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1.
Nigella sativa decreases DNA damage and thereby prevents initiation of carcinogenesis in colonic tissue secondary to exposure to toxic agents such as azoxymethane. N. sativa is of immense therapeutic benefit in diabetic individuals and those with glucose intolerance as it accentuates glucose-induced secretion of insulin besides having a negative impact on glucose absorption from the intestinal mucosa. N. sativa administration protects hepatic tissue from deleterious effects of toxic metals such as lead, and attenuates hepatic lipid peroxidation following exposure to chemicals such as carbon tetrachloride.  相似文献   

2.
AIM: To examine the anti-ulcerogenic and antioxidant effects of aqueous extracts of Foeniculum vu/gare (FVE) on ethanol-induced gastric lesions in rats.
METHODS: FVE was administered by gavage at doses of 75, i50 and 300 mg/kg, and famotidine was used at the dose of20mg/kg.Following a 60 min period, all the rats were given 1 mL of ethanol (80%) by gavage. One hour after the administration of ethanol, all groups were sacrificed, and the gastric ulcer index was calculated; whole blood malondialdehyde (MDA) and reduced glutathione (GSH), serum nitrate, nitrite, ascorbic acid, retinol and β-carotene levels were measured in all the groups.
RESULTS: It was found that pretreatment with FVE significantly reduced ethanol-induced gastric damage. This effect of FVE was highest and statistically significant in 300 mg/kg group compared with the control (4.18 ± 2.81 vs 13.15 ± 4.08, P 〈 0.001). Also, pretreatment with FVE significantly reduced the MDA levels, while significantly increased GSH, nitrite, nitrate, ascorbic acid, retinol and β-carotene levels.
CONCLUSION: FVE has clearly a protective effect against ethanol-induced gastric mucosal lesion, and this effect, at least in part, depends upon the reduction in lipid peroxidation and augmentation in the antioxidant activity.  相似文献   

3.
AIM: To investigate the effects of Nigella sativa L (NS) and Urtica dioica L (UD) on lipid peroxidation, antioxidant enzyme systems and liver enzymes in CCl4-treated rats. METHODS: Fifty-six healthy male Wistar albino rats were used in this study. The rats were randomly allotted into one of the four experimental groups: A (CCU-only treated), B (CCU+UD treated), C (CCU+NS treated) and D (CCl4+UD+NS treated), each containing 14 animals. All groups received CCU (0.8 mL/kg of body weight, sc, twice a week for 60 d). In addition, B, C and D groups also received daily i.p. injections of 0.2 mL/kg NS or/and 2 mL/kg UD oils for 60 d. Group A, on the other hand, received only 2 mL/kg normal saline solution for 60 d. Blood samples for the biochemical analysis were taken by cardiac puncture from randomly chosen-seven rats in each treatment group at beginning and on the 60th d of the experiment. RESULTS: The CCl4 treatment for 60 d increased the lipid peroxidation and liver enzymes, and also decreased the antioxidant enzyme levels. NS or UD treatment (alone or combination) for 60 d decreased the elevated lipid peroxidation and liver enzyme levels and also increased the reduced antioxidant enzyme levels. The weight of rats decreased in group A, and increased in groups B, C and D. CONCLUSION: NS and UD decrease the lipid peroxidation and liver enzymes, and increase the antioxidant defense system activity in the CCl4-treated rats.  相似文献   

4.
5.
The conventional physical and chemical synthetic methods for the preparation of metal nanoparticles have disadvantages as they use expensive equipment and hazardous chemicals which limit their applications for biomedical purposes, and are not environment friendly. However, for the synthesis of biocompatible nanomaterials, plant-based techniques are eco-friendly and easy to handle. Herein a simple, single-step biosynthesis of gold nanoparticles using aqueous extracts of Nigella sativa (NSE) and Zingiber officinale (GE) as a reducing and capping agent has been demonstrated. The formation of gold nanoparticles (Au NPs) was confirmed by X-ray diffraction, UV-Vis, and EDS spectroscopies. Spectroscopic and chromatographic analysis of GE and NSE revealed the presence of bioactive phytochemical constituents, such as gingerol, thymoquinone, etc., which successfully conjugated the surface of resulting Au NPs. TEM analysis indicated the formation of smaller-sized, less-aggregated, spherical-shaped Au NPs both in the case of GE (~9 nm) and NSE (~11 nm). To study the effect of the concentration of the extracts on the quality of resulting NPs and their anticancer properties, three different samples of Au NPs were prepared from each extract by varying the concentration of extracts while keeping the amount of precursor constant. In both cases, high-quality, spherical-shaped NPs were obtained, only at a high concentration of the extract, whereas at lower concentrations, larger-sized, irregular-shaped NPs were formed. Furthermore, the as-prepared Au NPs were evaluated for the anticancer properties against two different cell lines including MDA-MB-231 (breast cancer) and HCT 116 (colorectal cancer) cell lines. GE-conjugated Au NPs obtained by using a high concentration of the extract demonstrated superior anticancer properties when compared to NSE-conjugated counterparts.  相似文献   

