Improvement in the endothelium-dependent relaxation in hypercholesterolemic rabbits treated with vitamin E

The authors studied the time course of the vitamin E mediated improvement in endothelium-dependent relaxation in hypercholesterolemic rabbits. A total of 40 male New Zealand white rabbits were randomly assigned to hypercholesterolemic (control) and vitamin E treated groups. The latter group was further divided in three subgroups in accordance with the duration of the vitamin E treatment (2, 4 or 6 days) at the end of the experiment. The dose of vitamin E utilized was 50 IU/day administered once a day by gavage. All the rabbits were fed a diet supplemented with cholesterol (0.5%) and coconut oil (2%) for 4 weeks. At the end of this period, the animals were sacrificed and the aorta removed for determination of the cholesterol and malondialdehyde (MDA) contents. The relaxation of the aortic strips in response to acetylcholine was also studied. In addition, the cholesterol and MDA contents of native and oxidized LDL were measured. At the end of the 4th week, the MDA level was significantly reduced in native and oxidized LDL in the rabbits treated with vitamin E for 2 days, while in aortic tissue a reduction was seen after 4 days of treatment. Endothelium-dependent relaxation improved significantly after 6 days of vitamin E administration, and there was a reduction in the total plasma and aortic cholesterol levels during this same period. We conclude that vitamin E at a dose of 50 IU/day for 6 days improves the endothelium-dependent relaxation seen in hypercholesterolemic rabbits. This effect may be mediated through an antioxidant action on LDL particles and on the aortic arterial wall.     

Protective effects of melatonin against spinal cord injury induced oxidative damage in rat kidney: A morphological and biochemical study

Spinal cord injury (SCI) induced oxidative stress affects multiple organ systems including the kidney. We studied the possible protective effects of melatonin on SCI-induced oxidative damage in renal tissues of rats. Wistar albino rats (n = 24) were exposed to SCI and divided into vehicle- or melatonin-treated SCI groups. Melatonin was administred intraperitoneally at a dose of 10 mg/kg for seven days. Renal tissues were investigated by light and electron microscopy. Furthermore, tissue malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) and superoxide dismutase (SOD) activities were also determined. In the vehicle-treated SCI group, the renal histology was disturbed compared to controls, whereas the melatonin-treated SCI group showed significantly reduced degeneration of renal tissue as seen by both light and electron microscopy. MDA levels, MPO and SOD activities were increased and GSH levels were decreased in the vehicle-treated SCI group compared to controls. On the other hand, decreased MDA levels and MPO activities and increased GSH levels were observed in the melatonin-treated SCI group compared to vehicle-treated SCI group. These results showed that experimentally induced SCI caused oxidative stress in the rat kidney, whereas melatonin treatment reduced oxidative stress, suggesting that it may be used as a complementary therapy of renal problems occurring following SCI.     

Silymarin improved 6-OHDA-induced motor impairment in hemi-parkisonian rats: behavioral and molecular study

Background

Neuroinflammation and oxidative stress has been shown to be associated with the development of Parkinson disease (PD). In the present study, we investigated the effect of intraperitoneal (i.p.) administration of silymarin, on 6-OHDA-induced motor-impairment, brain lipid per-oxidation and cerebrospinal fluid (CSF) levels of inflammatory cytokine in the rats.

Results

The results showed that silymarin is able to improve motor coordination significantly (p < 0.001) in a dose dependent manner. There was a significant (p < 0.001) increase in MDA levels of 6-OHDA-lesioned rats whereas; in silymarin (100, 200 and 300 mg/kg, i.p. for 5 days) pre-treated hemi-parkinsonian rats MDA levels was decreased markedly (p < 0.001). Furthermore the CSF levels of IL-1β was decreased (p < 0.001) in silymarin (100, 200 and 300 mg/kg) pre-treated rats up to the range of normal non-parkinsonian animals.

Conclusion

We found that pre-treatment with silymarin could improve 6-OHDA-induced motor imbalance by attenuating brain lipid per-oxidation as well as CSF level of IL-1β as a pro-inflammatory cytokine. We suggest a potential prophylactic effect for silymarin in PD. However, further clinical trial studies should be carried out to prove this hypothesis.     

Protective effects of 2-deoxy-D-glucose on nephrotoxicity induced by cyclosporine A in rats

Objective: This study aims to explore the protective effect mechanism of 2-deoxy-D-glucose on nephrotoxicity of cyclosporin A in vivo. Method: Renal toxicity of SD rats model induced by CsA was established. Serum creatinine, blood urea nitrogen, urine NAG, GSH and MDA were determined and the histopathological changes of rat renal cortex were observed to explore the protective effects of 2-DG on CsA-induced nephrotoxicity. Results: Serum creatinine, BUN and urinary NAG of rats were significantly changed in experimental groups. Pathological results showed that there was obvious renal tubular injury in model group, however, the renal injury was significantly reduced in pre-treated with 2-DG. Conclusions: 2-DG had obvious protective effect on nephrotoxicity especially with high dose. This protective effect could be related to the reduction of ROS induced by CsA. However, 2-DG had no effect on the expression of RIP3.     

