二甲氨基乙醇和复方氨基酸溶液对衰老 大鼠皮肤胶原代谢和自由基的影响

目的 探讨真皮内注射二甲氨基乙醇（DMAE）和复方氨基酸溶液（AA）对皮肤胶原代谢和自由基的影响.方法 80只大鼠随机分成衰老治疗组（60只）、衰老对照组（10只）和正常对照组（10只）.皮下注射半乳糖制备衰老模型.衰老治疗组从第18天开始,在两侧臀部真皮内分别注射0.2％ DMAE＋AA、0.1％ DMAE＋AA、0.2％ DMAE、0.1％ DMAE、AA、生理盐水（NS）,每周1次,连续4周.观察各组皮肤苏木精-伊红染色法（HE）切片组织学变化并测定皮肤中含水量、超氧化物歧化酶（SOD）活力、羟脯氨酸（HYP）和丙二醛（MDA）含量.结果 0.2％DMAE＋ AA组、0.1％ DMAE＋AA组表皮、真皮厚度和胶原纤维面积均高于衰老对照组,差异有统计学意义（P＜0.05）.0.2％ DMAE＋AA组、0.1％ DMAE＋ AA组与其他各衰老组相比,HYP含量增加、SOD活力升高、MDA含量降低,其组间差异具有统计学意义（P＜0.05）.正常对照组、0.2％ DMAE＋AA组、0.1％DMAE＋ AA组之间HYP含量差异无统计学意义（P＞0.05）.各组大鼠皮肤含水量差异无统计学意义（P＜0.05）.结论 真皮内注射0.2％ DMAE＋AA、0.1％ DMAE＋AA能显著增加表皮、真皮厚度和胶原纤维面积及HYP含量,提高SOD活力、降低MDA含量,表明其有清除皮肤自由基、提高抗氧化能力和促进皮肤胶原代谢的作用,从而延缓皮肤衰老.     

丹参对梗阻性黄疸肾损害保护作用的实验研究

目的 :探讨梗阻性黄疸 (梗黄 )肾损害及丹参保护作用机制。方法 :将 36只大鼠随机分为对照组、胆总管结扎组和丹参治疗组 ,以结扎胆总管方法建立梗黄肾损害鼠模型 ,丹参治疗组每日每只腹腔内注射 2g丹参注射液。 3组大鼠分别于术后第 7、14、2 1和 2 8天活杀 ,检测血清和肾组织中丙二醛 (MDA)及超氧化物歧化酶 (SOD)的变化 ,并观察肾功能和肾病理组织学改变。结果 :与非治疗组相比 ,丹参治疗组的血清及肾组织中SOD活性显著升高 ,而MDA则显著下降 (P <0 .0 5 ) ,肾功能和肾病理组织改变也较轻。结论 :氧自由基所引发的脂质过氧化作用是梗黄鼠肾损害发病过程中的重要因素之一 ,应用丹参可明显降低肾脏病理组织损害程度。     

胆胃宁对乙醇性胃黏膜损伤的治疗作用

目的 探讨胆胃宁对乙醇致胃黏膜损伤的修复作用及其机制.方法 40只雄性SD大鼠随机分为正常组、模型组、胆胃宁组、雷尼替丁组和硫糖铝组.正常组大鼠采用生理盐水灌胃,其余组以无水乙醇灌胃.2h后分别采用胆胃宁、雷尼替丁及硫糖铝灌胃治疗,间隔5h重复上述治疗一次,对比观察各组胃黏膜修复情况.检测治疗前后胃黏膜内丙二醛(MDA)及前列腺素E2(PGE2)水平.结果 胆胃宁组大鼠胃黏膜损伤指数均显著低于模型组,胆胃宁组胃黏膜损伤轻于雷尼替丁及硫糖铝组.胆胃宁能提高大鼠胃黏膜内PGE2水平,降低MDA含量.结论 胆胃宁能促进急性胃黏膜损伤的修复,其机制可能与降低脂质过氧化,提高抗氧化活力和促进PGE2合成有关.     

不同时辰针刺对豚鼠血清SOD、MDA的影响

目的:观察不同时辰按灵龟八法开穴针刺的抗氧化效应差异。方法:选用健康豚鼠182只,随机分为12个时辰针刺组和1个空白对照组,每组14只。时辰针刺组在子、丑、寅、卯、辰、巳、午、未、申、酉、戌、亥12个时辰里按照灵龟八法开穴针刺,每日1次,连续7d。观察超氧化物歧化酶(SOD)和丙二醛(MDA)治疗前后的变化。结果:健康豚鼠在12个时辰里SOD活力和MDA含量各不相同,SOD活力午时最高,子时最低;MDA含量子时最高,午时最低。灵龟八法针刺可提高健康豚鼠SOD活力,卯时升高幅度最大,午时升高幅度最小;亦可降低丙二醛的含量,午时降低幅度最大,亥时降低幅度最小。结论:不同时辰按灵龟八法开穴针刺对豚鼠血清SOD和MDA的影响存在差异,灵龟八法可以提高健康豚鼠SOD活力,降低MDA含量。     

