Asawin Wanbanjob

Identification ofStreptomyces sp. Tc022, an endophyte inAlpinia galanga, and the isolation of actinomycin D

Some endophytic actinomycetes (120) were isolated from the roots ofAlpinia galanga. Identification of these endophytes was based on their morphology and amino acid composition of the whole-cell extract. Most isolates were classified aStreptomyces sp. (82), with the remainder belonging toNocardia sp. (11),Microbispora sp. (3) andMicromonospora sp. (2). Eight isolates were unclassified and 14 were lost during subculture. The strain identified as endophyticStreptomyces sp. Tc022 strongly inhibitedColletotrichum musae andCandida albicans. This endophyte was cultured, the agar was extracted with organic solvent and the extract was purified on a column of silica gel to give a major component, which was identified to be actinomycin D on the basis of spectroscopic dat Actinomycin D showed antifungal activity againstColletotrichum musae andCandida albicans with the MIC of 10 and 20 mg ml−1, respectively.

Anti-inflammatory activity of lansais from endophytic Streptomyces sp. SUC1 in LPS-induced RAW 264.7 cells

Abstract This research was undertaken to find the in vitro inflammatory action of lansai A–D produced by Streptomyces sp. SUC1. We investigated the effects of lansai C not only on the formation of nitric oxide (NO), prostaglandin E2 (PGE2), tumour necrosis factor (TNF-α), interleukin (IL)-1α, IL-6 and IL-10, but also on inducible NO synthase and cyclooxygenase-2 (COX-2) in lipopolysaccharide (LPS)-induced murine macrophage RAW 264.7 cells. The data obtained were consistent with the modulation of inducible nitric oxide synthase enzyme expression. A similar fashion was also observed when LPS-induced PGE2 release and COX-2 expression were tested. The significant inhibitory effects were shown in concentration-dependent manners. In addition, lansai C also mildly but significantly reduced the formation of TNF-α. These findings support the application of lansai C as anti-inflammatory agent.

Anti-inflammatory effects of lansai C and D cause inhibition of STAT-1 and NF-κB activations in LPS-induced RAW 264.7 cells

Abstract In inflammation, proinflammatory cytokines induce the formation of large amounts of nitric oxide (NO) by inducible nitric oxide synthase (iNOS), and compounds that inhibit NO production have anti-inflammatory effects. In the present study, we investigated the effects of lansai C and D on NO production in lipopolysaccharide-induced RAW 264.7 cells, and evaluated the mechanisms of action of the compounds. Lansai C and D inhibited iNOS protein and mRNA expression and also NO production in a dose-dependent manner. These compounds inhibited the activation of nuclear factor-κB, which is a significant transcription factor for iNOS and also inhibited the activation of the signal transducer and activator of transcription-1, another important transcription factor for iNOS. The present study characterises the effects and mechanisms of lansais on iNOS expression and NO production in activated macrophages. The results explain the pharmacological efficacy of lansais as anti-inflammatory compounds.

Total Synthesis and the Biological Activities of (±)-Norannuradhapurine

The structure previously assigned to the phenolic noraporphine alkaloid, (-)-norannuradhapurine has been confirmed by a total synthesis of the racemic alkaloid in which the key step involved the formation of the C ring by a radical-initiated cyclization. although inactive against Staphylococcus aureus ATCC25932, Escherichia coli ATCC10536 and Candida albicans ATCC90028, (±)-norannuradhapurine inhibits the production of NO, PGE2, TNF-a, IL-1b and IL-6 and the expression of iNOS and COX-2 in RAW 264.7 macrophages stimulated with LPS in vitro.

Total Synthesis and Antimicrobial Activity of (±)-Laurelliptinhexadecan-1-one and (±)-Laurelliptinoctadecan-1-one

The structures previously assigned to (+)-laurelliptinhexadecan-1-one (1a) and (+)-laurelliptinoctadecan-1-one (1b) from Cocculus orbiculatus (L.) DC. (Menispermaceae) have been confirmed by total synthesis of the racemic alkaloids. The key step of the synthesis involved formation of ring C of the aporphines by a radical-intiated cyclisation. Both (±)-laurelliptinhexadecan-1-one (1a) and (±)-laurelliptinoctadecan-1-one (1b) were inactive against Staphylococcus aureus ATCC25932, Escherichia coli ATCC10536 and Candida albicans ATCC90028.

Total Syntheses of (±)-Gusanlung A, (±)-Gusanlung D and 8-Oxyberberrubine and the Uncertainty Concerning the Structures of (-)-Gusanlung A, (-)-Gusanlung D and 8-Oxyberberrubine

(±)-Gusanlung A, 8-oxyberberrubine and (±)-gusanlung D have been synthesized by radical cyclisation of the corresponding 2-aroyl-1-methylenetetra- hydroisoquinolines. The 1H and 13C spectra of (-)-gusanlung D were found to be different from those of synthetic (±)-gusanlung D. Careful analyses of the 13C spectra of (–)-gusanlung A and natural 8-oxyberberrubine also cast doubt on the correctness of the structures previously assigned to these two compounds. (±)-Gusanlung A and (±)-gusanlung D were inactive against Staphylococcus aureus ATCC25932, Escherichia coli ATCC10536 and Candida albicans ATCC90028.