6.
7.
Background Proanthocyanidin, a grape-seed polyphenol, has been reported to have protective properties against vascular injury and ulcers, preventive effects against atherosclerosis and cancer, and antioxidative effects, such as improving lipid metabolism and slowing aging. However, little has been reported on its antiulcer effects. We aimed to elucidate the antiulcer mechanism of proanthocyanidin.Methods Gravinol, containing 89.3% proanthocyanidin, was used. Proanthocyanidin solution, in distilled water, at 0.002%, 0.02%, 0.2%, or 1%, was given to rats ad libitum for 2 weeks. Distilled water was given to control rats. The effect of proanthocyanidin on gastric mucosal injury was investigated with the water-immersion restraint stress model. The ratios of areas of hemorrhagic erosion were compared as the lesion index. Myeloperoxidase activities were also examined, as an index of tissue injury. Superoxide dismutase activity was measured to examine its antioxidative effect. Furthermore, serum gastrin, somatostatin, histamine, and prostaglandin E2 levels were measured in this rat model.Results Proanthocyanidin administration significantly suppressed gastric mucosal injury, induced by water-immersion restraint stress, in a dose-dependent manner. Myeloperoxidase activities were also significantly inhibited, whereas superoxide dismutase activities were significantly stimulated. As to gastrointestinal hormones, the secretion of gastrin, somatostatin, and histamine was significantly inhibited, while prostaglandin E2 secretion was significantly stimulated.Conclusions Proanthocyanidin was shown to have a protective effect on the gastric mucosa. The mechanisms underlying the effect of proanthocyanidin were considered to be the following: anti-gastrin and anti-histamine effects to prevent attacks by water-immersion restraint stress, and mucoprotective properties, bestowed by increased prostaglandin and increased superoxide dismutase activities in the gastric mucosa.  相似文献   

8.
We aimed to evaluate the protective effects of pentoxifylline on alcohol-induced gastric injury, its relation with nitric oxide and prostaglandin synthesis, as well as gastric acidity in rats. Acute gastric mucosal injury was induced by intragastric infusion of 2 ml 98% alcohol. Pentoxifylline was given at 100 mg/kg intraperitoneally. Indomethacin and NG-nitro-L arginine were used to inhibit prostaglandin and nitric oxide synthesis, respectively. Macroscopic and microscopic gastric injuries were evaluated. Gastric pH, tissue malondialdehyde levels, oxidized and reduced glutathion (GSSG/GSH) levels, and effects of pentoxifylline on gastric acid output were measured. Pentoxifylline pretreatment significantly reduced macroscopic and microscopic gastric injury. Malondialdehyde level was lower in pentoxifylline treated rats (351.1 ± 94.1 nmol/g vs 624.3 ± 234.2 nmol/g). Pentoxifylline has a protective role on alcohol-induced gastric mucosal injury in rats. This effect is not related to synthesis of prostaglandins and changes in gastric acidity but does seem to be related to nitric oxide-mediated pathways. In contrast, pentoxifylline increases gastric acid output significantly.  相似文献   

