虾青素对眼组织保护作用的实验研究及存在的问题

虾青素是一种源于天然生物的类胡萝卜素的含氧衍生物,具有抗氧化、抗炎、抗细胞凋亡,预防心、脑血管疾病及癌症等多种作用,是一类具有一定发展前景的药品和保健食品成份.目前研究表明,虾青素可以透过血-视网膜屏障对眼组织发挥保护作用,已引起研究者的重视.本文针对虾青素在动物实验饲药环节中存在的问题、虾青素的抗氧化作用基础和组织细胞的氧化损伤机制以及在常见眼科疾病中的有关研究现况进行综述.     

Neuroprotective effect of edaravone in experimental glaucoma model in rats: a immunofluorescence and biochemical analysis

AIM: To evaluate the neuroprotective activity of systemically administered edaravone in early and late stage of experimental glaucoma in rats. METHODS: In this study, 60 Wistar albino rats were used. Experimental glaucoma model was created by injecting hyaluronic acid to the anterior chamber once a week for 6wk in 46 of 60 subjects. Fourteen subjects without any medication were included as control group. Edaravone administered intraperitoneally 3 mg/kg/d to the 15 of 30 subjects starting at the onset of glaucoma induction and also administered intraperitoneally 3 mg/kg/d to the other 15 subjects starting at three weeks after the onset of glaucoma induction. The other 16 subjects who underwent glaucoma induction was administered any therapy. Retinal ganglion cells (RGCs) have been marked with dextran tetramethylrhodamine (DTMR) retrograde at the end of the sixth week and after 48h, subjects were sacrificed by the method of cardiac perfusion. Alive RGC density was assessed in the whole-mount retina. Whole-mount retinal tissues homogenized and nitric oxide (NO), malondialdehyde (MDA) and total antioxidant capacity (TAC) values were measured biochemically. RESULTS: RGCs counted with Image-Pro Plus program, in the treatment group were found to be statistically significantly protected, compared to the glaucoma group (Bonferroni, P<0.05). The neuroprotective activity of edaravone was found to be more influential by administration at the start of the glaucoma process. Statistically significant lower NO levels were determined in the glaucoma group comparing treatment groups (Bonferroni, P<0.05). MDA levels were found to be highest in untreated glaucoma group, TAC levels were found to be lower in the glaucoma induction groups than the control group (Bonferroni, P<0.05). CONCLUSION: Systemic administration of Edaravone in experimental glaucoma showed potent neuroprotective activity. The role of oxidative stress causing RGC damage in glaucoma was supported by this study results.     

Silymarin attenuates paraquat‐induced lung injury via Nrf2‐mediated pathway in vivo and in vitro

The present study aims to investigate the impacts and mechanisms of silymarin on paraquat (PQ)‐induced lung injury in vivo and in vitro. In in vivo experiments, a total of 32 male Sprague‐Dawley (SD) rats were randomly divided into four groups. The rats were killed on day 3. Histopathological changes in lung tissue were examined using HE and Masson's trichrome staining. Biomarkers of neutrophil activation, pulmonary oedema, pulmonary fibrosis, lung permeability and oxidative stress were detected. Several proinflammatory mediators and antioxidant related proteins were measured. In in vitro experiments, A549 cells were transfected with Nrf2 special siRNA to investigate the roles of Nrf2. The results show that silymarin administration abated PQ‐induced lung histopathologic changes, decreased inflammatory cell infiltration and lung wet weight/dry weight (W/D) ratio, suppressed myeloperoxidase (MPO) activity and nitric oxide (NO)/inducible nitric oxide synthases (iNOS) expression, downregulated hydroxyproline (HYP) levels, reduced total protein concentration and proinflammatory mediator release, and improved oxidative stress (malondialdehyde, MDA; superoxide dismutase, SOD; catalase, CAT; and glutathione peroxidase, GSH‐Px) in lung tissue and serum. Meanwhile, treatment with silymarin upregulated the levels of nuclear factor‐erythroid‐2‐related factor 2 (Nrf2), heme oxygenase‐1 (HO‐1) and NAD(P)H:quinone oxidoreductase‐1(NQO1). However, the addition of Nrf2 siRNA reduced the expression of Nrf2‐mediated antioxidant protein HO‐1 and thus reversed the protective effects of silymarin against oxidative stress and inflammatory response. These results suggest that silymarin may exert protective effects against PQ‐induced lung injury. Its mechanisms were associated with the Nrf2‐mediated pathway. Therefore, silymarin may be a potential therapeutic drug for lung injury.     

