虾青素抑制氧化应激改善陈旧红细胞保存质量

目的:观察虾青素能否抑制陈旧悬浮红细胞内的氧化应激,改善红细胞保存质量。方法:采集志愿者血液,制备去白悬浮红细胞,将其随机分为4组,对照组加入DMSO,另外3组悬浮红细胞的保存液内加入抗氧化剂虾青素使其终浓度分别为5、10和20μmol/L,悬浮红细胞于2℃~6℃内保存。保存至28 d、42 d采用倒置荧光显微镜观察悬浮红细胞内活性氧族的表达状况,采用荧光酶标仪测定红细胞内活性氧族的含量,采用硫代巴比妥酸比色法测定红细胞内丙二醛含量,扫描电镜观察红细胞的超微结构,采用化学比色法测定三磷酸腺苷含量,采用紫外测试法测定2,3-二磷酸甘油酸含量。结果:与各自对照组相比,加虾青素的三组储存28 d和42 d悬浮红细胞内活性氧族和丙二醛含量降低,三磷酸腺苷和2,3-二磷酸甘油酸水平升高,改善了红细胞的形态。结论:虾青素可以通过降低储存悬浮红细胞内的氧化应激水平改善红细胞保存质量。     

Dose-dependent effects of astaxanthin on cortical spreading depression in chronically ethanol-treated adult rats

Background: The consumption of alcoholic drinks is a frequent drug‐abuse situation, which is associated to a wide variety of pathological disturbances affecting several organs, including the brain. We have previously shown in the developing rat brain that ethanol intake facilitates the propagation of cortical spreading depression (CSD), an excitability‐related neural phenomenon present in several animal species. This electrophysiological effect was attenuated by a shrimp (Litopenaeus vannamei) carotenoids extract. Here we investigated the effects of pure astaxanthin, the main carotenoid found in shrimp, on CSD. Methods: Adult Wistar rats were treated per gavage, during 18 days, with 2.5, 10 or 90 μg/kg/d astaxanthin dissolved in ethanol (3 g/kg) and CSD was recorded on the cortical surface 1 to 3 days thereafter. Four groups, treated respectively with ethanol, distilled water and soybean oil with‐ and without astaxanthin were also studied for comparison with the ethanol + astaxanthin groups. Results: Ethanol‐treated rats displayed higher CSD‐velocities (mean values, in mm/min, per hour of recording ranging from 4.08 ± 0.09 to 4.12 ± 0.16), compared to the distilled water‐group (from 3.19 ± 0.13 to 3.27 ± 0.06). Addition of astaxanthin to ethanol lead to lower CSD‐velocities in a dose‐dependent manner, ranging from 3.68 ± 0.09 to 3.97 ± 0.22 for the 2.5 μg/kg/d‐dose, from 3.29 ± 0.09 to 3.32 ± 0.07 for the 10 μg/kg/d‐dose, and from 2.89 ± 0.13 to 2.92 ± 0.11 for the 90 μg/kg/d‐dose. The velocities of the soybean oil groups (with and without astaxanthin) were not statistically different from the 10 μg/kg/d astaxanthin + ethanol and distilled water groups. Conclusion: The results demonstrate the antagonistic effect of astaxanthin against the ethanol‐induced facilitation of CSD propagation. Probably carotenoid antioxidant properties are involved in such effects.     

Nephroprotective effect of astaxanthin against trivalent inorganic arsenic-induced renal injury in wistar rats

Inorganic arsenic (iAs) is a toxic metalloid found ubiquitously in the environment. In humans, exposure to iAs can result in toxicity and cause toxicological manifestations. Arsenic trioxide (As₂O₃) has been used in the treatment for acute promyelocytic leukemia. The kidney is the critical target organ of trivalent inorganic As (iAs^III) toxicity. We examine if oral administration of astaxanthin (AST) has protective effects on nephrotoxicity and oxidative stress induced by As₂O₃ exposure (via intraperitoneal injection) in rats. Markers of renal function, histopathological changes, Na⁺-K⁺ ATPase, sulfydryl, oxidative stress, and As accumulation in kidneys were evaluated as indicators of As₂O₃ exposure. AST showed a significant protective effect against As₂O₃-induced nephrotoxicity. These results suggest that the mechanisms of action, by which AST reduces nephrotoxicity, may include antioxidant protection against oxidative injury and reduction of As accumulation. These findings might be of therapeutic benefit in humans or animals suffering from exposure to iAs^III from natural sources or cancer therapy.     

