AMPK as a metabolic switch in rat muscle,liver and adipose tissue after exercise

An increasing body of evidence has revealed that activation of adenosine monophosphate (AMP)‐activated protein kinase (AMPK)‐activated protein kinase increases fatty acid oxidation by lowering the concentration of malonyl coenzyme A (CoA), an inhibitor of carnitine palmitoyl transferase 1. Studies carried out primarily in skeletal muscle suggest that AMPK modulates the concentration of malonyl CoA by concurrently phosphorylating and inhibiting acetyl CoA carboxylase (ACC), the rate limiting enzyme in malonyl CoA synthesis, and phosphorylating and activating malonyl CoA decarboxylase (MCD), an enzyme involved in its degradation. We have recently observed that AMPK and MCD activities are increased and ACC activity diminished in skeletal muscle, liver and, surprisingly, in adipose tissue 30 min following exercise (treadmill run) in normal rats. In liver and adipose tissue these changes were associated with a decrease in the activity of glycerol‐3‐phosphate acyltransferase (GPAT), which catalyses the first committed reaction in glycerolipid synthesis and, which like ACC, is phosphorylated and inhibited by AMPK. Similar changes in ACC, MCD and GPAT were observed following the administration of 5‐aminoimidazole 4‐carboxamide‐riboside (AICAR), further indicating that the exercise‐induced alterations in these enzymes were AMPK‐mediated. Conclusions: (1) AMPK plays a major role in regulating lipid metabolism in multiple tissues following exercise. (2) The net effect of its activation is to increase fatty acid oxidation and diminish glycerolipid synthesis. (3) The relevance of these findings to the regulation of muscle glycogen repletion in the post‐exercise state and to the demonstrated ability of AMPK activation to decrease adiposity and increase insulin sensitivity in rodents remains to be determined.     

灯盏花素对糖尿病大鼠肾脏氧化应激的影响

目的　在链脲菌素诱导的糖尿病大鼠模型上 ,灯盏花素与化学合成药氨基胍相比较来探讨灯盏花素对糖尿病大鼠肾脏的保护作用及与氧化应激的关系。方法　用链脲菌素诱导糖尿病大鼠模型后 ,将糖尿病大鼠分为 :糖尿病组、灯盏花素组 (0 1g·kg-1)和氨基胍组 (饮水含 1g·L-1的氨基胍 )。在给药 15～ 17wk后进行与氧化应激相关的各项实验观察。结果　① 15～ 17wk的糖尿病大鼠与正常对照组相比 :肾指数显著增加 ,肾脏的抗氧化能力显著降低且氧化应激增强。②灯盏花素组与糖尿病组相比 :肾指数显著降低 ,总抗氧化能力和肾脏超氧化物歧化酶活性显著提高 ,脂质过氧化产物丙二醛显著降低。③氨基胍组与糖尿病组相比 :肾脏超氧化物歧化酶活性显著提高 ,肾脏的脂质过氧化产物丙二醛显著性降低 ,总抗氧化能力差异无显著性。结论　糖尿病大鼠与正常大鼠相比肾脏抗氧化能力降低且氧化应激增强 ,灯盏花素可显著提高糖尿病大鼠肾脏的抗氧化能力和降低氧化应激     

蕲蛇酶减轻大鼠局灶性脑缺血再灌注损伤的实验研究

目的 :探讨蕲蛇酶 (acutobin)在局灶性脑缺血再灌注损伤模型中的保护作用及其机制。方法 :线栓法制备大鼠大脑中动脉闭塞 (MCAO)模型 ,缺血3h后恢复血流再灌 2 4h。观察蕲蛇酶对脑梗死面积、脑组织中髓过氧化物酶 (MPO)、诱导型一氧化氮合酶 (iNOS)活性、一氧化氮 (NO)、丙二醛 (MDA)含量和超氧化物歧化酶 (SOD)活性的影响。结果 :蕲蛇酶能有效减小脑梗死灶 ,缓解MPO升高、降低MDA含量、抑制iNOS活性 ,降低NO含量。结论 :蕲蛇酶对脑缺血再灌注损伤有保护作用 ,其机制可能与缓解MPO升高以及抑制脑组织中iNOS活性 ,降低NO、MDA含量有关     

