Influence of astragaloside on gastric mucosa of stress ulcer rats

Objective To investigate the effect of astragaloside(AST)on the gastric mucosal injury of water immersion restraint stress ulcer rat.Methods The stress ulcer model was made by water immersion and restraint.The gastric mucosal injury index was observed.The SOD activity,the MDA contents and the gene expression of melatonin receptor 1 and 2 were detected in gastric mucosa.Results Compared with the normal group,the model group showed mucous edema,hyperemia and even ulcer damage.The injury index and the MDA content of gastric mucosa in model group were significantly increased(P<0.05),the SOD activity of gastric obviously depressed(P<0.01),and the melatonin receptor 1 and 2 mRNA expressions of damaged gastric mucosa were also lower.After administration of AST,the gastric mucosal ulcer index and MDA contents relieved obviously(P<0.01,P<0.05),the SOD activity and the expressions of melatonin receptor 1 and 2 mRNA raised up(P<0.01,P<0.05).Conclusions AST could prevent the gastric mucosal damage of rat in stress ulcer.And the mechanism of the gastric mucosal protection should be concerned with regulating the melatonin receptor and lessening the injury of oxygen free radical.     

单宁酸对糖尿病模型大鼠肾脏氧化应激水平及炎性因子表达的抑制作用

目的 观察单宁酸对糖尿病模型大鼠抗氧化能力的影响及对机体微炎症状态的改善作用.方法 选择6周龄健康雄性Wistar大鼠68只,随机选取其中8只作为正常对照组,其余60只给予高糖高脂饲料喂养4周后以链脲佐菌素（STZ）按52 mg/kg单次腹腔注射制造糖尿病大鼠模型,造模成功的大鼠进一步随机分为模型组、氨基胍组、单宁酸低剂量组、单宁酸高剂量组,各15只.氨基胍组及单宁酸低、高剂量组分别腹腔注射氨基胍40 mg/（kg·d）及单宁酸[20、30 mg/（kg·d）],正常对照组和模型组给予0.9％氯化钠注射液[30 mg/（kg·d）],10周后处死大鼠取材.化学比色法检测各组大鼠血清及肾皮质丙二醛含量及谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）活性;酶联免疫吸附测定法检测肾组织匀浆8-羟基脱氧鸟苷（8-OHdG）含量、血清C反应蛋白（CRP）水平;免疫组织化学检测肾组织细胞间黏附分子1（ICAM-1）、单核细胞趋化蛋白1（MCP-1）的蛋白表达,逆转录-聚合酶链反应检测肾组织ICAM-1、MCP-1 mRNA表达.结果 单宁酸低、高剂量组大鼠血清丙二醛含量明显低于模型组[（23.5±8.5）、（19.8±5.3） μmol/L比（35.5±14.6） μmol/L]（P＜0.05或P＜0.01）,GSH-Px、总SOD及CAT活性明显高于模型组[GSH-Px：（295 ±58）、（322±52） U/L比（232 ±72） U/L,总SOD：（75±13）、（86±15） U/ml比（49±13） U/ml,CAT：（6.9±2.2）、（7.2±2.9） U/ml比（3.7±1.4） U/ml]（P＜0.05或P＜0.01）;单宁酸低、高剂量组大鼠肾组织匀浆丙二醛含量明显低于模型组[（344±120）、（269±52） μmol/L比（464±62） μmol/L]（P＜0.05或P＜0.01）;单宁酸高剂量组GSH-Px活性明显高于模型组[（32 ±8）U/L比（17±4） U/L]（P＜0.01）;单宁酸低剂量组总SOD活性明显高于模型组[（23±4）U/ml比（17±4） U/ml] （P＜0.05）;单宁酸高剂量组大鼠肾组织8-O     

