氧化应激对动物消化道结构与功能影响的研究
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摘要
氧化应激是人类和动物范围极广的综合病症的主要原因之一。这些综合病症包括肠炎、肠蠕动紊乱、各种急性炎症,诸如创伤愈合过程中出现的炎症、心血管疾病、神经紊乱及一些与代谢有关的疾病等。其中对消化道的氧化损伤在动物生产中发生率极高,由于慢性应激状态下,表征不易察觉,危害性极大。消化道是动物体内营养素的消化、吸收和代谢的主要器官,因此,过量的自由基极易诱发胃肠疾病及消化道功能紊乱。本课题拟建立体外和体内氧化应激模型,选用大鼠和仔猪为试验对象,从消化道发育、结构、功能、功能激素基因表达等多方面研究自由基对动物胃肠功能的调控及氧化干预机制。
1.自由基对离体大鼠小肠上皮细胞的损伤及干预研究
选用5只初生未经哺乳的Wistar大鼠,于当日屠宰取出小肠,并进行小肠上皮细胞分离。细胞体外培养72h后,建立黄嘌呤/黄嘌呤氧化酶(X/XO)体外氧化损伤模型,细胞随机分为七组:对照组A加入等量的高温灭菌的三蒸水,氧化损伤B、C、D各组加入X (10μmol/L),并分别加入XO(10,40,70 U/L),抗氧化E、F、G各组加入X(10μmol/L)和谷胱甘肽(GSH,1.5μmol/ml),并分别加入XO(10,40,70U/L)。应激培养24h后,通过测定细胞活力、DNA片段化、凋亡率及细胞内外氧化还原指标,研究氧化应激对离体小肠上皮细胞增值、功能、凋亡的影响以及对细胞的氧化损伤干预机制。结果表明,不同剂量的X/XO均可导致离体大鼠IEC氧化应激的发生。在相对轻度的氧化应激条件下(XO,10U/L),离体大鼠IEC增殖明显降低,而抗氧化酶合成出现应激响应,其中SOD的活性略高于对照组(P>0.05),适度的氧化应激可能选择性的刺激氧化酶的合成。高活性的XO(40、70 U/L)导致细胞膜氧化脂质化程度显著提高,细胞膜通透性增强,细胞内Ca2+浓度的明显增加(P<0.05);随着添加的XO活性提高,DNA片段化和细胞凋亡率均呈上升趋势。添加GSH提高了离体大鼠IEC抗氧化酶活性及的总抗氧化能力;与相应的X/XO单独处理组比较,GSH显著降低了细胞内钙离子浓度和细胞凋亡率;同时GSH显著降低了XO(10, 40 U/L)两剂量组脂质氧化程度(P<0.05)。上述结果表明:X/XO系统导致离体培养大鼠IEC氧化损伤和细胞凋亡,轻度的氧化应激即可显著的降低小肠上皮细胞的增殖,外源性GSH能够有效抑制诱发性氧化应激对IEC造成的氧化损伤。
2.半胱胺对吲哚美辛诱发的胃粘膜氧化损伤及其能量代谢影响
选用45只体重200-250克的雄性SD大鼠。试验随机分为3组,对照组(A):灌服生理盐水1ml/只;单纯应激组(B):灌服吲哚美辛(IND,45mg/kg体重);抗氧化组(C):灌服半胱胺(CS,100mg/kg体重),1小时后灌服IND(45mg/kg体重)。分别在6、12、24小时3个时相点屠宰,分别测定:胃液PH值,血浆生长抑素浓度,胃粘膜溃疡指数(UI),胃壁细胞H+,K+-ATP酶活性,前列腺素E2(PGE2),黄嘌呤氧化酶(XO)活性,抗氧化指标(SOD, GSH, CAT),MDA含量,胃粘膜组织中及其线粒体内腺苷酸(ATP/ADP/AMP)含量和诱导型一氧化氮合成酶(iNOS)的基因表达。结果表明:灌服IND的大鼠胃泌酸能力迅速增强,6h即出现胃粘膜损伤,胃粘膜UI随应激时间延长而明显增加(P<0.05);CS在试验后期显著抑制了胃泌酸,同时降低了UI。IND处理大鼠提高了胃粘膜中H+,K+-ATP和黄嘌呤氧化酶(XO)酶活性,CS有效的抑制了H+,K+-ATP酶和XO活性的提高,但与对照组比较各时相点仍然均有提高。氧化损伤导致血浆中生长抑素的浓度迅速提高,CS使生长抑素在24h降低到生理水平。灌服IND后,各时相点胃粘膜PGE2含量均出现显著降低(P<0.05),CS有效的抑制PGE2下降,但仍然低于对照组。IND导致胃粘膜组织的氧化损伤,脂质化明显增强,CS对粘膜起到显著抗氧化保护作用,降低了脂质化程度。氧化应激发生时胃粘膜和胃粘膜线粒体中ATP、ADP、AMP、总腺苷酸池含量及能荷值均有明显降低,CS处理后使得ADP含量和能荷值与对照组差异不明显(P>0.05);其它各项指标在线粒体中含量显著高于损伤组,但在胃粘膜中与损伤组比较差异不显著。在24h时相点,IND处理组大鼠胃粘膜中iNOS mRNA基因表达量显著高于对照组和CS处理组;CS抑制了大鼠iNOS mRNA基因表达量,但仍然显著高于对照组(P<0.05)。综上所述,急性的氧化应激导致胃粘膜的氧化损伤,影响了胃正常的分泌功能和结构完整性,组织内氧化还原状态失衡,粘膜内的能量代谢紊乱,能荷降低,促使iNOS mRNA基因表达增强,抗氧化剂(CS)有效的抑制了氧化应激,显著抑制了部分氧化指标的变化。