9.
目的 评价铝碳酸镁等常用黏膜保护剂对乙醇、阿司匹林、盐酸、泼尼松龙诱发的大鼠胃黏膜损伤的保护作用,并观察铝碳酸镁的黏膜保护作用与胃黏膜上皮细胞间隙变化的关系.方法 采用四种方法造模.①乙醇造模:采用雄性Wistar大鼠84只,分为7组,每组12只,分别给予铝碳酸镁、麦滋林、替普瑞酮、吉法酯、硫糖铝、瑞巴派特、0.9%氯化钠溶液3 d,第4天动物在给药后再经口给予无水乙醇l ml造模.之后处死动物观察药物对大鼠胃黏膜损伤的作用.计算各组胃黏膜损伤长度(mm)作为损伤指数.②阿司匹林造模:经口给予阿司匹林(300 mg/kg)及0.1 mol/L盐酸0.5 ml/100 g造模,余实验方法同①.③盐酸造模:经口给予0.7 mol/L盐酸1 ml造模,余实验方法同①.④泼尼松龙造模:动物分组及给药剂量同其他模型,给药或0.9%氯化钠溶液5 d,第2~5天每天皮下注射泼尼松龙(250 mg/kg),第5天处死动物,用Guth法计算损伤指数.取每种动物模型对照组及铝碳酸镁组的第1、5和10号动物胃黏膜组织,用透射电镜检测细胞间隙的变化.结果 四种胃黏膜损伤模型中,各黏膜保护剂用药组胃黏膜损伤指数均显著小于对照组(P值均<0.05),其中铝碳酸镁组与对照组比较差异有统计学意义(P<0.01).同时铝碳酸镁组胃黏膜上皮细胞间隙显著小于对照组(P<0.05).结论 六种常用黏膜保护剂对乙醇、盐酸、阿司匹林、泼尼松龙诱发的胃黏膜损伤均有保护作用,其中铝碳酸镁的保护作用更显著.观察胃黏膜上皮细胞间隙可从细胞学水平进一步证实铝碳酸镁的黏膜保护作用.  相似文献   

10.
The efficacy of omeprazole in preventing gastric mucosal injury induced by hemorrhagic shock in rats and the putative mechanisms involved in this effect were investigated in the present study. Omeprazole did not affect mean arterial blood pressure under both basal conditions and induction of hemorrhagic shock, but it evoked a marked increase in Alcian blue recovery from gastric preepithelial mucus. The morphometric analysis of histological sections revealed that omeprazole caused a significant reduction of hemorrhagic shock-induced damage of gastric mucosa. Ranitidine, used as the reference drug, failed to affect mean arterial blood pressure, Alcian blue recovery from gastric mucus, or hemorrhagic shock-induced damage of gastric mucosa. Both omeprazole and ranitidine exerted a significant inhibition of gastric acid output from anesthetized pylorus-ligated rats. Overall, the present results indicate that omeprazole is effective in protecting gastric mucosa from necrotic damage induced by hemorrhagic shock and suggest that an enhancement of gastric mucus secretion contributes to this protective action.  相似文献   

11.
Introduction: We investigated the effect of Ricetrienol, which is an anti‐oxidant extracted from rice bran, and α‐tocopherol on the adipocytokine abnormalities and fatty liver in Otsuka Long‐Evans Tokushima Fatty (OLETF) rats. Materials and Methods: A total of 18 OLETF rats were bred using a 30% sucrose solution (the diabetic group; DM), whereas another 18 OLETF rats were bred using ordinary water (the non‐diabetic obese group; OB) as drinking water, respectively. After the sucrose‐fed rats developed diabetes, all of the rats from the diabetic and obese groups were randomly divided into three groups. Then each group was fed either standard chow (DM‐S, OB‐S group), 0.05% Ricetrienol‐containing chow (DM‐R, OB‐R group) or 0.05%α‐tocopherol‐containing chow (DM‐A, OB‐A group), respectively. After 12 weeks of feeding, all the rats were killed. Plasma insulin, adiponectin, resistin and leptin were assayed by enzyme immunoassay. Histopathological findings of liver tissue were scored according to Brunt and Kleiner’s method, and triglyceride contents of the liver tissue were investigated. Results: Plasma adiponectin was significantly reduced in DM‐S compared with OB‐S, but it had significantly increased in DM‐R and DM‐A as opposed to DM‐S. Plasma resistin showed a significant increase in DM‐S compared with OB‐S, but it was significantly reduced in DM‐A than in DM‐S. Though the triglyceride contents of liver tissue significantly increased in DM‐S as opposed to OB‐S, they were significantly reduced in DM‐R compared with DM‐S. Histopathological scores were significantly higher in DM‐S than OB‐S. Conclusions: The present study shows that Ricetrienol might prevent adipocytokine abnormalities and fatty liver in OLETF diabetic rats. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.00090.x, 2011)  相似文献   

12.
目的:探讨复方丹参注射液对门脉高压性胃病(PHG)模型大鼠胃黏膜的保护作用及其分子机制,方法:采用一期部分门静脉缩窄法制备PHG大鼠模型,♂Wistar大鼠70只,随机分为3组:模型对照组(n=30)、复方丹参治疗组(n)=30)、正常对照组(n=10).造模后各时段(5、10、15、20、30、45 d)处死大鼠取胃...  相似文献   