自拟调脂饮对高脂血症大鼠血脂及过氧化物水平的影响

目的 观察自拟调脂饮对高脂血症模型大鼠血清TC、TG、HDL-C、LDL-C、血浆超氧化物歧化酶(SOD)活性和丙二醛含量的影响.方法 采用高脂饮食喂饲法建立大鼠高脂血症模型.建模成功后,将60只大鼠完全随机分为模型组、辛伐他汀组和血脂康组以及自拟调脂饮高、中、低剂量组,每组10只.另选10只大鼠作为空白对照组,以普通饲料喂养.自造模成功后第1天起,灌胃连续给药4周后处死动物,测定血清TC、TG、HDL-C和LDL-C含量,同时测定SOD活性和丙二醛含量.结果 自拟调脂饮高、中、低剂量组大鼠血清TC、TG、LDL-C、丙二醛含量明显低于模型组[TC:(5.52±0.17)、(6.45±0.36)、(7.28±0.31) mmol/L比(10.64±0.85) mmol/L;TG:(1.56±0.23)、(1.77±0.35)、(1.95±0.57) mmol/L比(2.85±0.36) mmol/L;LDL-C:(2.31±0.67)、(2.57±0.4)、(3.38±0.40) mmol/L比(4.95±0.81)mmol/L;丙二醛:(3.5±1.2)、(4.8±1.3)、(5.4±1.9)μmol/L比(6.9±2.4)μmol/L],HDL-C水平及SOD活性明显高于模型组[HDL-C:(0.79±0.57)、(0.44±0.26)、(0.62 ±0.21) mmol/L比(0.44±0.26) mmol/L; SOD:(83±22)、(80±19)、(76±18)U/ml比(52±21)U/ml],差异均有统计学意义(P＜0.05或P＜0.01).自拟调脂饮高、中、低剂量组与辛伐他汀组和血脂康组比较,TC、TG、LDL-C、HDL-C、SOD活性和丙二醛含量差异均无统计学意义(均P＞0.05).结论 自拟调脂饮能有效地调节血脂异常,具有明显的抗脂质过氧化能力.     

花天胶囊对前列腺增生大鼠超氧化物歧化酶和丙二醛的影响

目的 观察花天胶囊对前列腺增生大鼠超氧化物歧化酶(SOD)和丙二醛(MDA)的药理作用。方法 应用甲睾酮8 mg/kg灌胃给药,构建前列腺增生模型,各组大鼠(对照组,模型组,前列康组,花天胶囊高、中、低剂量组)连续28 d给予相应药物或0.9%氯化钠注射液。检测SOD活力和MDA含量。结果 给药后花天胶囊高剂量组大鼠SOD活力为(110.58±31.87)U/mgprot,中剂量组大鼠SOD活力为(115.70±45.76)U/mgprot,均比模型组明显增加(P<0.05);且高剂量组的MDA含量为(112.22±32.75)nmo L/mg,明显减少(P<0.01)。结论 花天胶囊可明显增加SOD活力、降低MDA含量,可能是其抗前列腺增生的作用机制之一,还需进一步研究。     

慢性肾脏病对患者氧化应激程度的影响及可能意义

目的 探讨慢性肾脏病患者氧化应激的变化以及可能意义.方法 选择我院肾内科住院的慢性肾脏病患者73例,以同期我院体检中心47例体检健康者为对照组.收集受试者血和尿标本,分别用硫代巴比妥酸法和黄嘌呤氧化酶法测定脂质过氧化产物丙二醛和超氧化物歧化酶(SOD)的水平;同时收集患者临床资料,分析慢性肾脏病患者氧化应激程度的变化,同时探讨慢性肾脏病不同分期对氧化应激程度的影响.结果 慢性肾脏病组血丙二醛明显高于对照组[(16.7±20.3)μmol/L比(5.9±1.2)μmol/L,P＜0.05],尿丙二醛和对照组差异无统计学意义[(3.7±3.2)μmol/L比(5.2±4.5)μmol/L,P＞0.05].慢性肾脏病组血SOD和尿SOD活性分别为(37 300±18 200)U/L、(16 200±5600)U/L明显低于对照组[分别为(44 000±9400)U/L、(24 600±7200)U/L,均P＜0.05].结论 慢性肾脏病患者氧化应激程度明显增高,氧化应激随着肾功能的恶化而进一步加重.

