胃应激性溃疡的防治原则

胃应激性溃疡的命名曾一度比较混乱,先后被命名为急性溃疡、应激性胃炎、急性出血性胃炎、急性胃粘膜糜烂、急性胃粘膜局灶性坏死、急性胃粘膜病变等。但由于各种命名都不能完整地表现这一综合征,因而现在仍沿用最早命名的、为广大医师所熟悉的名称“胃应激性溃疡”。

降钙素基因相关肽在大鼠胃应激性溃疡发生过程中的作用

目的:观察降钙素基因相关肽(calcitoningene-related peptide,CGRP)在大鼠冷束缚应激过程中的动态改变及作用;观察阻断环氧化酶及一氧化氧合酶对应激大鼠血浆CGRP含量的影响。方法:制作大鼠冷束缚应激动物模型,用放免法检测大鼠冷束缚应激前及应激后2、4、6、8小时血浆CGRP含量。不同实验组大鼠。

胸腔手术和外伤并发胃应激性溃疡8例报告

报告胸腔手术和胸外伤后并发胃应激性溃疡８例。作者认为缺血、缺氧、精神因素、皮质激素药物应用等，均与本病有关。临床上以上腹隐痛、柏油样便为主。一经确诊，应积极处理，应用Ｈ２受体拮抗剂等药物，综合治疗，效果满意。

重症矽肺并发应激性溃疡的护理对策与体会

肠胃应激性溃疡多因外伤、休克、感染等重症并发。病理表现胃肠粘膜屏障功能破坏,引起胃肠粘膜溃疡、出血和坏死,病人可因大量呕血、便血而危及生命。我科自2000年1月～2009年10月共收治154例矽肺病人,其中28例重症并发应激性溃疡,现结合文献学习将护理对策和体会进行报告：

Octreotide ameliorates gastric lesions in chronically mild stressed rats

AIM:To evaluate the effect of chronic mild stress(CMS) on the emergence of gastric ulcers and possible modulation by octreotide,a synthetic somatostatin analogue. METHODS:Adult male Wistar rats were subjected to nine different unpredictable random stress procedures for 21 d,a multifactorial interactional animal model for CMS.Octreotide was administered daily for 21 d at two dose levels(50 and 90μg/kg)before exposure to stress procedure.Macro-and microscopical assessments were made,in addition to quantification of plasma corticosterone and gastric mucosal inflammatory,oxidative stress, and apoptotic biomarkers. RESULTS:Exposure to CMS elevated plasma corticosterone(28.3±0.6μg/dL,P=0.002),an event that was accompanied by gastric lesions(6.4±0.16 mm,P=0.01) and confirmed histopathologically.Moreover,the insult elevated gastric mucosal lipid peroxides(13±0.5 nmol/g tissue,P=0.001),tumor necrosis factor-α(3008.6±78.18 pg/g tissue,P<0.001),prostaglandin E2(117.1 ±4.31 pg/g tissue,P=0.002),and caspase-3 activity (2.4±0.14 OD/mg protein,P=0.002).Conversely,CMS mitigated interleukin-10(627.9±12.82 pg/g tissue,P= 0.001).Furthermore,in animals exposed to CMS,octreotide restored plasma corticosterone(61%and 71%from CMS,P=0.002)at both dose levels.These beneficial effects were associated with a remarkable suppression of gastric lesions(38%and 9%from CMS,P=0.01)and reversal of derangements in gastric mucosa. CONCLUSION:The current investigation provides evidence that exposure to CMS induces gastric ulceration, which was alleviated by administration of octreotide possibly possessing antioxidant,anti-inflammatory,and anti-apoptotic actions.

Doxycycline blocks gastric ulcer by regulating matrix metalloproteinase-2 activity and oxidative stress

AIM: To examine the effect of doxycycline on the activity of matrix metalloproteinases (MMPs) and oxidative stress in gastric tissues of rats following gastric injury.METHODS: Gastric ulcers were generated in rats by administration of 70% ethanol,and activity of doxycycline was tested by administration 30 min prior to ethanol.Similarly,the effect of doxycycline was tested in an indomethacin-induced gastric ulcer model.The activities and expression of MMPs were examined by zymography and Western blot analysis.RESULTS: Gastric injury in rats as judged by elevated ulcer indices following exposure to ulcerogen,either indomethacin or ethanol,was reversed significantly by doxycycline.Indomethacin-induced ulcerated gastric tissues exhibited about 12-fold higher proMMP-9 activity and about 5-fold higher proMMP-3 activity as compared to control tissues.Similarly,ethanol induced about 22-fold and about 6-fold higher proMMP-9 and proMMP-3 activities,respectively,in rat gastric tissues.Both proMMP-9 and MMP-3 activities were markedly decreased by doxycycline in ulcerogen treated rat gastric tissues.In contrast,the reduced MMP-2 activity in ulcerated tissues was increased by doxycycline during ulcer prevention.On the other hand,doxycycline inhibited significantly proMMP-9,-2 and -3 activities in vitro.In addition,doxycycline reduced oxidative load in gastric tissues and scavenged H2O2 in vitro.Our results suggest a novel regulatory role of doxycycline on MMP-2 activity in addition to inhibitory action on MMP-9 and MMP-3 during prevention of gastric ulcers.CONCLUSION: This is the first demonstration of dual action of doxycycline,that is,regulation of MMP activity and reduction of oxidative stress in arresting gastric injury.