3.自由基对实验性肠炎仔猪肠道结构、功能调控作用研究
选取21±2日龄的断奶仔猪50头,利用右旋糖苷硫酸钠(DSS)诱导仔猪肠炎模型,随机分为5个处理组,1组,基础日粮,饮用自来水;2组,基础日粮,饮用含4%DSS水;3组,基础日粮+0.03%FeSO4+含4%DSS的水;4组,基础日粮+0.2%FeSO4+含4% DSS水;5组,基础日粮+1%FeSO4+含4%DSS的水,试验期10天。测定仔猪生产性能、腹泻率、消化率、肠道菌群、肠道通透性、和吸收率、脂质氧化程度、肠粘膜自由基和抗氧化指标,并进行肠道形态观察。结果表明:在诱导性肠炎仔猪日粮中添加铁前后,肠道粘膜出现不同程度的氧化应激,这和持续的应激减弱了抗氧化防御体系的功能有关,自由基在炎症加剧中起到重要作用。低剂量的铁可以适当提高仔猪的生产性能和消化率,但对治疗腹泻效果不显著(P>0.05)。过量的铁加重了实验性肠炎断奶仔猪肠道粘膜的损伤,加剧了肠炎的症状,致使消化率、日增重显著降低,微生物菌群失衡。高铁导致的过氧化产物MDA增多,脂质氧化降低了仔猪肠道吸收和屏障功能,证明适度剂量的补铁对缺铁和患消化道炎症的仔猪是有利的。
4.高能日粮对仔猪消化器官发育、功能及氧化还原状态的影响
试验选取21±2日龄的三元断奶仔猪30头,随机分为3组。1组,基础日粮(含1.5%豆油);2组,5%豆油日粮;3组,10%豆油日粮。试验期21天。测定仔猪生产性能,营养消化率,消化器官重量,血清中总胆固醇(TC)、甘油三脂(TG)血浆丙二醛(MDA)、超氧化物歧化酶(SOD)及皮质醇浓度,肠粘膜中消化酶活性、IGF-1和GHr基因表达;以研究高能日粮诱发的慢性应激对仔猪生长效果及其可能机制。结果表明:添加5%油脂组显著提高了仔猪的生产性能,包括ADG、FI,F/G三项指标,而添加10%油脂组与对照组比较无明显差异(P>0. 05 )。不同剂量油脂添加对小肠重量及脂肪酶的活性均显著增加(P<0.05),10%油脂组小肠粘膜重量反而降低;添加油脂对其它器官重及肠道蛋白酶活性无影响;均提高了仔猪血液中的TC、TG浓度,并随油脂浓度增加呈上升趋势。而5%油脂组CP、EE消化率均显著高10%油脂组。10%油脂组诱发血液中皮质醇和MDA显著提高,抗氧化酶SOD活性明显下降。5%油脂组小肠粘膜GHR mRNA表达量略提高,而添加10%油脂却出现明显下降(P<0.05);添加油脂剂量对IGF-1基因表达没有影响。综上所述,可以推断,高能饲料诱发仔猪氧化应激,对仔猪的生长产生负效应,随着时间的延长这种副作用越显著。
Gastrointestinal tract is main digestive, absorbtive and metabolic organ in animal. It is difficult to be conscious of gastrointestinal disfunction induced by moderate stress, Oxidative stress of gastrointestinal mucosa is involved in inflammatory bowel disease, and appropriate antioxidant may modulate intestinal redox status. The aim of our experiment was to study the effect and regulation mechanism of free radical and antioxidant on gastrointestinal growth, structure, function, hormone exudation and expression of gene.
1. Oxidative injury of free radical on the rat IECs, and protection by GSH in vitro