Abstract：

Objective To study the oxidative stress in patients with chronic kidney disease (CKD) and its potential significance. Methods Seventy-three in-patients with CKD at the division of nephrology and 47 health controls were enrolled in this study between 2007 and 2010. The blood and urine samples were collected to detect malonaldehyde (MDA) and the activity of superoxide dismutase (SOD). Meanwhile the clinical datum was analyzed to evaluate the impact of CKD on oxidative stress. Results Serum MDA dramatically increased in patients with CKD than that in controls [( 16.7 ± 20.3 ) μmol/L vs ( 5.9 ± 1.2 ) μmol/L,P ＜ 0.05], while SOD of serum and urine in CKD group decreased significantly compared with controls [(37 300 ± 18 200) U/L vs (44 000 ±9 400) U/L, ( 16200 ± 5 600) U/L vs ( 24 600 ± 7 200) U/L, P ＜ 0.05].. Conclusion Oxidative stress is enhanced in patients CKD and it aggravates with the deterioration of kidney function.     

注射用丹参多酚酸盐延缓衰老作用的实验研究

目的 观察丹参多酚酸盐延缓大鼠衰老的作用.方法 取健康6个月龄雄性Wistar大鼠100只,完全随机分为空白对照组、衰老模型组、阳性对照药（维生素E 200 mg/kg）组、丹参多酚酸盐30.0 mg/kg和15.0 mg/kg两个剂量组,每组20只.采用皮下注射5.0%D-半乳糖的方法制作大鼠衰老模型,观察给药后大鼠大脑组织中的超氧化物歧化酶（SOD）活性及丙二醛含量以及大脑蒲肯野细胞的凋亡指数.结果 与空白对照组比较,衰老模型组大鼠大脑组织SOD活性降低、丙二醛含量增加、蒲肯野细胞的凋亡指数增加[SOD：（140.60±2.67）U/mgprot比（189.00±3.95）U/mgprot;丙二醛：（0.83±0.04）nmol/mgprot比（0.38±0.04）nmoL/mgprot凋亡指数：（18.53±1.64）%比（6.00±0.38）%;P＜0.01];维生素E 100 mg/kg组、丹参多酚酸盐30.0 mg/kg和15.0 mg/kg两个剂量组与衰老模型组相比,大脑组织SOD活性均明显增加[（157.21±3.12）、（159.33±3.99）、（149.36±2.72）U/mgprot,均P＜0.01]、丙二醛含量显著降低（0.5999±0.030）、（0.606±0.042）、（0.657±0.046）,均P＜0.01,蒲肯野细胞凋亡指数显著降低[（36.24±1.76）%,（38.97±1.81）%,（45.70±1.96）%,均P＜0.01].丹参多酚酸盐30.0 mg/kg组与维生素E200 mg/kg组的作用差异无统计学意义（P＞0.05）,而丹参多酚酸盐15.0 mg/kg组与前两者的作用有统计学意义（P＜0.05）.结论 丹参多酚酸盐具有延缓大鼠大脑衰老的作用.     

中药虎杖水煎液对CCL4诱导肝纤维化的保护作用

目的 观察虎杖水煎液对四氯化碳(CCL4)诱导肝纤维化的作用.方法 40只大鼠随机均分为正常对照(A)组、肝纤维化模型(B)组、虎杖水煎液低剂量3 g/kg(C)组和高剂量6 g/kg(D)组.10周后,检测血清ALT、AST以及肝纤维化血清标志物透明质酸(HA)与Ⅵ型胶原(C-Ⅳ)水平,测定肝组织匀浆中超氧化物歧化酶(SOD)活性与丙二醛(MDA)含量,并取肝组织做病理形态学检查.结果 与B组相比,C、D组血清ALT、AST、HA和C-Ⅳ水平降低,肝组织中MDA含量减少,而SOD活性增加(P＜0.05或P＜0.01),肝纤维化的组织学改变亦减轻.结论 虎杖水煎液对CCL4诱导的肝纤维化具有一定保护作用.     