黄芪对糖尿病大鼠心肌MDA及SOD,GSH-PX,Na+ - k+ ATP酶活性的影响

目的 观察黄芪对糖尿病大鼠心肌组织MDA含量及SOD,GSH,Na^＋-k^＋ -ATP酶活性的影响。方法 用链脲佐菌素腹腔注射制备糖尿病大鼠模型。正常大鼠、糖尿病大鼠及用黄芪注射液治疗8周的糖尿病大鼠各8只,测定心肌组织丙二醛（MDA）含量及超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-PX）、Na^＋-k^＋-ATP酶活性。结果 黄芪能显著降低糖尿病大鼠心肌组织MDA含量,并能提高心肌组织SOD,GSH-PX及Na＋-k＋ATP酶活性。结论 黄芪对糖尿病大鼠心肌脂质过氧化反应具有抑制作用。 基     

Corn oil enhancing hepatic lipid peroxidation induced by CCl4 does not aggravate liver fibrosis in rats

Lipid peroxidation (LPO) is known to be associated with liver fibrosis in chronic liver injury. However, direct effects of the products of LPO on liver fibrogenesis have not been demonstrated. In this study, we examined the LPO products of carbon tetrachloride (CCl4)+corn oil to evaluate the effect of LPO products on liver fibrosis. CCl4 was given twice a week for 8 weeks. Corn oil was given daily to rats at a dose of 2 or 10ml/kg via gastrogavage throughout the whole experiment period. CCl4 induced both cyclooxygenase (COX)-2 independent and COX-2 dependent LPO. COX-2 independent LPO was enhanced by corn oil treatment while no effect was reflected on COX-2 dependent LPO. CCl4-induced liver fibrosis in rats was not aggravated by corn oil treatment. In addition, the amount of fatty liver induced by CCl4 was increased by corn oil treatment. Though the inflammation-related UCP-2 mRNA expression was induced by CCl4, it was not aggravated by the enhancement of corn oil. Conclusion: corn oil enriches polyunsaturated fatty acids through COX-2 independent pathways to increase LPO products that do not enhance liver fibrosis induced by CCl4.     

Subacute effects of methyl parathion on antioxidant defense systems and lipid peroxidation in rats

In this study we aimed to examine how methyl parathion (MP) at sublethal dosages affects on malondialdehyde (MDA) content and antioxidant defense system (ADS) such as reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD) and glutathione-S-transferase (GST) in various tissues of rats exposed to 19 and 38 millimole (mM) MP dosages as drinking water ad libitum for 28 days continuously. MDA significantly increased in all the tissues except for in the lungs of rats treated with both dosages of MP. With regard to the ADS, SOD significantly decreased in the lungs tissue whereas increased in the erythrocytes with two dosages of MP. GR activity significantly decreased in the erythrocytes treated with both dosages of MP, but decreased in the lungs and liver tissues with 38 mM MP treatment. GST activity significantly elevated in all the tissues except for in the liver treated with 38 mM dosage but did not change with 19 mM. Meanwhile, GSH depletion in all the tissues except lungs of rats treated with both dosages of MP was found to be significant. The observations presented led us to conclude that after the administrations of MP promote MDA content and fluctuate in the ADS in rats.     

高山红景天提取物对糖尿病大鼠谷胱甘肽过氧化物酶活性及丙二醛含量的影响

目的观察高山红景天提取物对链脲佐菌素(STN)诱导的糖尿病大鼠肝组织中的谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)活性及丙二醛(malodialdehyde,MDA)含量的影响。方法采用链脲佐菌素诱导糖尿病大鼠模型,分别测定各组大鼠使用高山红景天提取物处理前后大鼠肝组织中GSH-Px活性和MDA含量。结果高山红景天提取物可提高糖尿病大鼠肝组织中的GSH-Px活性,降低MDA含量。结论高山红景天提取物对糖尿病大鼠具有清除自由基及抗脂质过氧化作用。     

Effects of trichlorfon on malondialdehyde and antioxidant system in human erythrocytes

Organophosphorus insecticides may induce oxidative stress leading to generation of free radicals and alteration in antioxidant system. The aim of this study was to examine the potency of trichlorfon, an organophosphate insecticide, to induce oxidative stress response in human erythrocytes in vitro. For this purpose trichlorfon solutions in different concentrations and erythrocyte solutions were incubated at 37 °C for 60 min. At the end of the incubation time, malondialdehyde (MDA), an end product of lipid peroxidation, total glutathione, reduced glutathione (GSH) levels, activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzymes were determined by spectrophotometric methods. Trichlorfon increased MDA formation depended on the concentration. On the other hand, decreases in the GSH-Px activity, GSH levels and increases in the total glutathione levels, SOD and CAT activities were seen in the studied concentrations. The present findings indicate that the in vitro toxicity of trichlorfon may be associated with oxidative stress.