13.
Active oxygen species generated by circulating leukocytes and released from the gastric mucosa were measured in the process of acute gastric mucosal lesion formation after thermal injury in rats. Alterations of luminol-dependent chemiluminescence activities generated by leukocytes obtained from the gastric vein and the inferior vena cava were approximately same. A decrease in chemiluminescence activity 15 min after thermal injury and a significant increase in chemiluminescence activity 5 hr after thermal injury were observed in leukocytes from both veins. From 15 min to 12 hr after thermal injury, luciferin-dependent chemiluminescence activities were significantly higher than that of the control group. Oral administration of rebamipide resulted in decreased mucosal lesion formation. Rebamipide, an antiulcer agent that protects the mucosa from damage in various animal models decreased chemiluminescence activities only released from the gastric mucosa but not from circulating leukocytes. These results suggest that two different pathways of active oxygen species formation may exist in the pathogenesis of acute gastric mucosal lesions after thermal injury.Part of this study was presented at the Second Osaka International Symposium on Gastroenterology held in Osaka, Japan, on November 22–23, 1993.  相似文献   

14.
The present study was designed to determine the role of leukotrienes in aspirin-induced acute gastric mucosal injury in rats. We examined the effects of aspirin, indomethacin, and sodium salicylate on gastric mucosal injury, and on eicosanoid synthesis and content. Aspirin, indomethacin, and acidified salicylate caused significant mucosal injury, while salicylate at pH 7 did not induce significant injury. Aspirin and indomethacin significantly reduced mucosal prostaglandin synthesis and content. No significant changes in mucosal leukotriene C4 synthesis and content were observed. There were no correlations between changes in mucosal leukotriene B4 synthesis and the extent of mucosal injury. We also evaluated the effects of MK-571 (a leukotriene D4 receptor antagonist) and MK-886 (a leukotriene biosynthesis inhibitor) on aspirin-induced gastric mucosal injury. Neither MK-571 nor MK-886 could reduce the mucosal lesions induced by aspirin. These findings suggest that leukotrienes are not involved in aspirin-induced acute gastric mucosal injury in rats.This work was supported in part by grants from the Research Service of the Department of Veterans Affairs and the National Institutes of Health (DK 16816).  相似文献   

15.
Inhibition of monoamine oxidase B (MAO B) by selective inhibitors pargyline and l-deprenyl increases dopamine (DA) and norepinephrine (NE) concentrations in nucleus accumbens (NACB) and is associated with reduction in cold water restraint-induced gastric mucosal injury, inhibition of basal gastric acid output, and regional gastric mucosal blood flow. Similar effects were not observed with administration of MAO A inhibitors. These observations suggest that activation of central dopamine and norepinephrine receptors, particularly in NACB, are involved in the control of gastric mucosal function.Supported by PHS grant DK 38198 (G.K.).  相似文献   

16.
Leptin mRNA表达的组织分布及在大鼠急性肠道损伤中的变化   总被引:3,自引:0,他引:3  
目的:探讨leptin在急性炎症反应中的作用.方法:采集正常大鼠下丘脑、肺、肝、脾、胃、十二指肠、肾、附睾脂肪垫、睾丸等重要脏器标本,以RT-PCR法检测leptinmRNA表达的组织分布;并建立大鼠盲肠结扎穿孔模型,设立假手术组(A)和脂肪乳组(B)、单纯损伤组(C)、雌二醇组(D)、胰岛素组(E)等实验组,采用RT-PCR检测脂肪、肝及肺内leptinmRNA表达的变化.结果:正常大鼠的上述9种重要脏器内均有leptinmRNA表达,肾脏内含量最高而睾丸内含量最低.大鼠盲肠结扎穿孔12h后,与A组leptinmRNA表达水平相比,其在B组脂肪内表达显著增高而在肝、肺内表达显著降低,在C组肝内表达无显著差异而在脂肪、肺内表达显著降低,在D组肺内表达显著增高而在脂肪、肝内表达显著降低,在E组肺内表达无显著差异而在脂肪、肝内表达显著降低.脂肪乳对leptinmRNA表达的影响具有中枢分泌组织(脂肪)内诱导而外周脏器内抑制的双向模式.结论:LeptinmRNA表达水平在干预急性肠道损伤后能量代谢和神经-内分泌功能时发生敏感变化,提示leptin可能作为一种核心保护因子促进内环境的稳定.  相似文献   