The objective of the this study was to investigate the direct oxidative injury of the different dose xanthine and xanthine oxidase (X/XO) on rat intestinal epithelial cells (IECs), and protection by glutathione(GSH)in vitro. IECs were maintained in culture medium for 72 h. Subsequently, culture cells were divided into 7 groups, and cultured in the presence and absence of xanthine (10μmol/L), xanthine oxidase (10, 40, 70 U/L) or GSH (1.5μmol/ml) for 24h. The oxidative injury of reactive oxygen species on IECs were evaluated by studying production of malondialdehyde (MDA), DNA fragmentation, total antioxidant capacity (TRAP), proliferation, activity of superoxide dismutase (SOD) and catalase (CAT), the level of Ca2+ and apoptosis of IECs. The results show the proliferation of IECs was significantly inhibited, but the activity of SOD and the value of total antioxidant capacity (TRAP) was slightly increased at low activity of XO (10U/L). However, the oxidative stress significantly inhibited cell proliferation, decreased TRAP, increased lipid peroxidation, concentration of Ca2+ and DNA fragment at XO (40,70 U/L). Both of DNA fragment and apoptosis of IECs increased gradually with the increase of XO concentration (P<0.05). Presence of GSH remarkably enhanced TRAP value (P<0.05), but failed to affect the activity of SOD corresponding X/XO (10 U/L) alone-treated. The reduction in lipid peroxidation and DNA damage and the increase in cell proliferation were also observed in IECs. These results strongly suggest that IECs exposed to X/XO could induce its oxidative stress and injury, GSH could provide significant protection against oxidative injury of IECs by scavenging ROS in vitro. Moderate oxidative stress might selectively stimulated the synthesis of antioxidant enzyme, but significantly decreased cell proliferation.
