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Results for “Panduratin A”

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PubMed2006

Induction of apoptosis and cell cycle arrest by a chalcone panduratin A isolated from Kaempferia pandurata in androgen-independent human prostate cancer cells PC3 and DU145.

Because of unsatisfactory treatment options for prostate cancer (CaP) there is a need to develop novel preventive approaches for this malignancy. One such strategy is through chemoprevention by the use of non-toxic dietary substances and botanical products. We have shown previously that panduratin A isolated from the extract of Kaempferia pandurata (Zingiberaceae) is a strong inhibitor of cyclooxygenase-2 in RAW264.7 cells and induces apoptosis in HT-29 cells. In the present study, we provide evidence that panduratin A treatment to androgen-independent human CaP cells PC3 and DU145 result in a time and dose-dependent inhibition of cell growth with an IC50 of 13.5-14 microM and no to little effect on normal human prostate epithelial cells. To define the mechanism of these anti-proliferative effects of panduratin A, we determined its effect on critical molecular events known to regulate the cell cycle and the apoptotic machinery. Annexin V/propidium iodide staining provided the evidence for the induction of apoptosis which was further confirmed by the observation of cleavage of poly (ADP-ribose) polymerase and degradation of acinus. Panduratin A treatment to cells was found to result in inhibition of procaspases 9, 8, 6 and 3 with significant increase in the ratio of Bax:Bcl-2, suggesting the involvement of a mitochondrial-dependent apoptotic pathway. Panduratin A-mediated apoptosis was accompanied with upregulation of Fas death receptor and TNF-related apoptosis-inducing ligand (TRAIL). Furthermore, cell cycle analysis using flow cytometry showed that panduratin A treatment of cells resulted in a G2/M arrest in a dose-dependent manner. The immunoblot analysis data revealed that in both cell lines panduratin A treatment resulted in a dose-dependent (i) induction of p21WAF1/Cip1 and p27Kip1, (ii) downregulation of cdks 2, 4 and 6 and (iii) decrease in cyclins D1 and E. These findings suggest that panduratin A may be an effective chemopreventive or therapeutic agent against CaP.

Adenocarcinoma↗

PubMed2005

Induction of apoptosis by Panduratin A isolated from Kaempferia pandurata in human colon cancer HT-29 cells.

We previously showed that panduratin A isolated from an extract of Kaempferia pandurata (Zingiberaceae) was a strong inhibitor of cyclooxygenase-2 (COX-2) in RAW264.7 cells, suggesting a potential use of panduratin A as an anti-inflammatory agent. In the present study, we have investigated the effects of panduratin A on cytoplasmic levels of COX-2, as well as proliferation and apoptosis in human colon cancer cells HT-29. Cell proliferation and induction of apoptosis was determined by the MTT assay, DNA fragmentation measurement, flow cytometric analysis, nuclear staining and Western blotting. The MTT assay indicated that panduratin A exhibited cytotoxicity with an IC50 value of 28 microM. The cytotoxic effects of panduratin A were found to be accompanied by the dose-dependent induction of apoptosis as assessed by DNA fragmentation and apoptotic bodies. In addition, treatment with an apoptosis-inducing concentration of panduratin A resulted in cleavage of poly(ADP-ribose) polymerase (PARP) with a concomitant decrease in procaspase-3 protein. Our study provides evidence for cell growth inhibition and induction of apoptosis by panduratin A in human colon cancer cells, suggesting its potential use as a cancer chemopreventive and therapeutic agent.

Antineoplastic Agents, Phytogenic↗

PubMed2003

In vitro anti-inflammatory activity of panduratin A isolated from Kaempferia pandurata in RAW264.7 cells.

An active compound identified as panduratin A was isolated from a methanol extract of Kaempferia pandurata (Zingiberaceae). We examined the effect of panduratin A on nitric oxide (NO) and prostaglandin E (2) (PGE (2)) production induced by lipopolysaccharide (LPS) in RAW264.7 cells. Modulations of iNOS and COX-2 enzyme expression were evaluated by Western blotting. Panduratin A strongly inhibited both NO (IC (50): 0.175 microM) and PGE (2) (IC (50): 0.0195 microM) production and suppressed both iNOS and COX-2 enzyme expression without any appreciable cytotoxic effect on RAW264.7 cells in a dose-dependent manner. Panduratin A also suppressed the phosphorylation of inhibitor kappaBalpha (IkappaBalpha) and degradation of IkappaBalpha associated with nuclear factor kappaB (NF-kappaB) activation. Furthermore, panduratin A inhibited LPS-induced NF-kappaB transcriptional activity in a dose-dependent manner. These results suggest that panduratin A could exert its inhibitory effects on the production of NO and PGE (2) through the suppression of NF-kappaB activation, indicating its potential for use as an anti-inflammatory agent.

