Biomedical subjects

Yun-Lian Lin

Publications and source records attributed to Yun-Lian Lin.

At least 19 recordsLinked to original sources

PubMed2007

Antifibrotic effects of tetrandrine on hepatic stellate cells and rats with liver fibrosis.

BACKGROUND: Anti-inflammation strategies are one of the proposed therapeutic approaches to hepatic fibrosis. Tetrandrine (C(38)H(42)O(8)N(2), molecular weight: 622; Tet), an alkaloid isolated from the Chinese medicinal herb Stephania tetrandra, has been shown to exert anti-inflammatory activity in pulmonary diseases. The purpose of the present study was to investigate the in vitro and in vivo effects of Tet on hepatic fibrosis. METHODS: A cell line of rat hepatic stellate cells (HSC-T6) was stimulated with transforming growth factor-beta1 (TGF-beta1) or tumor necrosis factor-alpha (TNF-alpha). The inhibitory effects of Tet on the nuclear factor kappaB (NFkappaB) signaling cascade and molecular markers including intercellular adhesion molecule-1 (ICAM-1) and alpha-smooth muscle actin (alpha-SMA) secretion were assessed. Fibrosis was induced by dimethylnitrosamine (DMN) administration in rats for 4 weeks. Fibrotic rats were randomly assigned to one of the four groups: vehicle (0.7% carboxyl methyl cellulose, CMC), Tet (1 mg/kg), Tet (5 mg/kg), or silymarin (50 mg/kg), each given by gavage twice daily for 3 weeks starting after 1 week of DMN administration. At the end of the study, liver tissues were scored for fibrosis and analyzed for molecular markers of fibrosis. RESULTS: Tetrandrine (0.5-5.0 micromol/L) concentration-dependently inhibited NFkappaB transcriptional activity induced by TNF-alpha, including IkappaBalpha phosphorylation and mRNA expressions of ICAM-1 in HSC-T6 cells. In addition, Tet also inhibited TGF-beta1-induced alpha-SMA secretion and collagen deposition in HSC-T6 cells. Fibrosis scores of livers from DMN-treated rats with high-dose Tet (1.3 +/- 0.3) were significantly reduced in comparison with DMN-treated rats receiving saline (2.0 +/- 0.2). Hepatic collagen content of DMN rats was significantly reduced by either Tet or silymarin treatment. Double-staining results showed that alpha-SMA- and NFkappaB-positive cells were decreased in the fibrotic livers by Tet and silymarin treatment. In addition, mRNA expression of ICAM-1, alpha-SMA, and TGF-beta1 was attenuated by Tet treatment. Moreover, levels of plasma aspartate aminotransferase and alanine aminotransferase activities were reduced by Tet and silymarin treatment. CONCLUSION: Tetrandrine exerts antifibrotic effects in both HSC-T6 cells and in rats with DMN-induced fibrosis.

Actins↗

PubMed2006

Antitumor agents. 254. Synthesis and biological evaluation of novel neo-tanshinlactone analogues as potent anti-breast cancer agents.

In our previous study, neo-tanshinlactone (1) showed potent and selective anti-breast cancer activity. To explore the SAR of 1, nine analogues (15-18, 24-28) were designed and synthesized. Together with 1 and tamoxifen (TAM), all newly synthesized compounds and some intermediates were evaluated for in vitro anticancer activity against several human tumor cell lines. Compounds without a ring D did not show promising activity, while compounds with a methylated furan ring D showed better activity than those with unsubstituted furan or hydroxy-dihydrofuran rings. Among all newly synthesized compounds, compound 15 with an ethyl group at the 4-position showed the best activity and selectivity with ED50 values of 0.45 and 0.18 microg/mL against MCF-7 and ZR-75-1 (ER+) and 13.5 and 10.0 microg/mL against MDA MB-231 and HS 587-1 (ER-), respectively. Furthermore, 15 also showed potent activity against SK-BR-3 (ER-, HER2+) with an ED50 value of 0.10 microg/mL. Our preliminary SAR studies showed that a methylated furan ring D and the C-4 substituent in ring A are critical for anti-breast cancer activity. Further development of 1 and 15 as anti-breast cancer drug candidates is warranted.

Antineoplastic Agents↗

PubMed2006

Ligusticum chuanxiong prevents rat pheochromocytoma cells from serum deprivation-induced apoptosis through a protein kinase A-dependent pathway.