2. Regulation of of CS on IND-induced gastric oxidative injury and energy metabolism in rats
To study the gastroprotective effect of cysteamine (CS) on indomethacin-induced gastric ulcers in rats. A total of 45 male, SD rats weighing 180–220 g, have been used for the experiments. The Forty-five were randomly divided into three groups of 15 each:Control (A), stress (B) oral Indomethacin (IND, 45mg/kg weight); antioxidation (C), oral IND (45mg/kg weight) after oral CS (100mg/kg weight) for 1h. The concent of endogenous prostaglandin E2 (PGE2), the changes of ulcer index, the activities of H+,K+-ATPase and XO, the antioxidative index, the expressions of iNOS mRNA, somatostatin (SS) and the size of adenylic acid pool(ATP, ADP, AMP) in gastric mucosa tissue or mitochondria at postinjury 6, 12, 24h. The results showed that gastric lesions were significantly reduced by CS as compared with the group B. IND significantly damaged gastric mucosa excretive function and integrality, decreased the levels of SOD, glutathione (GSH) and the size of adenylic acid (AMP, ADP, ATP) in gastric mucosal mitochondria. However, CAT and lipid peroxidation (LPO) were increased corresponding the control (P< 0.05). The administration of CS reversed the trend, inducing a significant increase of SOD, GSH and total adenylic acid, a reduction of LPO and SS in gastric mucosa, and inhibitied the expressions of iNOS mRNA compared to the group B. Based on above results, it was concluded that the oxidative stress damged gastric normal structure and function, furthermore induced gastric energy metabolism disfunction. Gastroprotective effect of cysteamine can be attributed to its reducing effect on the oxidative damage.
3. Regulation of oral iron on the intestinal structure and function in piglets with DSS -induced colitis
To estimate the effect of oral iron on the intestinal function and oxidative redox status in piglets with dextran sulphate sodium (DSS)-induced colitis, fifty 21-day-old weaned piglets with an average initial weight of 4.80±0.76kg were randomly divided into five groups of ten each. The piglets received regular diet and water, or four diets with 0, 0.03, 0.2 or 1% FeSO4·2H2O and water with 4% DSS, respectively, for 10 days. Growth performance, digestibility, intestinal microflora, permeability, absorptive capacity, lipid peroxidation, free radical, antioxidation index and intestinal structure of piglet were determined. We observed oral iron induced oxidative stress in colonic mucosa, and a markedly higher lactulose/mannitol (Lac/Man) excretion ratio and lower serum concentration of D-xylose in Fe 0.2 and 1% supplementated piglets than piglets on DSS alone, but not in Fe 0.03% supplemented piglets. Supplementation of oral iron resulted in intestinal villus injury in piglets, and dose-response manner. The activities of SOD, CAT and glutathione peroxidase (GPx) significantly increased in the DSS group compared with the control group (P< 0.05). Iron supplementation significantly decreased the activities of GPx and CAT, as was vitamin E content, but not SOD. Furthermore, excess iron significantly increased the production of MDA and hydroperoxides (HP), in a dose-response related manner. In conclusion, excess iron supplementation caused injury on intestinal mucosa in piglets with colitis, these might be involved in the antioxidant defence system weaken in condition which the oxidative stress was stronger and sustained. Thus, lower iron supplementation in diarrhetic and iron-deficient piglets might be beneficial.
4. Effect of high-caloric feeding on peptic growth, function and redox of piglet
A total of 30 weaned piglets of an average initial body weight of 5.53±0.53kg, weaned at 21±2 day of age, were allocated to three dietary treatments of ten each in a randomized complete block design. 1) control group: regular diet; 2) 5% grease; 3) 10% grease. The piglets were fed the respective diets for 21 days. To study the mechanism and effect of the high caloric feeding-induced chronic stress on the growth performance, digestibility, the weight of peptic and intestinal mucosa; the content of MDA, total cholesterol (TC), total glycerol(TG) and cortisol in serum, activities of SOD and digestive enzyme, the expression of GHr and IGF-1 were determined. The results showed that 5% grease significantly increased the performance of piglets when compared with the piglets on control diet (P<0.05), but not in 10% gaease group (P>0. 05). Different dose of grease didn’t increase significantly the intestinal weight and the activity of lipase, but not in protease and the weight of other peptic; on the contrary, administration of 10% grease decreased the weight of intestinal mucosa. The level of TC and TG increased with the development of additive grease. The digestibility of CP and EE were increased in the 5% grease group when compared with the 10% grease group, so was the expression of GHR mRNA. However, 10% grease significantly increased the level of cortisol and MDA in serum, reduced activity of SOD and expression of GHR mRNA. Addition of grease had no effect on the expression of IGF-1 mRNA in intestinal mucosa. In conclusion, the high-caloric feeding could cause chronic stress in piglets, induce considerable gastrointestinal side effects, in a time-response related manner.
