Prothrombin (Human) ELISA Kit

Rutin trihydrate a herbal drug having abundant medicinal properties, mainly used for topical treatment of inflammation, presents a hindrance and reduced anti-inflammatory activity. It is a BCS class II drug having low oral bioavailability, poor water solubility (0.125 g/L), and low stability of rutin in aqueous alkaline medium, restricting its application in use. So, it is successfully formulated as an emulgel to improve its antiinflammatory properties. The current study aims to design, formulate, and to optimize Rutin trihydrate emulgel to enhance its efficacy and stability. Emulgel was designed, optimized by using central composite design taking three independent variables and one dependent variable. Five responses were generated, and the optimized formulation was prepared using carbopol 934(0.8%), clove oil (12.5 ml), and span (2.32%). The emulsifying agent being Tween 20, Span 20, and preservatives used are methyl and propyl parabens. The formulation (F2) with this combination gave emulgel of yellow color, homogeneous with good consistency, possessed pH of 6.51 +/- 0.04, drug content of 98.7%, a viscosity of 14, 980 cps, spreadability 13.5 gm.cm/sec and extrudability 36.2 and in-vitro drug release of 74.8% for 8 h. Since, F2 emulgel possesses an edge in terms of spreadability, viscosity, extrusion, in-vitro drug release it would become a solution for loading hydrophobic drugs in a water-soluble gel base.

Erysimum cheiranthoides L (Brassicaceae; wormseed wallflower) accumulates not only glucosinolates, which are characteristic of the Brassicaceae, but also abundant and diverse cardenolides. These steroid toxins, primarily glycosylated forms of digitoxigenin, cannogenol, and strophanthidin, inhibit the function of essential Na+/K+-ATPases in animal cells. We screened a population of 659 ethylmethanesulfonate-mutagenized E. cheiranthoides plants to identify isolates with altered cardenolide profiles. One mutant line exhibited 66% lower cardenolide content, resulting from greatly decreased cannogenol and strophanthidin glycosides, partially compensated for by increases in digitoxigenin glycosides. This phenotype was likely caused by a single-locus recessive mutation, as evidenced by a wildtype phenotype of F1 plants from a backcross, a 3:1 wildtype:mutant segregation in the F2 generation, and genetic mapping of the altered cardenolide phenotype to one position in the genome. The mutation created a more even cardenolide distribution, decreased the average cardenolide polarity, but did not impact most glucosinolates. Growth of generalist herbivores from two feeding guilds, Myzus persicae Sulzer (Hemiptera: Aphididae; green peach aphid) and Trichoplusia ni Hubner (Lepidoptera: Noctuidae; cabbage looper), was decreased on the mutant line compared to wildtype. Both herbivores accumulated cardenolides in proportion to the plant content, with T. ni accumulating higher total concentrations than M. persicae. Helveticoside, a relatively abundant cardenolide in E. cheiranthoides, was not detected in M. persicae feeding on these plants. Our results support the hypothesis that increased digitoxigenin glycosides provide improved protection against M. persicae and T. ni, despite an overall decrease in cardenolide content of the mutant line.