Effects of the serum derived from rats treated with electroacupuncture at different meridian acupoints on EGFR signal transduction pathway in gastric mucosal cells

Objective To study the effect of the serum derived from the rats treated with electroacupunctre at Stomach Meridian acupoints on the EGFR signal transduction pathway in gastric mucosal cells. Methods Sixty rats were randomly divided into 5 groups： model group, Stomach （ST） Meridian group, Gallbladder （GB） Meridian group, ST＋ PD153035 group and GB＋ PD153035 group. Water-immersion and restrained stress method was adopted for preparation of the stress-induced gastric ulcer rat model, and the gastric mucosa cells were separated by using pronase digestion method. Gastric mucosa cells were incubated respectively with PD153035, EGFR inhibitor and the serum; PLCγ-1＇s expression level in gastric mucosa cells was tested by enzyme-linked immunosorbant assay （ELISA）, and PKC activity by isotope mingling method; and reverse transcription polymerase chain reaction assay （RT-PCR） was used for testing expression level of c-myc gene. Results The expression levels of PLCγ-1 ,PKC and c- myc gene were lower in gastric mucosa cells in the model group; there were relatively high expression levels of PLCγ-1 ,PKC and c-myc gene in the ST Meridian group and the GB Meridian group, with the highest expression levels of PLCγ-1 ,PKC and c-myc gene in the ST Meridian, and with a significant difference between the ST Meridian group and the GB Meridian group （P〈0.01 ） ; and relative lower expression levels of PLCγ-1, PKC and c-myc gene were seen in the ST ＋ PD153035 group and the GB ＋ PD153035 group; and there was a significant difference between the ST Meridian group and the ST ＋ PD153035 group （P〈0.01）. Conclusion There was a close correlation between the healing effect of electroacupuncture and activation of the EGFR signal transduction pathway in the impaired gastric mucosa cells, which was also one proof for the TCM theory： ＂There is relative specificity between the meridians and viscera＂.

Effect of moxa-burning heat stimulating Liangmen(ST 21) and Zusanli(ST 36) on proliferation and apoptosis signaling proteins in rats with stress-induced gastric ulcer

OBJECTIVE: To observe the effect of moxa-burning heat stimulating acupoints of Liangmen(ST 21)and Zusanli(ST 36) on the proliferation and apoptosis signaling proteins in rats with stress-induced gastric ulcer.METHODS: Forty rats were randomly divided into four groups: negative control(NC), ulcer control(UC), acupoints of stomach meridian(ASM), and acupoints control(AC). The acute gastric ulcer model was established by bound and water immersion.Rats in NC and UC groups didn't receive any moxa-burning heat stimulating treatment, while rats in ASM and AC groups were treated with buringmoxa heat stimulating the acupoints of Liangmen(ST 21) and Zusanli(ST 36) and their controlled points, respectively. Rats in all groups were sacrificed after 12 consecutive days treatment. The ulcer index was evaluated by using Guth's method.The expression of tumor necrosis factor-alpha(TNF-α), apoptotic protease activating facter-1(Apaf-1), Caspase-3, p21 activated kinase 1(PAK1),extracellular regulated protein kinases 2(ERK2),phosphorylated ERK2(p ERK2), phosphoinositide3-kinase(PI3K) and RAC-alpha serine/threonine-protein kinase(Akt) in gastric mucosa was detected by enzyme linked immunosorbent assay(ELISA).RESULTS: Compared with UC group, the ulcer index of ASM and AC groups decreased, and the injured gastric mucosa was improved, the expression of TNF-α, Apaf-1 and Caspase-3 in gastric mucosa was significantly reduced(P < 0.05), while the ex-pression of PAK1, ERK2, p ERK2, PI3 K and Akt in gastric mucosa was significantly increased(P < 0.05).And ASM showed better effect than AC group(P <0.05).CONCLUSION: Moxa-burning Heat stimulating of Liangmen(ST 21) and Zusanli(ST 36) could promote the recovery of gastric mucosal lesion probably by inhibiting cell apoptosis and promoting cell proliferation in stress-induced gastric ulcer.