1.自由基对离体大鼠小肠上皮细胞的损伤及干预研究
选用5只初生未经哺乳的Wistar大鼠,于当日屠宰取出小肠,并进行小肠上皮细胞分离。细胞体外培养72h后,建立黄嘌呤/黄嘌呤氧化酶(X/XO)体外氧化损伤模型,细胞随机分为七组:对照组A加入等量的高温灭菌的三蒸水,氧化损伤B、C、D各组加入X (10μmol/L),并分别加入XO(10,40,70 U/L),抗氧化E、F、G各组加入X(10μmol/L)和谷胱甘肽(GSH,1.5μmol/ml),并分别加入XO(10,40,70U/L)。应激培养24h后,通过测定细胞活力、DNA片段化、凋亡率及细胞内外氧化还原指标,研究氧化应激对离体小肠上皮细胞增值、功能、凋亡的影响以及对细胞的氧化损伤干预机制。结果表明,不同剂量的X/XO均可导致离体大鼠IEC氧化应激的发生。在相对轻度的氧化应激条件下(XO,10U/L),离体大鼠IEC增殖明显降低,而抗氧化酶合成出现应激响应,其中SOD的活性略高于对照组(P>0.05),适度的氧化应激可能选择性的刺激氧化酶的合成。高活性的XO(40、70 U/L)导致细胞膜氧化脂质化程度显著提高,细胞膜通透性增强,细胞内Ca2+浓度的明显增加(P<0.05);随着添加的XO活性提高,DNA片段化和细胞凋亡率均呈上升趋势。添加GSH提高了离体大鼠IEC抗氧化酶活性及的总抗氧化能力;与相应的X/XO单独处理组比较,GSH显著降低了细胞内钙离子浓度和细胞凋亡率;同时GSH显著降低了XO(10, 40 U/L)两剂量组脂质氧化程度(P<0.05)。上述结果表明:X/XO系统导致离体培养大鼠IEC氧化损伤和细胞凋亡,轻度的氧化应激即可显著的降低小肠上皮细胞的增殖,外源性GSH能够有效抑制诱发性氧化应激对IEC造成的氧化损伤。
2.半胱胺对吲哚美辛诱发的胃粘膜氧化损伤及其能量代谢影响
选用45只体重200-250克的雄性SD大鼠。试验随机分为3组,对照组(A):灌服生理盐水1ml/只;单纯应激组(B):灌服吲哚美辛(IND,45mg/kg体重);抗氧化组(C):灌服半胱胺(CS,100mg/kg体重),1小时后灌服IND(45mg/kg体重)。分别在6、12、24小时3个时相点屠宰,分别测定:胃液PH值,血浆生长抑素浓度,胃粘膜溃疡指数(UI),胃壁细胞H+,K+-ATP酶活性,前列腺素E2(PGE2),黄嘌呤氧化酶(XO)活性,抗氧化指标(SOD, GSH, CAT),MDA含量,胃粘膜组织中及其线粒体内腺苷酸(ATP/ADP/AMP)含量和诱导型一氧化氮合成酶(iNOS)的基因表达。结果表明:灌服IND的大鼠胃泌酸能力迅速增强,6h即出现胃粘膜损伤,胃粘膜UI随应激时间延长而明显增加(P<0.05);CS在试验后期显著抑制了胃泌酸,同时降低了UI。IND处理大鼠提高了胃粘膜中H+,K+-ATP和黄嘌呤氧化酶(XO)酶活性,CS有效的抑制了H+,K+-ATP酶和XO活性的提高,但与对照组比较各时相点仍然均有提高。氧化损伤导致血浆中生长抑素的浓度迅速提高,CS使生长抑素在24h降低到生理水平。灌服IND后,各时相点胃粘膜PGE2含量均出现显著降低(P<0.05),CS有效的抑制PGE2下降,但仍然低于对照组。IND导致胃粘膜组织的氧化损伤,脂质化明显增强,CS对粘膜起到显著抗氧化保护作用,降低了脂质化程度。氧化应激发生时胃粘膜和胃粘膜线粒体中ATP、ADP、AMP、总腺苷酸池含量及能荷值均有明显降低,CS处理后使得ADP含量和能荷值与对照组差异不明显(P>0.05);其它各项指标在线粒体中含量显著高于损伤组,但在胃粘膜中与损伤组比较差异不显著。在24h时相点,IND处理组大鼠胃粘膜中iNOS mRNA基因表达量显著高于对照组和CS处理组;CS抑制了大鼠iNOS mRNA基因表达量,但仍然显著高于对照组(P<0.05)。综上所述,急性的氧化应激导致胃粘膜的氧化损伤,影响了胃正常的分泌功能和结构完整性,组织内氧化还原状态失衡,粘膜内的能量代谢紊乱,能荷降低,促使iNOS mRNA基因表达增强,抗氧化剂(CS)有效的抑制了氧化应激,显著抑制了部分氧化指标的变化。
