19 research outputs found

    Evaluation of free-radical quenching properties of standard Ayurvedic formulation Vayasthapana Rasayana

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    <p>Abstract</p> <p>Background</p> <p>Cellular damage induced by free-radicals like Reactive Oxygen and Nitrogen Species (ROS and RNS) has been implicated in several disorders and diseases, including ageing. Hence naturally occurring anti-oxidant rich-herbs play a vital role in combating these conditions. The present study was carried out to investigate the <it>in vitro </it>free-radical quenching capacity of a known <it>Ayurvedic </it>poly-herbal formulation called <it>Vayasthapana Rasayana.</it></p> <p>Methods</p> <p>Methanol extracts of <it>Vayasthapana Rasayana </it>formulation (VRF) were studied for <it>in vitro </it>total antioxidant activity along with phenolic content and reducing power. <it>In vitro </it>assays like DPPH, FRAP, ABTS scavenging to evaluate radical quenching potential were performed.</p> <p>Results</p> <p>The formulation has shown 94% at 0.1 mg/ml DPPH free-radical scavenging activity as against 84% at 0.1 mg/ml for standard ascorbic acid (IC<sub>50 </sub>value 5.51 μg/ml for VRF and 39 μg/ml for standard). It has a significant higher ferric reducing potential also (OD 0.87 at 700 nm & 0.21 at 0.1 mg/ml for VRF and standard, respectively). The total phenolic content (gallic acid equivalent) of the VRF is 8.3 mg per g of dry mass. Total antioxidant capacity of the formulation, estimated by FRAP was 1150 ± 5 μM Fe(II)/g dry mass. ABTS radical scavenging activity of VRF was 69.55 ± 0.21% at 100 μg/ml concentration with a IC<sub>50 </sub>value of 69.87 μg/ml as against 9% and 95% by ascorbic acid and Trolox (at 70.452 μg/ml and 0.250 μg/ml concentrations, respectively).</p> <p>Conclusion</p> <p>In Indian traditional <it>Ayurvedic </it>system, use of VRF is in regular practice for mainly combating age-related disorders and diseases as many of the components of the <it>Rasayana </it>are known for their free-radical scavenging activity. This study has validated the potential use of VRF as an anti-oxidant to fight age-related problems.</p

    The omega-3 fatty acid docosahexaenoic acid favorably modulates the inflammatory pathways and macrophage polarization within aorta of LDLR-/- mice

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    International audienceThe omega-3 fatty acid docosahexaenoic acid (DHA) has potent anti-atherogenic properties but its mechanisms of action at the vascular level remain poorly explored. Knowing the broad range of molecular targets of omega-3 fatty acids, microarray analysis was used to open-mindedly evaluate the effects of DHA on aorta gene expression in LDLR-/- mice and better understand its local anti-atherogenic action. Mice were fed an atherogenic diet and received daily oral gavages with oils rich in oleic acid or DHA. Bioinformatics analysis of microarray data first identified inflammation and innate immunity as processes the most affected by DHA supplementation within aorta. More precisely, several down-regulated genes were associated with the inflammatory functions of macrophages (e. g., CCL5 and CCR7), cell movement (e. g., ICAM-2, SELP, and PECAM-1), and the major histocompatibility complex (e. g., HLA-DQA1 and HLA-DRB1). Interestingly, several genes were identified as specific biomarkers of macrophage polarization, and their changes suggested a preferential orientation toward a M2 reparative phenotype. This observation was supported by the upstream regulator analysis highlighting the involvement of three main regulators of macrophage polarization, namely PPAR gamma (z-score = 2.367, p = 1.50 x 10(-13)), INF gamma (z-score = -2.797, p = 2.81 x 10(-14)), and NF kappa B (z-score = 2.360, p = 6.32 x 10(-9)). Moreover, immunohistological analysis of aortic root revealed an increased abundance of Arg1 (+111 %, p = 0.01), a specific biomarker of M2 macrophage. The present study showed for the first time that DHA supplementation during atherogenesis is associated with protective modulation of inflammation and innate immunity pathways within aorta putatively through the orientation of plaque macrophages toward a M2 reparative phenotype
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