Metabolic Abnormalities in the Diabetic Heart

Congestive heart failure is a major health problem in the diabetic. Diabetics have a high incidence of heart disease, including an increased incidence and severity of congestive heart failure than the non-diabetic. Progression to heart failure after an acute myocardial infarction is also more frequent in diabetics then non-diabetics. While atherosclerosis and ischemic injury are important contributing factors to this high in incidence of heart failure, another important factor is diabetes-induced changes within the heart itself. A prominent change that occurs in the diabetic is a switch in cardiac energy metabolism. Increases in fatty acid oxidation accompanied by decreases in glucose metabolism can result in the myocardium becoming almost entirely reliant on fatty acid oxidation as a source of energy. This switch in energy metabolism contributes to congestive heart failure by increasing the severity of injury following an acute myocardial infarction, and by having direct negative effects on contractile function. This paper will review the evidence linking alterations in energy metabolism to alterations in contractile function in the diabetic.     

In vitro and in vivo Biocompatibility of Alginate Dialdehyde/Gelatin Hydrogels with and without Nanoscaled Bioactive Glass for Bone Tissue Engineering Applications

In addition to good mechanical properties needed for three-dimensional tissue engineering, the combination of alginate dialdehyde, gelatin and nano-scaled bioactive glass (45S5) is supposed to combine excellent cellular adhesion, proliferation and differentiation properties, good biocompatibility and predictable degradation rates. The goal of this study was to evaluate thein vitro and in vivo biocompatibility as a first step on the way to its use as a scaffold in bone tissue engineering. In vitro evaluation showed good cell adherence and proliferation of bone marrow derived mesenchymal stem cells seeded on covalently crosslinked alginate dialdehyde-gelatin (ADA-GEL) hydrogel films with and without 0.1% nano-Bioglass^®(nBG). Lactate dehydrogenase (LDH)- and mitochondrial activity significantly increased in both ADA-GEL and ADA-GEL-nBG groups compared to alginate. However, addition of 0.1% nBG seemed to have slight cytotoxic effect compared to ADA-GEL. In vivo implantation did not produce a significant inflammatory reaction, and ongoing degradation could be seen after four weeks. Ongoing vascularization was detected after four weeks. The good biocompatibility encourages future studies using ADA-GEL and nBG for bone tissue engineering application.     

甲醛和苯联合染毒对雄性小鼠睾丸的毒性作用

目的 研究甲醛和苯联合染毒对雄性小鼠睾丸组织的毒性作用,为综合评价甲醛和苯的安全性提供科学依据.方法 选用78只健康清洁级昆明种纯系雄性小鼠为研究对象,按染毒剂量分为低(0.2 mg/kg)、中(2 mg/kg)、高(20 mg/kg)剂量甲醛组,以生理盐水为阴性对照组;低(100.0mg/kg)、中(200.0mg/kg)、高(400.0mg/kg)剂量苯组,以花生油为阴性对照组;低(0.1 mg/kg甲醛 50.0 mg/kg苯)、中(1 mg/kg甲醛 100.0 mg/kg苯)、高(10 mg/kg甲醛 200.0 mg/kg苯)剂量联合染毒组,以生理盐水 花生油为阴性对照组;以环磷酰胺(40 mg/kg)为阳性对照组.采用腹腔注射染毒,注射容量为0.01 ml/g,每日1次,连续5 d.染毒结束次日,处死小鼠,测定睾丸组织中超氧化物歧化酶(SOD)活力、丙二醛(MDA)、Cu、Zn含量.结果 甲醛、苯单独染毒组及联合染毒组的SOD活力、Cu、Zn含量均低于其阴性对照组,且随染毒剂量的升高而下降;MDA含量均高于其阴性对照组,且随染毒剂量的升高而上升.联合染毒组染毒剂量与SOD活力呈负相关(r=-0.967,P＜0.01),与MDA含量呈正相关(r=0.941,P＜0.01).与甲醛、苯单独染毒比较,联合染毒组SOD活力、Cu、Zn含量呈下降趋势,MDA含量呈升高趋势.结论 甲醛和苯联合染毒对小鼠睾丸组织的毒性作用大于甲醛、苯单独染毒时的作用;二者对小鼠睾丸组织的联合毒性作用可能具有协同作用.     