3.自由基对实验性肠炎仔猪肠道结构、功能调控作用研究
选取21±2日龄的断奶仔猪50头,利用右旋糖苷硫酸钠(DSS)诱导仔猪肠炎模型,随机分为5个处理组,1组,基础日粮,饮用自来水;2组,基础日粮,饮用含4%DSS水;3组,基础日粮+0.03%FeSO4+含4%DSS的水;4组,基础日粮+0.2%FeSO4+含4% DSS水;5组,基础日粮+1%FeSO4+含4%DSS的水,试验期10天。测定仔猪生产性能、腹泻率、消化率、肠道菌群、肠道通透性、和吸收率、脂质氧化程度、肠粘膜自由基和抗氧化指标,并进行肠道形态观察。结果表明:在诱导性肠炎仔猪日粮中添加铁前后,肠道粘膜出现不同程度的氧化应激,这和持续的应激减弱了抗氧化防御体系的功能有关,自由基在炎症加剧中起到重要作用。低剂量的铁可以适当提高仔猪的生产性能和消化率,但对治疗腹泻效果不显著(P>0.05)。过量的铁加重了实验性肠炎断奶仔猪肠道粘膜的损伤,加剧了肠炎的症状,致使消化率、日增重显著降低,微生物菌群失衡。高铁导致的过氧化产物MDA增多,脂质氧化降低了仔猪肠道吸收和屏障功能,证明适度剂量的补铁对缺铁和患消化道炎症的仔猪是有利的。
4.高能日粮对仔猪消化器官发育、功能及氧化还原状态的影响
试验选取21±2日龄的三元断奶仔猪30头,随机分为3组。1组,基础日粮(含1.5%豆油);2组,5%豆油日粮;3组,10%豆油日粮。试验期21天。测定仔猪生产性能,营养消化率,消化器官重量,血清中总胆固醇(TC)、甘油三脂(TG)血浆丙二醛(MDA)、超氧化物歧化酶(SOD)及皮质醇浓度,肠粘膜中消化酶活性、IGF-1和GHr基因表达;以研究高能日粮诱发的慢性应激对仔猪生长效果及其可能机制。结果表明:添加5%油脂组显著提高了仔猪的生产性能,包括ADG、FI,F/G三项指标,而添加10%油脂组与对照组比较无明显差异(P>0. 05 )。不同剂量油脂添加对小肠重量及脂肪酶的活性均显著增加(P<0.05),10%油脂组小肠粘膜重量反而降低;添加油脂对其它器官重及肠道蛋白酶活性无影响;均提高了仔猪血液中的TC、TG浓度,并随油脂浓度增加呈上升趋势。而5%油脂组CP、EE消化率均显著高10%油脂组。10%油脂组诱发血液中皮质醇和MDA显著提高,抗氧化酶SOD活性明显下降。5%油脂组小肠粘膜GHR mRNA表达量略提高,而添加10%油脂却出现明显下降(P<0.05);添加油脂剂量对IGF-1基因表达没有影响。综上所述,可以推断,高能饲料诱发仔猪氧化应激,对仔猪的生长产生负效应,随着时间的延长这种副作用越显著。
Gastrointestinal tract is main digestive, absorbtive and metabolic organ in animal. It is difficult to be conscious of gastrointestinal disfunction induced by moderate stress, Oxidative stress of gastrointestinal mucosa is involved in inflammatory bowel disease, and appropriate antioxidant may modulate intestinal redox status. The aim of our experiment was to study the effect and regulation mechanism of free radical and antioxidant on gastrointestinal growth, structure, function, hormone exudation and expression of gene.
