute gastritis (증숙 횟수에 따른 천마 추출물의 급성 위염 개선효과)

  • Lee, Ah Reum;Kwon, O Jun;Noh, Jeong Sook;Roh, Seong-Soo
    • Korean Journal of Food Science and Technology
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    • v.48 no.6
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    • pp.597-603
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    • 2016
  • This study aimed to explore the protective effect of Gastrodia elata (GE) in an HCl/ethanol induced acute gastritis model by differing the steaming time. The samples GE1 (GE by steaming for 1 time) and GE9 (GE by steaming for 9 times), were selected based on the results of HPLC analysis, free radical scavenging activities, and total phenol and flavonoid contents. To evaluate the anti-inflammatory effect of GE, ICR mice were divided into 5 groups; normal mice (Nor), gastritic mice with distilled water (Con), gastritic mice with 100 mg/kg GE1, gastritic mice with 100 mg/kg GE9 and gastritic mice with 10 mg/kg sucralfate (SC). HCl/ethanol-induced gastric mucosal injury was markedly improved by GE9 treatment as observed during histological evaluation. The increased reactive oxygen species levels in the serum were diminished by GE9 treatment. Furthermore, peroxynitrite levels of the stomach tissue were decreased in the GE9-treated group. The analyses of stomach proteins indicated that GE9 treatment effectively reduced inflammatory cytokine levels as compared to that by GE1 treatment. These results suggest that GE9 improves health during acute gastritis.

Intermuscular Hematoma in Esophagus : without Tearing (식도 혈종)

  • 윤용한;김해균;강정신
    • Journal of Chest Surgery
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    • v.32 no.4
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    • pp.404-407
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    • 1999
  • Spontanous hematoma of the esophagus is a rare condition affecting middle aged or elderly women. We experienced one case of esophageal hematoma which attracted our attention due to its confusing presentation clinically. The pathogenesis has been in dispute so far. The diagnosis has traditionally been made by barium esophagogram. We proved the diagnosis of spontaneous hematoma of the esophagus by utilizing CT scan and MRI. This condition led to conservative treatment and full recovery ultimately, but we performed the surgical correction because the filling defect persisted and the dysphagia got worse on the 20th day of hospital stay. Hematoma was located between the inner layer of circular muscle and the outer layer of longitudinal muscle which we considered as intermuscular hematoma of the esophagus.

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Studies on Physicochemical and Biological Properties of Depolymerized Alginate from Sea Tangle, Laminaria japonicus by Heating Hydrolysis -4. Inhibition Effects of Acute Gastritis Induced by $HCl{\cdot}ethanol$ Solution and Gastric Ulcer Induced- (다시마 (Laminaria japonicus) Alginate의 가열가수분해에 따른 물리${\cdot}$화학적 및 생물학적 특성에 관한 연구 -4. $HCl{\cdot}ethanol$용액과 침수스트레스에 의해 유발되는 랫드 위궤양의 억제효과-)

  • KIM Yuck-Yong;CHO Young-Je
    • Korean Journal of Fisheries and Aquatic Sciences
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    • v.33 no.6
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    • pp.520-523
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    • 2000
  • Anti-ulcer effects of depolymerized alginate (HAG-10, average molecular weight 10,000; HAG-50, average molecular weight 50,000; HAG-100, average molecular weight 100,000) obtained by hydrolysis of alginate by heating at $121^{\circ}C$, against $HCl{\cdot}ethanol$ and water-immersion stress in rats were investigated. The acute gastritis, induced by $HCl{\cdot}ethanol$, and the gastric ulcer, induced by water-immersion stress, were inhibited dose-dependently by administration of HAG-50, HAG-100 and alginate. Histopathological lesions of the gastritis and gastric ulcer in rats treated with HAG-50, HAG-100 and alginate were significantly lower than those in rats fed with HAG-10. The inhibition rates (${\%}$) on acute gastritis induced by $HCl{\cdot}ethanol$ and gastritis ulcer induced by water-immersion stress in rats, were $13.00{\%}\;and\;15.74{\%}$of HAG-10, $41.15{\%}\;and\;35.72{\%}$ of HAG-50, $41.58{\%}\;and\;35.37{\%}$ of HAG-100, and $45.17{\%}\;and\;41.11{\%}$ of alginate, respectively. These results suggested that HAG-50, HAG-100 and slginate had a protective effect against the gastritis and gastric ulcer. The effect was not as visible when using HAG-10 in rats. From the present results, it was suggested that HAG-50 was an effective anti-ulcer agent against $HCl{\cdot}ethanol$and water-immersion stress in rats.

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The Signal Transduction Mechanisms on the Intestinal Mucosa of Rat Following Irradiation (방사선조사후 백서소장점막에서 발생하는 신호전달체계에 관한 연구)

  • Yoo Jeong Hyun;Kim Sung Sook;Lee Kyung Ja;Rhee Chung Sik
    • Radiation Oncology Journal
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    • v.15 no.2
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    • pp.79-95
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    • 1997
  • Purpose : Phospholipase C(PLC) isozymes play significant roles in signal transduction mechanism. $PLC-\gamma$ 1 is one of the key regulatory enzymes in signal transduction for cellular proliferation and differentiation. Ras oncoprotein, EGFR, and PKC are also known to be involved in cell growth. The exact mechanisms of these signal transduction following irradiation, however, were not clearly documented Thus, this study was Planned to determine the biological significance of PLC, ras oncoprotein, EGFR, and PKC in damage and regeneration of rat intestinal mucosa following irradiation. Material and Method : Sixty Sprague-Dawley rats were irradiated to entire body with a single dose of 8Gy. The rats were divided into S groups according to the sacrifice days after irradiation. The expression of PLC, ras oncoprotein, EGFR and PKC in each group were examined by the immunoblotting and immunohistochemistry. The histopathologic findings were observed using H&I stain, and the mitoses for the evidence of regeneration were counted using the light microscopy & PCNA kit. The Phosphoinositide(PI) hydrolyzing activity assay was also done for the indirect evaluation of $PLC-\gamma$ 1 activity. Results: In the immunohistochemistry , the expression of $PLC-{\beta}$ was negative for all grøups. The expression of $PLC-{\gamma}1$ was highest in the group III followed by group II in the proliferative zone of mucosa. The expression of $PKC-{\delta}1$ was strongly positive in group 1 followed by group II in the damaged surface epithelium. The above findings were also confirttled in the immunoblotting study. In the immunoblotting study, the expressions of $PLC-{\beta}$, $PLC-{\gamma}1$, and $PKC-{\delta}1$ were the same as the results of immunohis-tochemistry. The expression of ras oncoprctein was weakly positive in groups II, III and IV. The of EGFR was the highest in the group II, III, follwed by group IV and the expression of PKC was weakly positive in the group II and III. Conclusion: $PLC-{\gamma}1$ mediated signal transduction including ras oncoprotein, EGFR, and PKC play a significant role in mucosal regeneration after irradiation. $PLC-{\delta}1$ mediated signal transduction might have an important role in mucosal damage after irradiation. Further studies will be necessary to confirm the signal transduction mediating the $PKC-{\delta}1$.

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