Evaluation of efficacy of natural astaxanthin and vitamin E in prevention of colistin-induced nephrotoxicity in the rat model

ObjectiveWe evaluated the effect of astaxanthin (ASX) and vitamin E (vit E) on colistin methanesulfonate (CMS) induced-nephrotoxicity in rats.MethodsAnimals were treated with sterile saline, 300 000 or 450 000 IU/kg/day of CMS, CMS + ASX (20 mg/kg), CMS + vit E (100 mg/kg), or CMS + 1 ml/kg olive oil (OO) for 7 days. The plasma/urine creatinine (Cr) level, urine γ-glutamyl-transferase (GGT) level, and renal tissue activities in malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and reductase (GSH), as well as renal histology were performed.ResultsCMS induced a tubular damage, increased the GGT and MDA levels, and decreased the activities of SOD, CAT, GPx and GSH. Co-treatment with ASX or vit E restored all biochemical parameters cited above and improved the histopathological damage.ConclusionNephrotoxicity induced by CMS might be due to oxidative damage. The improvement by ASX or vit E seems to be related to their antioxidant properties.     

虾青素对高脂血症大鼠脂代谢的影响

目的研究虾青素对高脂饲料喂养下大鼠诱发高脂血症过程中血脂代谢的干预作用。方法将60只SD雄性大鼠,随机分为正常对照组、高血脂模型组、辛伐他汀阳性药组(200 mg/kg)、虾青素高、中、低剂量组(415、210、110 mg/kg),分别饲喂标准、高脂、高脂+辛伐他汀、高脂+虾青素,于实验开始前1 d和开始后第4、8、12周末取空腹血,检测血清甘油三酯(TG)、总胆固醇(TC)和高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)。结果与高血脂模型组比较,虾青素组的TC、TG、LDL-C在8、12 w时降低,差异显著(P<0.01),而HDL-C升高,差异显著(P<0.01)。结论虾青素可以对高脂饲料喂养大鼠诱发高脂血症过程中的血脂代谢产生影响,改善血脂变化。     

虾青素胶囊治疗膝关节骨性关节炎疗效观察

目的观察虾青素胶囊治疗膝关节骨性关节炎的疗效。方法将60例膝关节骨性关节炎患者随机分为治疗组(30例)和对照组(30例)。治疗组给予虾青素胶囊治疗,对照组给予芬必得治疗。比较两组治疗前后膝关节功能评分,观察主要症状缓解情况和治疗效果。结果 (1)治疗组的疼痛缓解持续时间较对照组缩短,而疼痛缓解时间较对照组延长(P均0.01);(2)两组治疗后关节功能较治疗前均有提高(P均0.01),而治疗组比对照组更优(P0.05);(3)总有效率治疗组为66.67%,对照组为83.33%,两组疗效比较差异无统计学意义(P0.05)。结论虾青素胶囊治疗骨性关节炎有一定的疗效。     

Treatment of H. pylori infected mice with antioxidant astaxanthin reduces gastric inflammation, bacterial load and modulates cytokine release by splenocytes

Helicobacter pylori is a Gram-negative bacterium affecting about half of the world population, causing chronic gastritis type B dominated by activated phagocytes. In some patients the disease evolves into gastric ulcer, duodenal ulcer, gastric cancer or MALT lymphoma. The pathogenesis is in part caused by the immunological response. In mouse models and in human disease, the mucosal immune response is characterized by activated phagocytes. Mucosal T-lymphocytes are producing IFN-γ thus increasing mucosal inflammation and mucosal damage. A low dietary intake of antioxidants such as carotenoids and vitamin C may be an important factor for acquisition of H. pylori by humans. Dietary antioxidants may also affect both acquisition of the infection and the bacterial load of H. pylori infected mice. Antioxidants, including carotenoids, have anti-inflammatory effects. The aim of the present study was to investigate whether dietary antoxidant induced modulation of H. pylori in mice affected the cytokines produced by H. pylori specific T-cells. We found that treatment of H. pylori infected mice with an algal cell extract containing the antioxidant astaxanthin reduces bacterial load and gastric inflammation. These changes are associated with a shift of the T-lymphocyte response from a predominant Th1-response dominated by IFN-γ to a Th1/Th2-response with IFN-γ and IL-4. To our knowledge, a switch from a Th1-response to a mixed Th1/Th2-response during an ongoing infection has not been reported previously.     

