替米沙坦对脑出血急性应激性胃黏膜病变大鼠胃黏膜细胞增殖和凋亡的影响被引量：4

Effect of telmisartan on proliferation and apoptosis of gastric mucosal cells in acute stress gastric lesion rats with intracerebral hemorrhage

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摘要目的探讨血管紧张素Ⅱ受体拮抗剂替米沙坦对脑出血急性应激性胃黏膜病变大鼠胃黏膜细胞增殖和凋亡的影响。方法健康成年SD大鼠96只,随机分为假手术组、脑出血组、替米沙坦组,每组32只,各组再分为1、2、3和5d4个时间点,每个时间点8只大鼠。制作脑出血大鼠模型,大体观察胃黏膜病变并计算溃疡指数;HE染色光镜下观察胃黏膜组织形态学改变;免疫组织化学法检测胃黏膜增殖细胞核抗原(PCNA)蛋白的表达;TUNEL检测胃黏膜凋亡细胞。结果与假手术组比较,脑出血组大鼠1、2、3和5d胃黏膜溃疡指数明显增大、PCNA表达明显减少、TUNEL凋亡细胞明显增多(P<0.01)。与脑出血组比较,替米沙坦组大鼠1、2、3和5d胃黏膜溃疡指数明显减小、PCNA表达增多、TUNEL凋亡细胞减少(P<0.05)。结论替米沙坦能够减小脑出血急性应激性胃黏膜病变大鼠胃黏膜溃疡指数、增加PCNA表达、减少TUNEL凋亡细胞,减轻应激性胃黏膜病变。 Objective To study the effect of telmisartan,an Ang Ⅱ receptor blocker,on proliferation and apoptosis of gastric mucosal cells in acute stress gastric lesion rats with intracerebral hemorrhage.Methods Ninety-six healthy adult SD rats were randomly divided into sham operation group,intracerebral hemorrhage group and telmisartan treatment group （32 in each group）.Rats in each group were further divided into 1-day group,2-day group,3-day group and 5-day group （8 in each group）.A rat intracerebral hemorrhage model was established.Gross gastric mucosal lesion was observed and ulcer index was calculated.Gastric mucosa morphology was observed by optical microscopy with HE staining.Expression of PCNA protein in gastric mucosa was detected with immunohistochemistry staining.Apoptosis of gastric mucosal cells was assayed by TUNEL.Results The gastric mucosa ulcer index was significantly higher while the expression level of PCNA was significantly lower and the number of apoptotic cells was significantly larger in intracerebral hemorrhage group than in sham operation group on days 1,2,3 and 5 （P〈0.01）.The lesion was most severe on day 3 and alleviated on day 5.The gastric mucosa ulcer index was significantly lower while the expression level of PCNA was significantly higher and the number of apoptotic cells was significantly smaller in telmisartan treatment group than in intracerebral hemorrhage group on days 1,2,3 and 5 （P〈0.05）.Conclusion Telmisartan can reduce the ulcer index,increase the expression of PCNA,decrease the number of apoptotic cells and alleviate the gastric mucosa lesion in acute stress gastric lesion rats with intracerebral hemorrhage.

作者邱月宁显忠杨文海

机构地区辽宁医学院附属第三医院神经内科

出处《中华老年心脑血管病杂志》 CAS 2015年第1期83-86,共4页 Chinese Journal of Geriatric Heart,Brain and Vessel Diseases

基金辽宁省科学技术计划项目(2012225019)

关键词脑出血胃黏膜细胞凋亡细胞增殖 cerebral hemorrhage gastric mucosa apoptosis cell proliferation

分类号 R743.34 [医药卫生—神经病学与精神病学]