Animals↗

PubMed2005

Protective effects of panduratin A against oxidative damage of tert-butylhydroperoxide in human HepG2 cells.

The protective effect of panduratin A, isolated from Kaempferia pandurata ROXB. (Zingiberaceae), against tert-butylhydroperoxide (t-BHP)-induced cytotoxicity was investigated in a human hepatoma cell line, HepG2. The tetrazolium dye colorimetric test (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay) was used to monitor cytotoxicity. Lipid peroxidation [malondialdehyde (MDA) formation] and intracellular glutathione level were estimated by fluorometric methods. Intracellular reactive oxygen species (ROS) formation was measured using a fluorescent probe 2',7'-dichlorofluorescein diacetate (DCFH-DA). Panduratin A significantly reduced the cell growth inhibition caused by t-BHP. Furthermore, panduratin A ameliorated lipid peroxidation as demonstrated by a reduction in MDA formation, and attenuated glutathione (GSH) depletion in a dose-dependent manner. It was also found that panduratin A reduced intracellular ROS formation caused by t-BHP. These results strongly suggest that panduratin A has significant protective ability against oxidative damage caused by reactive intermediates.

Antioxidants↗

PubMed2025

Panduratin A Induces Autophagy Through AMPK Activation Independent of mTOR Inhibition and Restricts Mycobacterium tuberculosis in Host Macrophages.

Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains a major global health burden, especially with the increasing prevalence of drug-resistant strains. There is an urgent need for new therapeutics that act via alternative mechanisms. Autophagy, a vital cell-autonomous defense process, allows macrophages to degrade intracellular pathogens such as Mtb and has gained attention as a potential target for host-directed therapy. In this study, we conducted a high-content imaging screen of herb-derived compounds to identify autophagy inducers in RAW264.7 macrophages. Panduratin A (NPA), a natural compound from Boesenbergia rotunda, was found to potently induce autophagy. NPA promoted autophagic vacuole formation in a dose-dependent fashion at low micromolar levels. Its autophagy-inducing effect was validated using RFP-GFP-LC3 dual fluorescence assays and immunoblotting in the presence of bafilomycin A1. Further mechanistic analysis revealed that NPA activates autophagy through AMPK activation, independent of mTOR inhibition. Importantly, NPA significantly promoted intracellular Mtb clearance and increased colocalization of Mtb with autophagosomes and lysosomes, in a manner dependent on Beclin-1. These findings highlight NPA as a potent enhancer of macrophage antimicrobial responses via autophagy, supporting its potential as a candidate for host-directed adjunctive therapy against TB.

Autophagy↗

PubMed2005

Anti-HIV-1 protease activity of compounds from Boesenbergia pandurata.

Searching for anti-HIV-1 protease (PR) inhibitors of Thai medicinal plants led to the isolation of a new cyclohexenyl chalcone named panduratin C (1) and chalcone derivatives (2-6) from the methanol extract of Boesenbergia pandurata rhizomes. The known compounds were identified to be panduratin A (2), hydroxypanduratin A (3), helichrysetin (4), 2',4',6'-trihydroxyhydrochalcone (5), and uvangoletin (6). The structures of all compounds were elucidated on the basis of chemical and spectroscopic methods. It was found that 3 possessed the most potent anti-HIV-1 PR activity with an IC50 value of 5.6 microM, followed by 2 (IC50 = 18.7 microM), whereas other compounds exhibited only mild activity. Structure-activity relationships of these compounds on anti-HIV-1 PR activity are summarized as follows: (1) hydroxyl moiety at position 4 conferred higher activity than methoxyl group; (2) prenylation of dihydrochalcone was essential for activity; (3) hydroxylation at position 4''' reduced activity; and (4) introduction of double bond at C1' and C6' of chalcone gave higher activity. As regards active constituents contained in B. pandurata rhizomes, hydroxypanduratin A (3) and panduratin A (2) are active principles against HIV-1 PR.

Chalcones↗

PubMed2002

Anti-inflammatory cyclohexenyl chalcone derivatives in Boesenbergia pandurata.

The cyclohexenyl chalcone derivative [(-)-hydroxypanduratin A], together with the previously known panduratin A, sakuranetin, pinostrobin, pinocembrin, and dihydro-5,6-dehydrokawain were isolated from the chloroform extract of the red rhizome variety of Boesenbergia pandurata (Robx.) Schltr. [currently known as Boesenbergia rotunda (L.) Mansf., Kulturpfl.]. Their structures were assigned on the basis of their spectroscopic data. (-)-Hydroxypanduratin A and (-)-panduratin A showed significant topical anti-inflammatory activity in the assay of TPA-induced ear edema in rats.