In Vivo Protective Effects of Diosgenin against Doxorubicin-Induced Cardiotoxicity

Doxorubicin (DOX) induces oxidative stress leading to cardiotoxicity. Diosgenin, a steroidal saponin of Dioscorea opposita, has been reported to have antioxidant activity. Our study was aimed to find out the protective effect of diosgenin against DOX-induced cardiotoxicity in mice. DOX treatment led to a significant decrease in the ratio of heart weight to body weight, and increases in the blood pressure and the serum levels of lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and creatine kinase myocardial bound (CK-MB), markers of cardiotoxicity. In the heart tissue of the DOX-treated mice, DOX reduced activities of antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GPx), were recovered by diosgenin. Diosgenin also decreased the serum levels of cardiotoxicity markers, cardiac levels of thiobarbituric acid relative substances (TBARS) and reactive oxygen species (ROS), caspase-3 activation, and mitochondrial dysfunction, as well as the expression of nuclear factor kappa B (NF-κB), an inflammatory factor. Moreover, diosgenin had the effects of increasing the cardiac levels of cGMP via modulation of phosphodiesterase-5 (PDE5) activity, and in improving myocardial fibrosis in the DOX-treated mice. Molecular data showed that the protective effects of diosgenin might be mediated via regulation of protein kinase A (PKA) and p38. Our data imply that diosgenin possesses antioxidant and anti-apoptotic activities, and cGMP modulation effect, which in turn protect the heart from the DOX-induced cardiotoxicity.     

茶多酚有效成分对淋巴细胞增殖的抑制和抗氧化作用

研究表明,茶多酚具有很强的消除有害自由基、抗衰老等多种药理作用[1],茶多酚临床治疗白癜风具有较明显的效果,但其各类组分在临床治疗白癜风所发挥的作用还未见报道。1材料与方法1.1动物C57BL/6(B6)小鼠,体质量(20±2)g,由浙江中医药大学实验动物中心提供。1.2主要药品与试剂H2O2、EGCG均购自美国Sigma公     

一株红树内生真菌BY5的鉴定及生物活性研究△

目的对分离自红树植物海马齿(Sesuvium portulacastrum)的1株内生真菌BY5进行鉴定,并对其发酵产物的生物活性进行研究。方法采用形态学、28SrDNA序列对红树内生真菌BY5进行鉴定;采用滤纸片琼脂扩散法、自由基清除法(DPPH、·OH和ABTS+)和MTT法对其发酵液上清乙酸乙酯抽提物的抗菌、抗氧化和抗肿瘤活性进行研究。结果菌株BY5的菌落形态和显微形态与曲霉属的基本相同,其28SrDNA序列与塔宾曲霉(Aspergillus tubingensis)的相似度达100%,确定该菌株为塔宾曲霉;其发酵液上清乙酸乙酯抽提物对金黄色葡萄球菌、枯草芽孢杆菌有较强抑制作用;对DPPH自由基、·OH自由基和ABTS+自由基具有较强清除作用(0mg/mL相似文献   

Space radiation-induced inhibition of neurogenesis in the hippocampal dentate gyrus and memory impairment in mice: ameliorative potential of the melatonin metabolite, AFMK

Evaluation of potential health effects from high energy charged particle radiation exposure during long duration space travel is important for the future of manned missions. Cognitive health of an organism is considered to be maintained by the capacity of hippocampal precursors to proliferate and differentiate. Environmental stressors including irradiation have been shown to inhibit neurogenesis and are associated with the onset of cognitive impairments. The present study reports on the protective effects of N(1)-acetyl-N(2)-formyl-5-methoxykynuramine (AFMK), a melatonin metabolite, against high energy charged particle radiation-induced oxidative damage to the brain. We observed that radiation exposure (2.0 Gy of 500 MeV/nucleon (56)Fe beams, a ground-based model of space radiation) impaired the spatial memory of mice at later intervals without affecting the motor activities. AFMK pretreatment significantly ameliorated these neurobehavioral ailments. Radiation-induced changes in the population of immature and proliferating neurons in the dentate gyrus were localized using anti-doublecortin (Dcx) and anti-Ki-67 expression. AFMK pretreatment significantly inhibited the loss of Dcx and Ki-67 positive cells. Moreover, AFMK pretreatment ameliorated the radiation-induced augmentation of protein carbonyls and 4-hydroxyalkenal + malondialdehyde (MDA + HAE) in the brain and maintained the total antioxidant capacity of plasma and nonprotein sulfhydryl contents in brain.     