Role of central and peripheral ghrelin in the mechanism of gastric mucosal defence

Ghrelin, identified in the gastric mucosa, has been involved in the control of food intake and growth hormone (GH) release, but whether this hormone influences the gastric secretion and gastric mucosal integrity has been little elucidated. We compared the effects of intraperitoneal (i.p.) and intracerebroventricular (i.c.v.) administration of ghrelin on gastric secretion and gastric lesions induced in rats by 75% ethanol or 3.5 h of water immersion and restraint stress (WRS) with or without suppression of nitric oxide (NO)-synthase or functional ablation of afferent sensory nerves by capsaicin. The number and the area of gastric lesions was measured by planimetry, the GBF was assessed by the H₂-gas clearance method and blood was withdrawn for the determination of the plasma ghrelin and gastrin levels. In addition, the gastric mucosal expression of mRNA for CGRP, the most potent neuropeptide released from the sensory afferent nerves, was analyzed in rats exposed to WRS with or without ghrelin pre-treatment. Ghrelin (5–80 μg/kg i.p. or 0.6–5 μg/kg i.c.v.) increased gastric acid secretion and attenuated gastric lesions induced by ethanol and WRS. This protective effect was accompanied by a significant rise in the gastric mucosal blood flow (GBF), luminal NO concentration and plasma ghrelin and gastrin levels. Ghrelin-induced protection was abolished by vagotomy and significantly attenuated by L-NNA and deactivation of afferent nerves with neurotoxic dose of capsaicin. The signal for CGRP mRNA was significantly increased in gastric mucosa exposed to WRS as compared to that in the intact gastric mucosa and this was further enhanced in animals treated with ghrelin. We conclude that central and peripheral ghrelin exerts a potent protective action on the stomach of rats exposed to ethanol or WRS, and these effects depend upon vagal activity and hyperemia mediated by the NOS-NO system and CGRP released from sensory afferent nerves.     

The protective effect of cuminaldehyde on gastric mucosa in Rattus norregicus of experimental gastric ulcer北大核心CSCD

Aim To explore the effect of cuminaldehyde in cumin fruit on gastric ulcer and the protective mechanism via establishing the gastric ulcer model of rats was by ethanol injury. Methods Thirty-six male R. norregicus were divided into six groups: control group, model group, omeprazole positive control group and cuminaldehyde low, medium and high dosage groups. After seven days of continuous intragastric administration, the acute gastric ulcer of R. norregicus was tested by absolute alcohol. Gastric ulcer area, inhibition rate, gastric tissue antioxidant activity, serum inflammatory factors and gastric mucosal protective factors were detected in different groups. Results The results showed that cuminaldehyde significantly reduced the area of gastric ulcer and increased the inhibition rate of gastric ulcer. The inhibition rate of cuminaldehyde at high dose group was up to 74.65%, the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH) in gastric tissue significantly increased, and the contents of serum prolandin E2(PGE2) and NO in gastric tissue also significantly increased. The content of malondialdehyde (MDA) decreased. Compared with the model group, cuminaldehyde decreased the content of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in rat serum, and decreased the activity of myeloperoxidase (MPO). Conclusions Cuminaldehyde has good antioxidant stress ability and anti-inflammatory activity, increases the expression of protective factors, enhances the defense ability of gastric mucosa, and has obvious protective effect on acute gastric ulcer in R. norregicus. © 2023 Publication Centre of Anhui Medical University. All rights reserved.     

胃得安片对应激性胃溃疡模型大鼠的保护作用

目的:研究胃得安片对应激性胃溃疡模型大鼠的保护作用。方法:采用空腹、水浸拘束法复制大鼠胃溃疡模型。60只大鼠随机均分为正常对照(等容氯化钠注射液)组、模型(等容氯化钠注射液)组、雷尼替丁(0.015 g/kg)组与胃得安片高、中、低剂量(1.70、0.87、0.43 g/kg)组。观察大鼠胃大体情况,测定大鼠胃黏膜损伤指数、血清一氧化氮(NO)含量、胃组织超氧化物歧化酶(SOD)、诱导型一氧化氮合酶(i NOS)活性与丙二醛(MDA)、前列腺素E2(PGE2)含量,光学显微镜下观察大鼠胃组织病理变化。结果:与正常对照组比较,模型组大鼠胃黏膜损伤指数升高,血清NO含量减少,胃组织SOD活性减弱、i NOS活性增强、MDA和PGE2含量增加,差异有统计学意义(P<0.01或P<0.05);大鼠胃内出现暗红物质,黏膜细胞出现严重变形坏死,并出现多发性大面积浅表性溃疡。与模型组比较,胃得安片高、中、低剂量组大鼠胃黏膜损伤指数降低,血清NO含量增加,胃组织SOD活性增强、i NOS活性减弱、MDA含量减少、PGE2含量增加,差异有统计学意义(P<0.01或P<0.05);大鼠胃大体情况与组织病理情况有所改善。结论:胃得安片对应激性刺激导致的胃溃疡大鼠具有一定保护作用,其机制与改善大鼠血清抗氧化指标水平有关。     

