DESIGN AND EVALUATION OF NOVEL TOPICAL GEL OF TINOSPORA CORDIFOLIA AS ANTIMICROBIAL AGENT

Objective: The present study deals with topical formulations of a bioactive extract of Tinospora cordifolia and its evaluation.Methods: Dried, powdered stem was extracted with chloroform using ultra-sonication method for 3 hrs. Topical formulations like gels containingchloroform extract were formulated using various gelling agents. These gels were evaluated for physicochemical parameters, viscosity, spreadaibility,and antimicrobial activity.Results: A topical gel was successfully formulated containing bioactive chloroform extract of T. cordifolia. The gel was very effective as antimicrobialformulations.Conclusion: These kinds of formulations can be very promising wound healing medicines with ease of use and no side effects.Keywords: Topical gel, Tinospora Cordifolia, Anitmictobia

The Rhizome Mixture of Anemarrhena asphodeloides

In the previous study, the mixture of the rhizome of Anemarrhena asphodeloides (AA, family Liliaceae) and the rhizome of Coptidis chinensis (CC, family Ranunculaceae) (AC-mix) improved TNBS- or oxazolone-induced colitis in mice. Therefore, to investigate its anticolitic mechanism, we measured its effect in acute and chronic DSS-induced colitic mice and investigated its anti-inflammatory mechanism in peritoneal macrophages. AC-mix potently suppressed DSS-induced body weight loss, colon shortening, myeloperoxidase activity, and TNF-α, IL-1β, and IL-6 expressions in acute or chronic DSS-stimulated colitic mice. Among AC-mix ingredients, AA, CC, and their main constituents mangiferin and berberine potently inhibited the expression of proinflammatory cytokines TNF-α and IL-1β, as well as the activation of NF-κB in LPS-stimulated peritoneal macrophages. AA and mangiferin potently inhibited IRAK phosphorylation, but CC and berberine potently inhibited the binding of LPS to TLR4 on macrophages, as well as the phosphorylation of IRAK1. AC-mix potently inhibited IRAK phosphorylation and LPS binding to TLR4 on macrophages. Based on these findings, AC-mix may ameliorate colitis by the synergistic inhibition of IRAK phosphorylation and LPS binding to TLR4 on macrophages

Ursolic Acid Isolated from the Seed of Cornus officinalis Ameliorates Colitis in Mice by Inhibiting the Binding of Lipopolysaccharide to Toll-like Receptor 4 on Macrophages

Ursolic acid, which was isolated from an ethanol extract of Cornus officinalis seed, potently inhibited nuclear factor κ light-chain enhancer of activated B cells (NF-κB) activation in lipopolysaccharide (LPS)-stimulated peritoneal macrophages. Therefore, we investigated the anti-inflammatory mechanism of ursolic acid in LPS-stimulated macrophages and colitic mice. Ursolic acid inhibited phosphorylation of interleukin 1 receptor-associated kinase (IRAK)­1, TAK1, inhibitor of nuclear factor κB kinase subunit β (IKKβ), and IκBα as well as activation of NF-κB and MAPKs in LPS-stimulated macrophages. Ursolic acid suppressed LPS-stimulated interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, cyclooxygenase (COX)-2, and inducible NO synthetase (iNOS) expression as well as PGE2 and NO levels. Ursolic acid not only inhibited the Alexa Fluor 488-conjugated LPS-mediated shift of macrophages but also reduced the intensity of fluorescent LPS bound to the macrophages transiently transfected with or without MyD88 siRNA. However, ursolic acid did not suppress NF-κB activation in peptidoglycan-stimulated macrophages. Oral administration of ursolic acid significantly inhibited 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colon shortening and myeloperoxidase (MPO) activity in mice. Ursolic acid also suppressed TNBS-induced COX-2 and iNOS expression as well as NF-κB activation in colon tissues. Ursolic acid (20 mg/kg) also inhibited TNBS-induced IL-1β, IL-6, TNF-α by 93, 86, and 85%, respectively (<i>p</i> < 0.05). However, ursolic acid reversed TNBS-mediated downregulation of IL-10 expression to 79% of the normal control group (<i>p</i> < 0.05). On the basis of these findings, ursolic acid may ameliorate colitis by regulating NF-κB and MAPK signaling pathways via the inhibition of LPS binding to TLR4 on immune cells