番茄红素对高脂兔血管脂质过氧化损伤的影响及机制探讨

目的：观察番茄红素对高脂喂饲所致家免主动脉脂质过氧化损伤的影响。方法：采用高脂喂饲模型，将30只新西兰家兔随机分为3组：对照组、高脂模型组和番茄红素组，分别给予普通饲料和高脂饲料喂养，番茄红素组另加用番茄红素；于实验开始前1d和开始后第2、4、6、8周末取空腹血测定血清总胆固醇、甘油三酯、高密度脂蛋白胆固醇、血清超氧化物歧化酶活性、丙二醛含量、血清一氧化氮含量和一氧化氮合酶活性。实验结束后，苏丹Ⅳ染色和HE染色观察主动脉血管病理变化。结果：与高脂模型组相比，番茄红素组血清甘油三酯含量减低；血清超氧化物歧化酶活性明显增加；血清丙二醛的含量减少；一氧化氮含量增加；主动脉脂质斑块面积减少。结论：番茄红素对兔主动脉脂质过氧化损伤具有较好的保护作用，能减轻高脂兔动脉粥样硬化病变形成。降甘油三酯，抗脂质过氧化损伤及保护血管内皮功能可能是番茄红素产生抗动脉粥样硬化作用的重要机制。     

汉防己甲素对急性百草枯中毒致肺损伤的实验治疗研究

目的 探讨汉防己甲素(TET)对急性百草枯中毒所致肺损伤的拮抗作用.方法 雄性Wistar大鼠随机分为对照组(7只)、未治疗组(32只)和治疗组(32只).治疗组与未治疗组大鼠用百草枯(15 mg/kg)一次性腹腔注射染毒.治疗组于百草枯染毒后6 h经口给予汉防己甲素30 mg/kg,1次/d;未治疗组给予等体积的生理盐水;对照组一次性腹腔注射等体积生理盐水.分别测定不同处理后3、7、14和21 d时大鼠血浆和肺匀浆中丙二醛(MDA)含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力,并观察肺组织结构改变.结果 染毒3 d时,未治疗组血浆及匀浆中MDA含量分别为(3.65±0.44)nmol/ml、(9.54±0.92)nmol/mgpro,均高于对照组,差异有统计学意义(P<0.01);未治疗组3 d时血浆和3、7 d时匀浆中GSH-Px活力与对照组相比明显降低,差异有统计学意义(P<0.05);未治疗组3 d时血浆和14 d时匀浆中的SOD活力与对照组相比明显降低.差异有统计学意义(P<0.05);各时点治疗组血浆、匀浆中MDA含量与未治疗组比较,差异无统计学意义(P>0.05).3 d时治疗组血浆SOD活力与未治疗组相比明显增高,差异有统计学意义(P<0.01).治疗组血浆中GSH-Px活力虽均高于未治疗组,但差异均无统计学意义(P>0.05).治疗组肺纤维组织积分均低于未治疗组,差异有统计学意义(P<0.01).结论 TET对急性百草枯中毒大鼠血浆中SOD和GSH-Px活力降低有一定的拮抗作用,可减轻肺纤维化.     

Antioxidant activity of Ganoderma lucidum in acute ethanol-induced heart toxicity

The hot water extract of the mushroom Ganoderma lucidum was shown to have antioxidative effect against heart toxicity. Investigations into the mechanisms of action, level of lipid peroxidation level in vivo, and superoxide scavenging activity were also conducted. The mice were divided into six groups with ten animals in each group. Ganoderma lucidum, at doses of 10, 25 and 50 mg/kg (p.o.) was administered. Superoxide anions were assayed by UV spectrophotometer using the cytochrome C reduction method. The results of this study showed that Ganoderma lucidum exhibited a dose-dependent antioxidative effect on lipid peroxidation and superoxide scavenging activity in mouse heart homogenate. Additionally, this result indicated that heart damage induced by ethanol shows a higher malonic dialdehyde level compared with heart homogenate treated with Ganoderma lucidum. It is concluded that the antioxidative activity may therefore contribute to the cardioprotective effect of Ganoderma lucidum, and may therefore protect the heart from superoxide induced damage.