1. Oxidative injury of free radical on the rat IECs, and protection by GSH in vitro
The objective of the this study was to investigate the direct oxidative injury of the different dose xanthine and xanthine oxidase (X/XO) on rat intestinal epithelial cells (IECs), and protection by glutathione(GSH)in vitro. IECs were maintained in culture medium for 72 h. Subsequently, culture cells were divided into 7 groups, and cultured in the presence and absence of xanthine (10μmol/L), xanthine oxidase (10, 40, 70 U/L) or GSH (1.5μmol/ml) for 24h. The oxidative injury of reactive oxygen species on IECs were evaluated by studying production of malondialdehyde (MDA), DNA fragmentation, total antioxidant capacity (TRAP), proliferation, activity of superoxide dismutase (SOD) and catalase (CAT), the level of Ca2+ and apoptosis of IECs. The results show the proliferation of IECs was significantly inhibited, but the activity of SOD and the value of total antioxidant capacity (TRAP) was slightly increased at low activity of XO (10U/L). However, the oxidative stress significantly inhibited cell proliferation, decreased TRAP, increased lipid peroxidation, concentration of Ca2+ and DNA fragment at XO (40,70 U/L). Both of DNA fragment and apoptosis of IECs increased gradually with the increase of XO concentration (P<0.05). Presence of GSH remarkably enhanced TRAP value (P<0.05), but failed to affect the activity of SOD corresponding X/XO (10 U/L) alone-treated. The reduction in lipid peroxidation and DNA damage and the increase in cell proliferation were also observed in IECs. These results strongly suggest that IECs exposed to X/XO could induce its oxidative stress and injury, GSH could provide significant protection against oxidative injury of IECs by scavenging ROS in vitro. Moderate oxidative stress might selectively stimulated the synthesis of antioxidant enzyme, but significantly decreased cell proliferation.
2. Regulation of of CS on IND-induced gastric oxidative injury and energy metabolism in rats
To study the gastroprotective effect of cysteamine (CS) on indomethacin-induced gastric ulcers in rats. A total of 45 male, SD rats weighing 180–220 g, have been used for the experiments. The Forty-five were randomly divided into three groups of 15 each:Control (A), stress (B) oral Indomethacin (IND, 45mg/kg weight); antioxidation (C), oral IND (45mg/kg weight) after oral CS (100mg/kg weight) for 1h. The concent of endogenous prostaglandin E2 (PGE2), the changes of ulcer index, the activities of H+,K+-ATPase and XO, the antioxidative index, the expressions of iNOS mRNA, somatostatin (SS) and the size of adenylic acid pool(ATP, ADP, AMP) in gastric mucosa tissue or mitochondria at postinjury 6, 12, 24h. The results showed that gastric lesions were significantly reduced by CS as compared with the group B. IND significantly damaged gastric mucosa excretive function and integrality, decreased the levels of SOD, glutathione (GSH) and the size of adenylic acid (AMP, ADP, ATP) in gastric mucosal mitochondria. However, CAT and lipid peroxidation (LPO) were increased corresponding the control (P< 0.05). The administration of CS reversed the trend, inducing a significant increase of SOD, GSH and total adenylic acid, a reduction of LPO and SS in gastric mucosa, and inhibitied the expressions of iNOS mRNA compared to the group B. Based on above results, it was concluded that the oxidative stress damged gastric normal structure and function, furthermore induced gastric energy metabolism disfunction. Gastroprotective effect of cysteamine can be attributed to its reducing effect on the oxidative damage.