Ligusticum chuanxiong (LC) is a traditional Chinese herbal medicine used to treat various cardiovascular diseases. In this study, the butanol extract of LC was found to protect neuronal-like pheochromocytoma cells from serum deprivation-induced apoptosis. Both a serine/threonine kinase inhibitor and a specific protein kinase A (PKA) inhibitor blocked the protective effect of LC. A transcription inhibitor (actinomycin D) and a protein synthesis inhibitor (cyclohexamide) also attenuated the protective effect of LC, suggesting the requirement of gene expression for the protection of LC. On the other hand, LC increased both the formation of cyclic-AMP and the phosphorylation of the cyclic-AMP response element-binding protein (CREB), a downstream target of PKA and a nuclear transcription factor known for neuroprotective mechanism. Furthermore, LC-induced CREB phosphorylation and protective effect could be blocked by a PKA inhibitor and overexpression of the dominant negative CREB, respectively. Taken together, the protective mechanism of LC in antagonizing serum deprivation-induced PC12 cell apoptosis might be mediated through a PKA/CREB-dependent pathway.

Animals↗

PubMed2006

Inhibition of (S)-armepavine from Nelumbo nucifera on autoimmune disease of MRL/MpJ-lpr/lpr mice.

T cell immune responses play important roles in the pathogenesis of systemic lupus erythematosus (SLE). (S)-Armepavine (C19H23O3N; MW313) from Nelumbo nucifera suppresses T cells proliferation. To study its potential benefit on SLE, we examined effects of (S)-armepavine on MRL/MpJ-lpr/lpr mice, which have similar disease features to human SLE. MRL/MpJ-lpr/lpr mice were treated orally with (S)-armepavine for 6 weeks and their SLE characteristics were evaluated. The results revealed that (S)-armepavine prevented lymphadenopathy and elongated life span of MRL/MpJ-lpr/lpr mice. It seemed to be mediated by inhibition of splenocytes proliferation, suppression of interleukin-2 (IL-2), interleukin-4, interleukin-10, and interferon-gamma (IFN-gamma) gene expressions, reduction of glomerular hypercellularity and immune complexes deposition, and decrease of urinary protein and anti-double stranded DNA autoantibody production. Furthermore, the data demonstrated (S)-armepavine impaired IL-2 and IFN-gamma transcripts in human peripheral blood mononuclear cells. We suggest that (S)-armepavine may be an immunomodulator for the management of autoimmune diseases like SLE.

Alkaloids↗

PubMed2006

Antidepressant principles of the roots of Polygala tenuifolia.

[(125)I]RTI-55-membrane binding assay-guided fractionation and separation of a water-soluble extract of the roots of Polygala tenuifolia gave five new oligosaccharide derivatives, polygalatenosides A-E (1-5). The structures of these new oligosaccharides were established on the basis of spectroscopic evidence. Polygalatenosides A and B (1 and 2) showed significant inhibitory activity, with IC(50) values of 30.0 and 6.04 microM, respectively, in this membrane binding assay and acted as norepinephrine reuptake inhibitors through blocking norepinephrine transport.

Antidepressive Agents↗

PubMed2006

Inhibitory effects of Ligusticum chuanxiong on the proliferation of rat hepatic stellate cells.

BACKGROUND AND AIMS: Platelet-derived growth factor (PDGF) is a very potent mitogen for hepatic stellate cells (HSC) in hepatic fibrogenesis. Ligusticum chuanxiong Hort. (LC), a traditional Chinese herb used for cerebrovascular diseases, has been shown to exert anti-inflammatory and free radical scavenging effects. The aims of the present study were to investigate the effects of LC extract on the proliferation-related biomarkers in a rat HSC cell line (HSC-T6) stimulated with PDGF. METHODS: DNA synthesis via bromodeoxyuridine (BrdU) incorporation, cell cycle related proteins and apoptosis markers were determined to evaluate the inhibitory effects of LC. RESULTS: The results revealed that LC extract (25-100 microg/mL) concentration-dependently decreased the PDGF-induced cell proliferation as well as alpha-smooth muscle actin expression in HSC. The inhibitory activity of LC on HSC was associated with: (i) inhibition of BrdU incorporation; (ii) induction of apoptosis with the activation of caspase-3, up-regulation of cell cycle inhibitory proteins p21 and p27, and down-regulation of cell cycle stimulatory proteins cyclins D1 and D2; and (iii) increased phosphorylation of mitogen-activated protein kinases (JNK). LC at the studied concentrations showed no direct cytotoxicity on primary hepatocytes. CONCLUSION: The results suggest that LC significantly inhibited PDGF-activated HSC proliferation, possibly through apoptotic mechanisms and the potential of LC as an antifibrotic agent warrants further investigation.

Animals↗

PubMed2006

Induction of cytochrome P450-dependent monooxygenase by extracts of the medicinal herb Salvia miltiorrhiza.

