Disease relevance of Astilbin

• Lymph node cells from donor mice administered astilbin failed to adoptively transfer the hypersensitivity [1].
• RESULTS: Astilbin significantly inhibited contact hypersensitivity when given in the elicitation phase but not in the sensitization phase, whereas cyclosporin A inhibited both phases [1].
• RESULTS: Astilbin dose-dependently inhibited the footpad swelling, arthritic incidence, and clinical scores without influencing the body weights, while CsA showed strong inhibition with a significant weight loss [2].
• CONCLUSIONS: Astilbin may act as an efficient therapeutic agent for arthritis like CsA but with less toxicity [2].
• Furthermore, the isolated spleen cells from normal mice were incubated with astilbin in the presence of concanavalin A, or those from mice with ear dermatitis were cultured with astilbin [3].

High impact information on Astilbin

• Flavonoid molecules obtained from medicinal herbs, including astilbin and epigallocatechin gallate, were discovered to have immunomodulatory properties [4].
• Astilbin in vivo remarkably induced IL-10 expression in lymph node cells at an earlier time and decreased TNF-alpha and IFN-gamma expression at a later time [1].
• Furthermore, the in vivo neutralization of IL-10 significantly impaired the effect of astilbin on contact hypersensitivity [1].
• Purification of astilbin and isoastilbin in the extract of smilax glabra rhizome by high-speed counter-current chromatography [5].
• The pretreatment of nonparenchymal cells but not hepatocytes with astilbin in vitro caused a concentration- and time-dependent inhibition against the damage [6].

Chemical compound and disease context of Astilbin

• When administered during the effector but not induction phase, astilbin significantly decreased the liver injury induced by delayed-type hypersensitivity to picryl chloride in mice [6].

Biological context of Astilbin

• This study examined the effects of astilbin, a flavanone, on delayed-type hypersensitivity reactions and its mechanisms of action on cell migration [3].
• The active substances isolated from the EtOAc-soluble fraction of the rhizomes were identified as eucryphin (1), bergenin (2), and astilbin (3), which enhanced norepinephrine-induced lipolysis at concentrations of 10-1000 microgram/mL, while they themselves did not cause lipolysis [7].
• Similar to astilbin (4), compounds 22, 24, 26, 30 and 32 significantly inhibited the single mixed lymphocytes reaction (sMLR) and enhanced the apoptosis of spleen cells isolated from mice with sheep red blood cell-induced delayed-type hypersensitivity respectively [8].
• This paper reports the synthesis and immunosuppressive activity of seven analogues of astilbin, which may shed light on the structure-activity relationship of the compounds [8].

Anatomical context of Astilbin

• These results suggest that astilbin provides improvement against liver injury through a selective dysfunction of liver-infiltrating cells rather than by protecting the hepatocyte membrane [6].
• Astilbin suppresses delayed-type hypersensitivity by inhibiting lymphocyte migration [3].
• Astilbin prevents concanavalin A-induced liver injury by reducing TNF-alpha production and T lymphocytes adhesion [9].
• In addition, astilbin inhibited the adhesion of spleen cells and purified T lymphocytes isolated from the liver-injured mice to fibronectin, laminin and type IV collagen.Moreover, the adhesion of human Jurkat T cells to endothelial cell line ECV-304 was also inhibited by astilbin [9].
• Astilbin selectively facilitates the apoptosis of interleukin-2-dependent phytohemagglutinin-activated Jurkat cells [10].

Associations of Astilbin with other chemical compounds

• The effects of astilbin in Kohki tea, which is produced from the leaves of Engelhardtia chrysolepis Hance (Chinese name, huang-qui), and of an aglycone of astilbin, taxifolin, on the serum and liver lipid concentrations, and on the erythrocyte and liver antioxidative enzyme activities were determined with rats fed on a cholesterol-free diet [11].
• The mixture of two glycoside-flavonoids, identified as astilbin (2) and quercitrin (3), also exhibited good analgesic activity, causing 63% of reduction of abdominal constriction in mice [12].

Gene context of Astilbin

• The aim of this study was to evaluate the effect of astilbin on concanavalin A (Con A)-induced hepatitis, a T cell-dependent model of liver injury [9].
• In the supernatants collected, the activity of matrix metalloproteinases (MMPs) MMP-2 and MMP-9 was remarkably inhibited by astilbin [3].
• In isolated spleen cells from arthritic mice, increased potentials in proliferation, NO production, and MMP-2 and 9 activities were suppressed dose-dependently by the oral administration of astilbin [2].
• To the Jurkat cells that had been cultivated for 72--144 h without PHA, however, astilbin did not show any facilitation of the cell apoptosis [10].
• Dihydroflavonol taxifolin and its glycoside, astilbin, from Engelhardtia chrysolepis inhibited rat lens and recombinant human aldose reductase [13].

Analytical, diagnostic and therapeutic context of Astilbin

• Astilbin suppresses collagen-induced arthritis via the dysfunction of lymphocytes [2].
• A high-performance liquid chromatographic (HPLC) method was developed for the simultaneous determination of five flavonoids, taxifolin, neoastilbin, astilbin, neoisoastilbin and isoastilbin, contained in Rhizoma Smilacis Glabrae [14].
• Quantitative determination of astilbin in rabbit plasma by liquid chromatography [15].
• The bioassay showed that the antimicrobial properties may be attributed to astilbin, a flavanone derivative identified on the basis of its spectroscopic data [16].

References