Negative regulators of the RIG‐I‐like receptor signaling pathway

Upon recognition of specific molecular patterns on microbes, host cells trigger an innate immune response, which culminates in the production of type I interferons, proinflammatory cytokines and chemokines, and restricts pathogen replication and spread within the host. At each stage of this response, there are stimulatory and inhibitory signals that regulate the magnitude, quality, and character of the response. Positive regulation promotes an antiviral state to control and eventually clear infection, whereas negative regulation dampens inflammation and prevents immune‐mediated tissue damage. An overexuberant innate response can lead to cell and tissue destruction, and the development of spontaneous autoimmunity. The retinoic acid‐inducible gene I (RIG‐I)‐like receptors (RLRs), RIG‐I and melanoma differentiation‐associated gene 5 (MDA5), belong to a family of cytosolic host RNA helicases that recognize distinct nonself RNA signatures and trigger innate immune responses against several RNA viruses by signaling through the essential adaptor protein mitochondrial antiviral signaling (MAVS). The RLR signaling pathway is tightly regulated to maximize antiviral immunity and minimize immune‐mediated pathology. This review highlights contemporary findings on negative regulators of the RLR signaling pathway, with specific focus on the proteins and biological processes that directly regulate RIG‐I, MDA5 and MAVS signaling function.     

非酒精性脂肪性肝病兔血浆丙二醛、超氧化物歧化酶与硫化氢、一氧化氮的关系

目的观察非酒精性脂肪性肝病(NAFLD)兔血浆超氧化物歧化酶(SOD)、丙二醛(MDA)、硫化氢(H2S)、一氧化氮(NO)关系。方法 40只日本大耳白兔随机分为重、轻度NAFLD组及对照组。重度组给予高脂饲料160 g/d,轻度组给予高脂饲料80 g/d+普通饲料80 g/d,对照组给予普通饲料160 g/d。饲养周期13 w,建立不同程度NAFLD模型。实验结束采集血浆标本,按设备、试剂操作常规检测SOD、MDA、H2S、NO。结果重、轻度组MDA较对照组明显增高(P<0.01,P<0.05),且重度组明显高于轻度组(P<0.05)。重、轻度组SOD活力较对照组明显减低,重度组明显低于轻度组(均P<0.01)。重度组、轻度组H2S水平较对照组明显降低(P<0.01),重、轻度组无显著差异(P>0.05)。重、轻度组NO较对照组明显升高(P<0.01)。重度组高于轻度组(P<0.01)。结论 NAFLD兔血浆MDA/SOD、H2S/NO平衡紊乱可能是NAFLD的发病机制。     

Lutein extends the lifespan of Drosophila melanogaster

Lutein is one of the major carotenoids in most fruits and vegetables. The effect of lutein on the lifespan of Drosophila melanogaster was investigated. Results revealed that 0.1 mg lutein/ml diet could prolong their mean lifespan from 49.0 to 54.6 days. This was consistent with a significant reduction in malonyldialdehyde (MDA) level and increase in antioxidant enzyme activities of the flies fed with lutein-treated diet compared with those fed with basal diet. Paraquat (PQ) and H₂O₂ treatment tests demonstrated that lutein could prolong the survival time of the flies. Real-time polymerase chain reaction (RT-PCR) analysis indicated the gene expression of superoxide dismutase (SOD; SOD1 and SOD2), and catalase (CAT) in the lutein-treated group was up-regulated relative to that of the control group. It was concluded that the lifespan-prolonging activity of lutein was partially by up-regulation of endogenous antioxidant enzymes.     

激动素对实验性肺纤维化的治疗作用研究简

目的 研究激动素（Kinetin）对博来霉素 A5 （ BLMA5） 诱导的大鼠肺纤维化的治疗作用.方法 雌性Wister大鼠60只随机分为3组：A组为生理盐水对照组;B 组为BLMA5造模组;C 组为Kinetin治疗组.分别于第3、7、14、28天处死大鼠,取肺组织行HE及Masson染色以观察肺泡炎和肺纤维化情况,检测肺组织匀浆HYP、SOD、MDA、TNF-α、TGF-β1的含量.结果与模型组比较,Kinetin治疗组的肺泡炎和肺纤维化程度明显减轻;肺组织SOD水平上升,MDA、TNF-α、TGF-β1水平下降.结论 Kinetin通过抗氧化、抑制TNF-α、TGF-β1减轻博来霉素A5所致大鼠肺纤维化.     

葛根素对实验性脑出血大鼠脑组织SOD、MDA水平变化和神经功能障碍的相关性研究

目的:探讨葛根素对脑出血的治疗作用及其作用机制。方法:采用立体定向胶原酶尾状核注射法制备动物模型。观察脑出血大鼠神经功能障碍程度,检测大鼠脑组织超氧化物歧化酶(SOD)活性和脂质过氧化产物丙二醛(MDA)含量的变化。结果:与模型组比较,葛根素组的偏瘫症状明显减轻,脑组织MDA含量明显降低[(54.80±6.72)nmol/g比(70.22+8.24)nmol/g](P<0.01),而SOD活性显著提高[(2.32±0.09)kNU/g比(1.29±0.07)kNU/g](P<0.01)。结论:葛根素对脑出血后神经功能损伤有保护作用。其机制可能与葛根素具有减少自由基的产生,加强机体对自由基的清除能力和增强机体抗脂质过氧化损伤能力有关。