唐古特大黄多糖对大鼠应激性胃溃疡的保护作用

目的：探讨唐古特大黄多糖(Rheum tanguticum polysaccharides，RTP)对大鼠应激性胃溃疡的保护作用。方法：用水浸束缚应激法(water immersion and restraint stress，WRS)复制大鼠应激性胃溃疡模型，提前灌胃给予大黄多糖，应激6h后处死动物，观察溃疡指数和胃粘膜损伤程度的变化，检测血清及胃粘膜组织中超氧物歧化酶(SOD)和丙二醛(MDA)的变化。结果：RTP能明显降低应激大鼠胃粘膜溃疡指数和胃粘膜MDA水平，升高血清和胃粘膜SOD活性。结论：RTP对水浸束缚应激引起的大鼠应激性胃溃疡有明显的保护作用，可能是大黄治疗应激性胃溃疡的有效成分之一。     

枸杞多糖对大鼠实验性胃溃疡的作用研究

目的 研究枸杞多糖对大鼠实验性胃溃疡的防治作用.方法 分别选取30只和50只SD大鼠建立水应激型和无水乙醇型胃溃疡模型,采用枸杞多糖对抗大鼠实验性胃溃疡,随机分为枸杞多糖大剂量组(LBP I组)、枸杞多糖中剂量组(LBP Ⅱ组)、枸杞多糖小剂量组(LBP Ⅲ组),通过计算抑制溃疡面积对其抗溃疡作用进行分析,结果枸杞多糖大剂量组能显著抑制水应激型大鼠胃溃疡,枸杞多糖大剂量组和中剂量组能显著抑制无水乙醇型大鼠胃溃疡.结论 枸杞多糖对大鼠实验性胃溃疡具有防治作用.     

尼美舒利对胃溃疡模型大鼠的保护作用研究

目的:研究环氧化酶-2选择性抑制剂尼美舒利对药物诱导胃溃疡的保护作用。方法:采用吲哚美辛灌胃给药制备大鼠胃溃疡模型,5min后按组别给予高、中、低(200、100、50mg·kg-1)不同剂量尼美舒利,6h后处死大鼠,观察胃溃疡面积和胃黏膜的损伤程度,检测血清及胃黏膜中超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽(GSH)值的变化。结果:与模型组比较,尼美舒利组大鼠胃溃疡面积明显减小,MDA水平降低,SOD和GSH活性升高(P<0.05或P<0.01)。结论:尼美舒利对吲哚美辛所致大鼠胃溃疡具有明显的保护作用。     

超氧化物歧化酶对急性胃粘膜损伤的保护作用

制作不同的动物急性胃粘膜损伤模型，应用外源性超氧化物歧化酶（ＳＯＤ）观测对急性胃粘膜损伤的保护作用。发现ＳＯＤ抑制应激、结扎幽门和阿斯匹林性胃溃疡的形成，降低大鼠胃溃疡形成过程中胃粘膜丙二醛（ＭＤＡ）含量，保护胃粘膜上皮并促进其粘液的分泌，但对胃酸的分泌量无明显影响。提示：ＳＯＤ的胃粘膜保护作用，可能与提高胃粘膜的防御能力有关。     