Animals↗

PubMed2006

Analysis of antioxidant activities contained in the Boesenbergia pandurata Schult. Rhizome.

The rhizome of Boesenbergia pandurata Schult. was found to possess potent antioxidant activity in a rat brain homogenate model. Bioassay-guided isolation of the active compounds from a CH2Cl2-MeOH (1:1) extract led to the isolation of 5-hydroxy-7-methoxyflavanone, panduratin A, 5,7-dihydroxyflavanone, 2',6'-dihydroxy-4'-methoxychalcone, 2',4'-dihydroxy-6'-methoxychalcone, and 4-hydroxypanduratin A. Panduratin A, 4-hydroxypanduratin A, and 2',6'-dihydroxy-4'-methoxychalcone were also found to exert neuroprotective effects.

Animals↗

PubMed2006

Inhibitory activity of cyclohexenyl chalcone derivatives and flavonoids of fingerroot, Boesenbergia rotunda (L.), towards dengue-2 virus NS3 protease.

Boesenbergia rotunda (L.) cyclohexenyl chalcone derivatives, 4-hydroxypanduratin A and panduratin A, showed good competitive inhibitory activities towards dengue 2 virus NS3 protease with the Ki values of 21 and 25 microM, respectively, whilst those of pinostrobin and cardamonin were observed to be non-competitive. NMR and GCMS spectroscopic data formed the basis of assignment of structures of the six compounds isolated.

Chalcone↗

PubMed2001

Structural analysis of a novel antimutagenic compound, 4-Hydroxypanduratin A, and the antimutagenic activity of flavonoids in a Thai spice, fingerroot (Boesenbergia pandurata Schult.) against mutagenic heterocyclic amines.

Six compounds were isolated from fresh rhizomes of fingerroot (Boesenbergia pandurata Schult.) as strong antimutagens toward 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) in Salmonella typhimurium TA98. These compounds were 2',4',6'-trihydroxychalcone (pinocembrin chalcone; 1), 2',4'-dihydroxy-6'-methoxychalcone (cardamonin; 2), 5,7-dihydroxyflavanone (pinocembrin; 3), 5-hydroxy-7-methoxyflavanone (pinostrobin; 4), (2,4,6-trihydroxyphenyl)-[3'-methyl-2'-(3' '-methylbut-2' '-enyl)-6'-phenylcyclohex-3'-enyl]methanone (5), and (2,6-dihydroxy-4-methoxyphenyl)-[3'-methyl-2'-(3' '-methylbut-2' '-enyl)-6'-phenylcyclohex-3'-enyl]methanone (panduratin A; 6). Compound 5 was a novel compound (tentatively termed 4-hydroxypanduratin A), and 1 was not previously reported in this plant, whereas 2-4 and 6 were known compounds. The antimutagenic IC(50) values of compounds 1-6 were 5.2 +/- 0.4, 5.9 +/- 0.7, 6.9 +/- 0.8, 5.3 +/- 1.0, 12.7 +/- 0.7, and 12.1 +/- 0.8 microM in the preincubation mixture, respectively. They also similarly inhibited the mutagenicity of 3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). All of them strongly inhibited the N-hydroxylation of Trp-P-2. Thus, the antimutagenic effect of compounds 1-6 was mainly due to the inhibition of the first step of enzymatic activation of heterocyclic amines.

Amines↗

PubMed2002

Activity-guided isolation of constituents of Renealmia nicolaioides with the potential to induce the phase II enzyme quinone reductase.

Three new prenylated dihydrochalcones, (+/-)-nicolaioidesins A, B, and C (1-3), as well as a new natural product, 5-styrylfuran-2-carboxylic acid methyl ester (4), along with four known compounds, 2'-hydroxy-4',6'-dimethoxychalcone (5), (+/-)-5-hydroxy-7-methoxyflavanone (6), (+/-)-5-hydroxy-7,4'-dimethoxyflavanone, and panduratin A, were isolated from the roots of Renealmia nicolaioides, using a bioassay to determine the induction of quinone reductase (QR) activity with cultured Hepa lclc7 mouse hepatoma cells. Among these isolates, 5 and 6 induced QR activity, with observed concentrations to double activity (CD) values of 1.7 and 0.9 microg/mL, respectively, while the other constituents were not regarded as being active (CD >10 microg/mL). The chemical structures of 1-4 were elucidated by spectroscopic methods. A biogenetic pathway for the formation of (+/-)-nicolaioidins A-C (1-3) is proposed.

Animals↗