Astaxanthin ameliorates lung fibrosis in vivo and in vitro by preventing transdifferentiation,inhibiting proliferation,and promoting apoptosis of activated cells

Astaxanthin, a member of the carotenoid family, is the only known ketocarotenoid transported into the brain by transcytosis through the blood–brain barrier. However, whether astaxanthin has antifibrotic functions is unknown. In this study, we investigated the effects of astaxanthin on transforming growth factor β1-mediated and bleomycin-induced pulmonary fibrosis in vitro and in vivo. The results showed that astaxanthin significantly improved the structure of the alveoli and alleviated collagen deposition in vivo. Compared with the control group, the astaxanthin-treated groups exhibited downregulated protein expressions of α-smooth muscle actin, vimentin, hydroxyproline, and B cell lymphoma/leukemia-2 as well as upregulated protein expressions of E-cadherin and p53 in vitro and in vivo. Astaxanthin also inhibited the proliferation of activated A549 and MRC-5 cells at median inhibitory concentrations of 40 and 30 μM, respectively. In conclusion, astaxanthin could relieve the symptoms and halt the progression of pulmonary fibrosis, partly by preventing transdifferentiation, inhibiting proliferation, and promoting apoptosis of activated cells.     

红球藻软胶囊抗氧化功能评价研究

目的观察红球藻软胶囊的抗氧化功能。方法 117名符合条件的受试者随机分为对照组(60人)和试验组(57人),试验组每人每日口服红球藻软胶囊1次,每次1粒,连续服用30天。观察受试者一般状况,检测安全性指标和功效性指标,采用自身前后对照和组间对照两种研究方法进行对比研究。结果试验期间受试者一般状况良好,体检各项安全性指标亦未见异常,表明受试样品对人体无不良影响。试验后试食组血超氧化物歧化酶(SOD)活性显著高于试验前、且显著高于对照组。结论红球藻软胶囊有一定的抗氧化功能。     

Astaxanthin restores the enzymatic antioxidant profile in salivary gland of alloxan-induced diabetic rats

Objective

To evaluate the effect of astaxanthin on antioxidant parameters of salivary gland from diabetic rats. The hypothesis of the study was whether the supplementation of diabetic rats with astaxanthin might antagonize, or at least prevent, the defect in their antioxidative status.

Design

Wistar rats (n = 32) were divided in 4 groups: untreated control, treated control, untreated diabetic and treated diabetic rats. Astaxanthin (20 mg/kg body weight) was administered daily by gavage for 30 days. On day 23, diabetes was induced by injection of alloxan (60 mg/kg body weight). After 7 days of diabetes induction, the rats were killed and submandibular and parotid removed. Superoxide dismutase (SOD), catalase, glutathione peroxidase and reductase activities and the content of thiol groups were determined. Data were compared by ANOVA and the Tukey test (p < 0.05).

Results

Diabetes caused a reduction of SOD, and thiol content and increase of catalase and glutathione peroxidase activities of submandibular gland whilst in the parotid gland diabetes caused an increase of thiol content and no effect in the antioxidant system. The astaxanthin restores the enzymatic activities in the salivary gland, however does not prevent its oxidative damage.

Conclusion

The submandibular gland presented more susceptibility to oxidative alterations induced by diabetes. Astaxanthin presented a positive effect on the oxidative protection of the salivary gland from diabetic rats.     

Mechanistic insights into the effects of Astaxanthin on lipid profile and glucose homeostasis parameters: A systematic review of animal and clinical trial studies

Background and aimsThe antioxidant Astaxanthin (ASTX) may have potential to improve cardiometabolic risk factors. This study aimed to systematically review the impact of ASTX supplementation on lipid profile and glycemic indices in animal and clinical trial studies.MethodElectronic databases, including PubMed, Scopus, Web of Science, and Google Scholar were searched from inception up to June 2021. All clinical trials and animal studies published in English that investigated the effects of ASTX on lipid profile and glycemic parameters were considered in the study.ResultsA total of 3258 studies were retrieved from the search strategy from which 20 animal and five human studies were included in this systematic review. Twenty animal studies evaluated the effect of ASTX on lipid profile, of which 17 studies reported significant beneficial impact on one or more lipids. In addition, of 20 animal studies assessing the effect of ASTX on glucose homeostasis parameters, only 11 detected significant improvements. Five clinical trials evaluated the effect of ASTX on lipid profile; from these, three reported significant beneficial effect on at least one lipid. Moreover, of five human studies in which glucose homeostasis parameters were measured, only two observed significant improvement.ConclusionEvidence supports positive effects of ASTX on lipid profile. Nevertheless, the results on glycemic parameters are controversial and more studies are needed to draw a definite conclusion. ASTX could have great potential for reducing the risk of CVD and prevent T2DM and obesity-associated metabolic disturbances.     