泮托拉唑对应激损伤大鼠胃黏膜修复作用的研究

目的:观察急性损伤的胃黏膜雌激素诱导基因相关肽(TFF1)表达及应用泮托拉唑后的变化,探讨,TFF1在应激胃黏膜损伤中的作用机制.方法:56只大鼠随机分为正常组、单纯造模组及造模干预组,各造模组制作大鼠水浸-束缚应激(WRS)模型,其中单纯造模组分为单纯造模1组(造模后即刻)、单纯造模2组(造模后4h)、单纯造模3组(造模后8 h),造模干预组分为造模十预1组(造模后即刻)、造模干预2组(造模后4 h)、造模干预3组(造模后8 h),观察胄黏膜损伤指数(UI)及组织学变化,采用免疫组化法检测TFF1蛋白的表达.结果:水浸束缚应激后胃黏膜广泛损伤:单纯造模组UI升高,TFF1表达降低.予泮托拉唑干预后,与相应单纯造模组相比UI降低(单纯造模1组与造模干预1组69.13±1.97 vs 23.38±1.30,单纯造模2组与造模干预2组57.50±8.81vs 10..38±3.02,单纯造模3组与造模干预3组43.50±6.76vs 5.88±1.25,均P＜0.01).TFF1染色计分增加(单纯造模1组与造模干预1组0.55±0.11vs 0.92±0.15,单纯造模2组与造模十预2组0.76±0.24vs 1.36±0.21,单纯造模3组与造模干预3组1.12±0.16vs 1.65±0.11,均P＜0.01).结论:TFF1可能参与胃黏膜保护,促进溃疡修复;泮托拉唑还可能通过上调雌激素诱导基因参与胃黏膜的防御屏障.     

褪黑素对脑出血大鼠应激性胃黏膜损伤的保护作用

目的 探讨褪黑素对脑出血大鼠应激性胃黏膜损伤的保护作用。方法 将60只健康成年SD大鼠随机分为空白对照组、模型组、奥美拉唑组、褪黑素组。空白对照组、模型组大鼠给予生理盐水灌胃,奥美拉唑组以奥美拉唑悬液灌胃,褪黑素组给予褪黑素灌胃,预防性给药,连续灌胃7 d,末次给药后禁食水24 h,除了空白对照组外,其余3组均制作脑出血大鼠模型,通过酶联免疫吸附法检测大鼠血清中超氧化物歧化酶(superoxidedismutase,SOD)、丙二醛(malonaldehyde,MDA)含量,大体观察大鼠胃黏膜病变并计算溃疡指数(UI),HE染色光镜下观察胃黏膜组织形态学改变,并比较各组胃黏膜损伤的发病率。结果 褪黑素的治疗增加了SOD含量,降低MDA含量、降低大鼠胃黏膜UI及胃黏膜损伤的发病率(P<0.05)。结论 褪黑素可通过清除氧自由基而对应激性胃黏膜起到保护作用。     

尼美舒利对吲哚美辛诱导的大鼠胃黏膜损伤的保护作用

目的探讨尼美舒利对胃黏膜的保护作用及其可能的作用机制。方法大鼠禁食12h后,ig给予吲哚美辛30mg·kg-1制备急性胃黏膜损伤模型,5min后分为模型对照、尼美舒利100mg·kg-1、塞来昔布100mg·kg-1、美洛昔康4mg·kg-1、双氯芬酸钠50mg·kg-1和布洛芬600mg·kg-1组,分别ig给予相应药物;另设正常对照组。6h后处死所有大鼠,测定胃溃疡面积。生化比色法检测大鼠胃组织和血清中谷胱甘肽(GSH)和丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。结果正常对照组大鼠胃黏膜表面光滑,黏膜皱襞纹理清晰;模型组大鼠均见急性胃溃疡,溃疡面积为(10.6±7.4)mm2;与模型组比较,尼美舒利和塞来昔布组胃溃疡面积显著减小,分别为4.1±1.7和(4.9±3.2)mm2(P<0.01);美洛昔康组未见明显变化,为(8.1±3.5)mm2;双氯芬酸钠和布洛芬组胃溃疡面积明显增加,分别为15.4±4.8和(16.0±7.3)mm2(P<0.01)。与正常对照组比较,模型组大鼠胃组织中GSH含量和SOD活性明显降低(P<0.05),MDA含量显著升高(P<0.01);血清中MDA含量显著升高(P<0.01),而GSH含量和SOD活性变化不明显。与模型组相比,尼美舒利组胃组织中GSH含量和SOD活性明显升高(P<0.05,P<0.01),MDA含量明显降低(P<0.01);血清中GSH含量明显增加(P<0.01),MDA含量明显降低(P<0.01);塞来昔布组大鼠胃组织中SOD活性明显升高(P<0.01),血清中MDA含量明显降低(P<0.01),其他指标无明显变化;美洛昔康、双氯芬酸钠和布洛芬对模型大鼠胃组织和血清中GSH,MDA含量及SOD活性均无明显影响。结论尼美舒利对吲哚美辛诱导的大鼠急性胃黏膜损伤具有明显的保护作用,作用机制可能与其抗氧化活性有关。     