3. Regulation of oral iron on the intestinal structure and function in piglets with DSS -induced colitis
To estimate the effect of oral iron on the intestinal function and oxidative redox status in piglets with dextran sulphate sodium (DSS)-induced colitis, fifty 21-day-old weaned piglets with an average initial weight of 4.80±0.76kg were randomly divided into five groups of ten each. The piglets received regular diet and water, or four diets with 0, 0.03, 0.2 or 1% FeSO4·2H2O and water with 4% DSS, respectively, for 10 days. Growth performance, digestibility, intestinal microflora, permeability, absorptive capacity, lipid peroxidation, free radical, antioxidation index and intestinal structure of piglet were determined. We observed oral iron induced oxidative stress in colonic mucosa, and a markedly higher lactulose/mannitol (Lac/Man) excretion ratio and lower serum concentration of D-xylose in Fe 0.2 and 1% supplementated piglets than piglets on DSS alone, but not in Fe 0.03% supplemented piglets. Supplementation of oral iron resulted in intestinal villus injury in piglets, and dose-response manner. The activities of SOD, CAT and glutathione peroxidase (GPx) significantly increased in the DSS group compared with the control group (P< 0.05). Iron supplementation significantly decreased the activities of GPx and CAT, as was vitamin E content, but not SOD. Furthermore, excess iron significantly increased the production of MDA and hydroperoxides (HP), in a dose-response related manner. In conclusion, excess iron supplementation caused injury on intestinal mucosa in piglets with colitis, these might be involved in the antioxidant defence system weaken in condition which the oxidative stress was stronger and sustained. Thus, lower iron supplementation in diarrhetic and iron-deficient piglets might be beneficial.
4. Effect of high-caloric feeding on peptic growth, function and redox of piglet
A total of 30 weaned piglets of an average initial body weight of 5.53±0.53kg, weaned at 21±2 day of age, were allocated to three dietary treatments of ten each in a randomized complete block design. 1) control group: regular diet; 2) 5% grease; 3) 10% grease. The piglets were fed the respective diets for 21 days. To study the mechanism and effect of the high caloric feeding-induced chronic stress on the growth performance, digestibility, the weight of peptic and intestinal mucosa; the content of MDA, total cholesterol (TC), total glycerol(TG) and cortisol in serum, activities of SOD and digestive enzyme, the expression of GHr and IGF-1 were determined. The results showed that 5% grease significantly increased the performance of piglets when compared with the piglets on control diet (P<0.05), but not in 10% gaease group (P>0. 05). Different dose of grease didn’t increase significantly the intestinal weight and the activity of lipase, but not in protease and the weight of other peptic; on the contrary, administration of 10% grease decreased the weight of intestinal mucosa. The level of TC and TG increased with the development of additive grease. The digestibility of CP and EE were increased in the 5% grease group when compared with the 10% grease group, so was the expression of GHR mRNA. However, 10% grease significantly increased the level of cortisol and MDA in serum, reduced activity of SOD and expression of GHR mRNA. Addition of grease had no effect on the expression of IGF-1 mRNA in intestinal mucosa. In conclusion, the high-caloric feeding could cause chronic stress in piglets, induce considerable gastrointestinal side effects, in a time-response related manner.
引文
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