Safety assessment of astaxanthin derived from engineered Escherichia coli K-12 using a 13-week repeated dose oral toxicity study and a prenatal developmental toxicity study in rats

Astaxanthin is a natural carotenoid with strong antioxidant activity that has been used for decades as a nutrient/color additive and it has recently been marketed as a health supplement. Astaxanthin can be synthesized in a wide range of microalgae, yeast, and bacteria. As genes directing astaxanthin biosynthesis in various organisms have been cloned, this study assessed the safety of astaxanthin crystal produced by Escherichia coli K-12 harboring plasmids carrying astaxanthin biosynthetic genes. The astaxanthin crystal contains a total carotenoid content of 950 mg/g and an astaxanthin content of 795 mg/g. Subchronic oral toxicity and prenatal developmental toxicity of the astaxanthin in rats were conducted in accordance with the Guidelines of Health Food Safety Assessment promulgated by Food and Drug Administration of Taiwan which is based on OECD guidelines 408 and 414. Both male and female Sprague-Dawley (SD) rats (12 for each gender) receiving the astaxanthin crystal at 1.2, 240.0, or 750.0 mg/kg/day in olive oil via oral gavage for 90 days showed no changes in body weight gains, hematology and serum chemistry values and hepatic enzyme stability, organ integrity and organ weight. Except the higher food consumption observed in rats receiving 750.0 mg/g astaxanthin crystal, administration of the astaxanthin crystal to 25–27 pregnant female rats in each group throughout the period of organogenesis (G6-G15) produced no adverse effects on fetal organogenesis. Based on the results, we propose that the no-observable-adverse-effect level (NOAEL) of the astaxanthin crystal extracted from genetically modified E. coli K-12 is 750.0 mg/kg bw/day.     

虾青素对四氯化碳诱导的慢性肝损伤大鼠的保护作用

探讨虾青素对慢性肝损伤大鼠肝功能的保护作用。方法采用四氯化碳（CCl4）制备大鼠慢性肝损伤模型,设正常组、模型组、虾青素干预组。通过酶联免疫法测定血清丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）、碱性磷酸酶（ALP）、总蛋白（TP）以及肝组织超氧化物歧化酶（ superoxide dismutase,SOD）、谷胱甘肽转移酶（ glutathione-S-transfcrase,GST）活性、谷胱甘肽（glutathione,GSH）及丙二醛（malondialdehyd,MDA）水平。对肝组织病理切片行Masson三色染色,检测肝纤维化情况,采用RT-PCR法检测Ⅰ型胶原mRNA水平。结果正常组大鼠肝胶原指数为（0.42±0.12）,模型组大鼠肝胶原指数为（1.84±0.24,P＜0.01）,虾青素治疗组肝胶原指数为（0.89±0.12）,显著低于模型组（P＜0.05）;正常大鼠肝组织Ⅰ型胶原mRNA水平为（0.12±0.02）,模型组为（0.48±0.06,P＜0.01）,虾青素治疗组为（0.35±0.09）,明显低于模型组（P＜0.05）;正常组肝组织MDA、GST、GSH和SOD水平分别为（1.93±0.76） nmol/mg、（18.43±5.34） U/mg、（75.45±9.67） mg/g、（678.80±76.56） U/mg,模型组MDA和GST分别为（6.56±1.09） nmol/mg、（54.34±7.65） U/mg,均显著升高（P＜0.05）,而GSH为（35.45±9.01） mg/g,SOD为（203.89±89.00） U/mg,均显著降低（P＜0.01）;与模型组比,虾青素治疗组MDA为（3.34±1.12） nmol/mg,GST为（30.89±4.78） U/mg,均显著低于模型组（P＜0.01）,而GSH为（56.78±7.78）mg/g,SOD为（432.34±92.56） U/mg,均较模型组显著升高（P＜0.01）。结论虾青素可以缓解四氯化碳诱导的大鼠慢性肝损伤,其可能机制与提高抗氧化能力有关。     

Physico-chemical stability of astaxanthin nanodispersions prepared with polysaccharides as stabilizing agents

Abstract

The emulsification and stabilization ability of four selected polysaccharides, namely, gum Arabic, xanthan gum, pectin and methyl cellulose, in the preparation of water-dispersible astaxanthin nanoparticles using the emulsification-evaporation technique was investigated in this study. The chemical and molecular structure of polysaccharides had significant effects (p?<?0.05) on the physicochemical properties of the prepared astaxanthin nanodispersions. Among all prepared nanodispersions, sample produced and stabilized using gum Arabic showed the smallest average particle size (295?nm) and highest physical stability. The observed considerable degradation of astaxanthin in the resulting nanodispersions during processing (24–70% w/w) and storage at 10?°C for 30?d (86–96% w/w) illustrated the limited chemical stability of polysaccharide-stabilized nanodispersions.