绞股蓝总皂苷对NCTC11637株HP延缓大鼠实验性胃溃疡愈合的治疗作用及其机制

目的探讨绞股蓝总皂苷（ｇｙｐｅｎｏｓｉｄｅｓ,ＧＰ）对ＣａｇＡ（＋）,ＶａｃＡ（＋）ＮＣＴＣ１１６３７株幽门螺杆菌（Ｈｅｌｉｃｏｂａｃｔｅｒｐｙ ｌｏｒｉ,ＨＰ）延缓动物实验性胃溃疡愈合的治疗作用及其机制。方法用醋酸诱发大鼠实验性胃溃疡,以溃疡面积、溃疡面积占腺胃部百分比、粘膜组织内白细胞介素 ８（ＩＬ ８）、ＰＧＥ２、ＭＤＡ、ＳＯＤ、·ＯＨ及溃疡愈合时间为指标,观察ｉｇ给予冻干ＮＣＴＣ１１６３７ＨＰ的影响及给予ＨＰ１ｈ后ｉｇＧＰ的治疗作用。结果单给ＨＰ组,溃疡面积加大,愈合延迟,粘膜组织内ＩＬ ８、ＭＤＡ升高,ＳＯＤ活性下降;·ＯＨ生成无明显变化;损伤粘膜组织内ＩＬ ８升高,ＰＧＥ２亦同时升高。ＨＰ＋ＧＰ组溃疡面积、溃疡面积百分率明显减小;粘膜内ＭＤＡ、·ＯＨ生成抑制,ＩＬ ８、ＰＧＥ２平行下降,ＳＯＤ活性提高。结论ＮＣＴＣ１１６３７株ＨＰ可明显延缓醋酸性大鼠胃溃疡的愈合;绞股蓝总皂苷通过抑制炎症反应过程中ＩＬ ８、ＭＤＡ、·ＯＨ生成,并通过提高ＰＧＥ２和ＳＯＤ活性增强胃粘膜保护机制,对感染ＮＣＴＣ１１６３７株ＨＰ大鼠实验性胃溃疡产生显著治疗作用。     

Effects of the anti-ulcer agents on the amine contents and regulating enzyme activity of gastric mucosa during the healing process of acetic acid induced gastric ulcer in rats

In order to elucidate the action of an H2 blocker (cimetidine) and gastric mucosal protection agents (sucralfate and sofalcone) on the relapse and recurrence of gastric ulcer, the effects of cimetidine, sucralfate and sofalcone on the contents of histamine and serotonin and histidine decarboxylase (HDC) activity in the gastric mucosa were examined in the ulcer region and the intact region at the 10th day after the operation to produce acetic acid-induced gastric ulcer in rats. The following results were obtained: 1) HDC activity in the gastric mucosa of rats treated with cimetidine (100 mg/kg twice daily) tended to increase in the intact region, and it was significantly increased in the ulcer region. 2) Increased HDC activity due to cimetidine treatment was observed at the 10th day after interruption of cimetidine administration. 3) The HDC activity in the gastric mucosa was not changed by the treatment with sucralfate (500 mg/kg/day) and sofalcone (200 mg/kg/day). The results suggest that the increased HDC activity in the gastric mucosa might participate in the relapse and recurrence of gastric ulcer after discontinuation of cimetidine administration.