17.
INTRODUCTION It has been accepted that the pathogenesis of ulcer is complex and related to different pathogenic factors. The most common side-effect of indomethacin (NSAID) is gastric mucosal damage. The inhibition of the biosynthesis of gastric prostagla…  相似文献   

18.
埃索美拉唑对胃黏膜的保护作用及其机制   总被引:1,自引:0,他引:1  
目的:探讨埃索美拉唑对大鼠胃黏膜保护的作用及其机制.方法:在乙醇诱导大鼠胃黏膜损伤前,预先给予埃索美拉唑(20 mg/kg)灌胃,L-硝基-精氨酸甲酯(L-NAME,4 mg/kg)和L-精氨酸(250 mg/kg)iv.采用激光多普勒血流计(LDF)测定胃黏膜血流量(GMBF),镉粒还原和比色法测定胃黏膜和血浆NO-2/NO-3含量,并观察胃黏膜损伤指数(ulcer index,UI)、溃疡坏死组织和中性粒细胞浸润严重程度的变化.结果:与模型损伤组比,埃索美拉唑组大鼠UI明显降低(5.6±2.2 vs 25.3±2.4,P<0.01),溃疡坏死组织和中性粒细胞浸润程度明显减轻(P<0.01).预先用L-NAME处理后,埃索美拉唑保护胃黏膜损伤作用明显减弱;L-NAME抑制作用可被L-精氨酸拮抗.向胃内灌注埃索美拉唑,可增加GMBF、胃黏膜和血浆NO-2/NO-3,L-NAME可逆转这种作用,但对埃索美拉唑抑制酸分泌作用无明显影响.结论:埃索美拉唑通过NO介导对大鼠胃黏膜损伤有重要的保护作用,而与埃索美拉唑抑制酸分泌作用无关.  相似文献   

19.
目的研究大鼠酒精性胃损害中,一氧化氮(NO)、内皮素(ET)和氧自由基的作用,以及NO对ET-1、丙二醛(MDA)水平的影响.方法以酒精给大鼠灌胃制备急性胃粘膜损害模型,实验分为五组,应用L-NAME或/和L-Arg依不同分组行尾静脉注射.取门脉血测定NO、ET-1和MDA水平,并取出胃进行形态学观察.结果酒精灌胃后,大鼠门脉血NO含量降低,ET-1和MDA量升高,粘膜损伤加重.L-NAME组NO进一步减少,ET-1和MDA更加升高,粘膜损伤明显加重.L-Arg与L-NAME合用后NO、ET-1及MDA水平均有不同程度恢复,粘膜损伤亦减轻.NO与ET-1及MDA水平呈负相关.结论在酒精性胃损害中,ET-1与氧自由基生成增加,起损害作用,内源性NO可调节ET-1的生成,清除氧自由基而发挥保护作用.  相似文献   

20.
潘托拉唑对胃黏膜损伤保护作用及其机制   总被引:2,自引:2,他引:0  
目的:探讨潘托拉唑对大鼠胃黏膜损伤保护的作用及其机制.方法:在乙醇诱导大鼠胃黏膜损伤前,预先给予(iv)潘托拉唑(20mg/kg)、L-硝基-精氨酸甲酯(L-NAME,4mg/kg)及L-精氨酸(250mg/kg).采用激光多普勒血流计(LDF)测定胃黏膜血流量(GMBF),采用镉粒还原和比色法测定胃黏膜和血浆NO-2/NO-3含量,并观察了胃黏膜损伤指数(ulcerindex,UI)、溃疡坏死组织和中性粒细胞浸润严重程度的变化.结果:与模型损伤组比,潘托拉唑组大鼠UI明显降低(5.7±2.1vs25.4±2.5,P<0.01),溃疡坏死组织和中性粒细胞浸润程度明显减轻.预先用L-NAME处理后,潘托拉唑保护胃黏膜损伤作用明显减弱;L-NAME抑制作用可被L-精氨酸拮抗.iv潘托拉唑,可增加GMBF、胃黏膜和血浆NO-2/NO-3,L-NAME可逆转这种作用,但对潘托拉唑抑制酸分泌作用无明显影响.结论:潘托拉唑通过一氧化氮介导对大鼠胃黏膜损伤有重要的保护作用,而与潘托拉唑抑制酸分泌作用无关.  相似文献   

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