Melatonin ameliorates oxidative organ damage induced by acute intra-abdominal compartment syndrome in rats

Acutely increased intra-abdominal pressure (IAP) can lead to multiple organ failure. As blood flow to intra-abdominal organs is reduced by high venous resistance, ischemia-reperfusion (I/R) injury plays an important role in the pathogenesis of abdominal compartment syndrome (ACS) following IAP. Melatonin, a secretory product of the pineal gland, is known to have free radical scavenging and antioxidative properties in several oxidative processes. The objective of this study was to examine the potential protective properties of melatonin on the oxidative organ damage in a rat model of ACS. Under ketamine anesthesia, an arterial catheter was inserted intraperioneally (i.p.) and using an aneroid manometer connected to the catheter, IAP was kept at 20 mmHg (ischemia group; I) for 1 hr. In the ischemia/reperfusion (I/R) group, pressure applied for an hour was decompressed and a 1-hr reperfusion period was allowed. In another IR group, melatonin was administered (10 mg/kg, i.p.) immediately before the decompression of IAP. The results demonstrate that tissue levels of malondialdehyde (MDA) and myeloperoxidase activity (MPO; index of tissue neutrophil infiltration) were elevated, while glutathione (GSH; a key to antioxidant) levels were reduced in both I and I/R groups (P < 0.05-0.001). Melatonin treatment in I/R rats reversed these changes (P < 0.01-0.001). Moreover, melatonin given to the I/R group reduced the elevations in serum aspartate aminotransferase, alanine aminotransferase and blood urea nitrogen levels and abolished the increase in serum creatinine levels. Our results indicate that melatonin, because of antioxidant and free radical scavenging properties, ameliorates reperfusion-induced oxidative organ damage. In conclusion, the results of the present study suggest that the therapeutic value of melatonin as a 'reperfusion injury-limiting' agent must be considered in ACS.     

Deficiency in antioxidant factors in patients with alcohol-related chronic pancreatitis

Free radicals have been suspected to play a role in the pathogenicity of alcohol-related chronic pancreatitis. The aim of this study was to determine the status of several antioxidant parameters in these patients and examine the factors that are likely to influence them. Thirty-five subjects (23 males and 12 females, mean age 48±8 years) with disease proven by endoscopic pancreatography and 14 healthy controls (6 males and 8 females, mean age 44±7 years) were included in the study. Biochemical antioxidant parameters included: selenium, zinc, and copper levels in plasma; glutathione peroxidase in plasma and erythrocytes; plasma malondialdehyde concentrations assessed by thiobarbituric acid reactants; and serum vitamin E and A levels. Selenium and vitamin E oral intake was assessed by a five-day diet analysis. Hemoglobin (130±16 vs 143±15 g/liter), vitamin E (8±5 vs 16±9 mg/liter), vitamin A (30±11 vs 49±12µg/dl), selenium (54±20 vs 87±11µg/liter), and plasma glutathione peroxidase (903±313 vs 1326±168 units/liter) were significantly lower in patients than in controls (P<0.05). In contrast, white blood cell count, C-reactive protein, and plasma copper levels were significantly higher in patients than in controls. Cholesterol, triglycerides, iron, ferritin, total proteins, zinc, and malondialdehyde were not different. Vitamin E was lower in patients with steatorrhea, while vitamin A was lower in patients with concomitant diabetes mellitus. Dietary intakes were not different between patients and controls. In conclusion, patients with alcohol-related chronic pancreatitis have low blood levels in many antioxidant factors. Dietary intakes of some of them (selenium and vitamin E) are adequate, however. Such deficiencies are secondary to pancreatic insufficiency and probably to increased requirements related to enhanced oxidative stress.