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参考文献12

1O'Donnell MJ,Kapral MK,Fang J,et al.Gastrointestinal bleeding after acute ischemic stroke.Neurology,2008,71:650-655.
2Bajaj JS,Zadvornova Y,Heuman DM,et al.Association of proton pump inhibitor therapy with spontaneous bacterial peritonitis in cirrhotic patients with ascites.Am J Gastroenterol,2009,104:1130-1134.
3宁显忠,邱月.脑出血患者预防性抑酸治疗对艰难梭菌相关性腹泻的影响研究[J].中国药房,2012,23(46):4376-4378. 被引量：1
4Buendgens L,Bruensing J,Matthes M,et al.Administration of proton pump inhibitors in critically ill medical patients is associated with increased risk of developing Clostridium difficile-associated diarrhea.J Crit Care,2014,29:e11-e15.
5Herzig SJ,Howell MD,Ngo LH,et al.Acid-suppressive medication use and the risk for hospital-acquired pneumonia.JAMA,2009,301:2120-2128.
6Wu T,Dong Z,Geng J,et al.Valsartan protects against ER stress-induced myocardial apoptosis via CHOP/Puma signaling pathway in streptozotocin-induced diabetic rats.Eur J Pharm Sci,2011,42:496-502.
7Wu B,Lin R,Dai R,et al.Valsartan attenuates oxidative stress and NF-κB activation and reduces myocardial apoptosis after ischemia and reperfusion.Eur J Pharmacol,2013,705:140-147.
8Kushwaha S,Jena GB.Telmisartan ameliorates germ cell toxicity in the STZ-induced diabetic rat:studies on possible molecular mechanisms.Mutat Res,2013,755:11-23.
9Krause EG,de Kloet AD,Scott KA,et al.Blood-borne angiotensinⅡacts in the brain to influence behavioral and endocrine responses to psychogenic stress.J Neurosci,2011,31:15009-15015.
10Zhang M,Mao Y,Ramirez SH,et al.AngiotensinⅡinduced cerebral microvascular inflammation and increased blood-brain barrier permeability via oxidative stress.Neuroscience,2010,171:852-858.

二级参考文献12

1Bajaj JS, Zadvornova Y, Heuman DM, et al. Association of proton pump inhibitor therapy with spontaneous bacte- rial peritonitis in cirrhotic patients with ascites[J]. Am J Gastroenterol,2009,104(5) : 1 130.
2Dial S, Delaney JA, Schneider V, et al. Proton pump in- hibitor use and risk of community-acquired Clostridium difficile-associated disease defined by prescription for oral vancomycin therapy[J]. CMAJ, 2006,175 (7) : 745.
3Lowe DO, Mamdani MM, Kopp A, et al. Proton pump in- hibitors and hospitalization for Clostridium difficile-asso- ciated disease: a population-based study[J]. Clin Infect Dis,2006,43(10):1 272.
4O' Donnell M J, Kapral MK, Fang J, et al. Gastrointesti- nal bleeding after acute ischemic stroke[J]. Neurology, 2008,71(9) :650.
5Prpin J, Saheb N, Coulombe MA, et al. Emergence of fl- uoroquinolones as the predominant risk factor for Clostridi- um difficile-associated diarrhea: a cohort study during an epidemic in Quebec[J]. Clin lnfect Dis, 2005,41 (9) : 1 254.
6WistrOm J, Norrby SR, Myhre EB, et al. Frequency of an- tibiotic-associated diarrhoea in 2 462 antibiotic-treated hospitalized patients: a prospective study[J]. JAntimicrob Chemother, 2001,47 ( 1 ) : 43.
7Dial S, Delaney JA, Barkun AN, et al.Use of gastric ac- id-suppressive agents and the risk of community-acquiredClostridium diffieile-assoeiated disease[J]..lAMA, 2005, 294(23) :2 989.
8Kelly CP, Pothoulakis C, LaMont JT.Clostridium difficile colitis[J]. N Engl J Med, 1994,330 (4) : 257.
9Barbut F, Petit JC. Epidemiology of Clostridium diffi-cile-associated infections[J]. Clin Microbiol Infect, 2001,7 (8):405.
10Lee KS, Shin WG, Jang MK, et al.Who are susceptible to pseudomembranous colitis among patients with presumed antibiotic-associated diarrhea?[J]. Dis Colon Rectum, 2006,49(10) : 1 552.