The potential antiepileptic activity of astaxanthin in epileptic rats treated with valproic acid

ObjectivesEpilepsy is a neurological disease characterized by sudden, abnormal, and hyper- discharges in the central nervous system (CNS). Valproic acid (VPA) is commonly used as a broad-spectrum antiepileptic therapeutic. However, in many cases, patients develop resistance to VPA treatment due to overwhelming oxidative stress, which in turn might be a major catalyst for disease progression. Therefore, antioxidants can potentially become therapeutic agents by counteracting reactive oxygen species (ROS)-mediated damage. The present study is aimed to evaluate the potential antiepileptic effect of astaxanthin (ASTA) in pentylenetetrazol (PTZ) induced epileptic model rats that are chronically treated with VPA for 8 weeks.MethodFifty-male Wistar rats were randomly divided into five groups: Non-PTZ group, PTZ, PTZ/VPA, PTZ/ASTA, and PTZ/VPA/ASTA treated groups.ResultsPTZ/VPA treated group showed a neuroprotective effect with improvement in antioxidant levels, behavioral test, and histopathological changes induced by PTZ. VPA also exhibited an anti-inflammatory effect as its treatment resulted in the reduction of tumor necrosis factor-α (TNF-α). ASTA exhibited an anticonvulsant effect and enhanced anti-inflammatory effect as compared to VPA. During the combined therapy, ASTA potentiated the antiepileptic effect of the VPA by reducing the oxidative stress and TNF-α as well as increased the glutathione (GSH) levels. Also, there were substantial improvements in the behavioral and histopathological changes in the VPA/ASTA treated group as compared to the VPA treated group.ConclusionASTA could have an antiepileptic and anti-inflammatory effect by reducing ROS generation. Therefore, co-administration of both the therapeutics (VPA/ASTA) has a synergistic effect in treating epilepsy and could potentially minimize recurrence and/or exacerbation of seizures.     

雨生红球藻中虾青素酯皂化工艺的研究

目的：研究雨生红球藻中虾青素酯的皂化工艺,优选雨生红球藻中虾青素酯皂化的最佳工艺条件。方法：采用HPLC测定皂化后虾青素的含量,以雨生红球藻中虾青素提取量为指标,应用正交试验设计进行筛选。结果：皂化的最佳工艺条件为10g·L^-１的KOH-CH30H皂化液在20℃争件下恒温振荡皂化60min。结论：优选得到的工艺稳定可行。     

虾青素脂质体对小鼠皮肤紫外线损伤干预机制的初步研究

目的 探讨虾青素脂质体对小鼠皮肤中波紫外线（UVB）损伤的干预作用及机制。方法 将40只C57BL/6J小鼠随机分为4组,即空白组（不行UVB照射,不用药）、模型组（UVB光损伤组,只照射不用药）、对照组（照射+虾青素）、实验组（照射+虾青素脂质体）,每组10只。UVB照射（辐照强度为2 mW·cm2,辐照时间为60 s;前5日每日照射1次,后9日隔日照射1次,2周共照射10次）及药物干预（每次辐照前10 min用4 mL 0.2‰虾青素或4 mL 0.2‰虾青素脂质体涂抹于暴露皮肤）2周后,HE染色分别观察皮肤组织病理学改变,免疫组织化学染色观察皮肤 Ki-67抗原、8-羟基-2-脱氧鸟苷（8-OHdG）表达情况,试剂盒测定皮肤超氧化物岐化酶（SOD）活力和血清基质金属蛋白酶-13（MMP-13）质量浓度。结果 模型组和对照组的HE染色显示真皮变薄、真皮胶原纤维细长、排列疏松紊乱,与空白组比较,Ki-67、MMP-13及8-OHdG表达增加以及SOD活力降低,其差异均有统计学意义（P＜0.05）。实验组与模型组相比皮肤组织病理变化得到明显改善,Ki-67、MMP-13及8-OHdG表达减少及SOD活力升高,其差异具有统计学意义（P＜0.05）。结论 外用虾青素脂质体可改善小鼠皮肤光损伤引起的病理变化及减轻胶原损伤,其强抗氧化作用可能是干预机制之一。