The herbal medicine Salvia miltiorrhiza (Danshen) is currently used for the treatment of cardiovascular and cerebrovascular diseases. To assess possible herb-drug interactions, the effects of the aqueous and ethyl acetate extracts of S. miltiorrhiza on cytochrome P450 (CYP) were studied. Oral treatment of C57BL/6J mice with the ethyl acetate extract caused a dose-dependent increase in liver microsomal 7-methoxyresorufin O-demethylation (MROD) activity. The ethyl acetate extract caused an 8-, 2-, 3- and 3-fold increase in hepatic MROD, tolbutamide hydroxylation, nifedipine oxidation and warfarin 7-hydroxylation activity, respectively. However, the aqueous extract had no effects on any of the activities determined. Pharmaceutical product of S. miltiorrhiza extract caused a dose-dependent increase in MROD activity without affecting other activity. Immunoblot analysis of microsomal proteins showed that ethyl acetate extract-treatment elevated the protein levels of CYP1A and CYP3A. Tanshinone IIA was the main diterpene quinone in S. miltiorrhiza. At the dose corresponding to its content in ethyl acetate extract, tanshinone IIA-treatment increased mouse liver microsomal MROD activity. These results demonstrated that there were mouse CYP1A, CYP2C and CYP3A-inducing agents present in the ethyl acetate extract, but not in the aqueous extract, of S. miltiorrhiza. Tanshinone IIA played a role in the induction of CYP1A by S. miltiorrhiza. The CYP induction by the ethyl acetate extract and pharmaceutical product suggested that possible drug interactions between S. miltiorrhiza and CYP substrates should be noticed.

Animals↗

PubMed2006

Antiproliferative effect of salvianolic acid A on rat hepatic stellate cells.

Suppression of activation or proliferation, or induction of apoptosis in hepatic stellate cells (HSCs) have been proposed as therapeutic strategies against liver fibrosis. Salvia miltiorrhiza has been reported to exert antifibrotic effects in rats with hepatic fibrosis, but its mechanisms of action remain to be clarified. We have investigated the effects of salvianolic acid A (Sal A), an active principle from S. miltiorrhiza, on the proliferation-related biomarkers in a cell line of rat HSCs (HSC-T6) stimulated with platelet-derived growth factor-BB homodimer (PDGF-BB). DNA synthesis (bromodeoxyuridine (BrdU) incorporation), cell cycle related proteins and apoptosis markers were determined to evaluate the inhibitory effects of Sal A. The results showed that Sal A (1-10 microM) concentration-dependently attenuated PDGF-BB-stimulated proliferation (BrdU incorporation) in HSC-T6 cells. Sal A at 10 microM induced cell apoptosis in PDGF-BB-incubated HSCs, together with a reduction of Bcl-2 protein expression, induction of cell cycle inhibitory proteins p21 and p27, and down-regulation of cyclins D1 and E, suppression of Akt phosphorylation, reduction in PDGF receptor phosphorylation, and an increase in caspase-3 activity. Sal A exerted no direct cytotoxicity on primary hepatocytes and HSC-T6 cells under experimental concentrations. Our results suggested that Sal A inhibited PDGF-BB-activated HSC proliferation, partially through apoptosis induction.

Animals↗

PubMed2005

Ester derivatives of tournefolic acid B attenuate N-methyl-D-aspartate-mediated excitotoxicity in rat cortical neurons.

The effects of tournefolic acid B (TAB) and two ester derivatives, TAB methyl ester (TABM) and TAB ethyl ester (TABE), on N-methyl-D-aspartate (NMDA)-mediated excitotoxicity and the underlying mechanisms were investigated. Treatment with 50 microM NMDA elicited neuronal death by 48.7 +/- 5.1%, coinciding with the appearance of injured morphology. TABM (50 microM) attenuated the NMDA-induced cell death by 60.9 +/- 19.7%, and to a lesser extent by TABE. The NMDA-mediated activation of calpain was not affected by TABM and TABE, as determined by the cleavage of alpha-spectrin. NMDA increased the activity of caspases 2, 3, 6, 8, and 9 and reached the maximum after 8-h treatment. TABM and TABE abrogated NMDA-induced activation of caspases 2, 3, 6, and 8 by approximately 80 to 90% and 50 to 60%, respectively, and to a higher extent for caspase 9. TABM and TABE also blocked the NMDA-mediated activation of caspase 12. Furthermore, TABM and TABE eliminated the NMDA-induced accumulation of superoxide anion (O2-*). NMDA evoked significant depolarization of mitochondria, whereas TABM elicited a mild decrease of mitochondrial membrane potential as determined by tetramethylrhodamine methyl ester perchlorate. NMDA treatment induced elevation of Ca2+ levels in cytosol, endoplasmic reticulum (ER), and mitochondria. TABM (50 microM) significantly diminished the NMDA-induced elevation of Ca2+ levels in mitochondria and ER but not cytosol. Therefore, TABM decreased mitochondrial membrane potential and attenuated the NMDA-mediated Ca2+-loading in ER and mitochondria. These events subsequently eliminated the accumulation of O2-* and blocked the activation of caspase cascade, thereby conferring their neuroprotective effects on NMDA-mediated excitotoxicity.

Animals↗

PubMed2005

In vitro protective effects of salvianolic acid B on primary hepatocytes and hepatic stellate cells.

The production of reactive oxygen species (ROS) is believed to be involved in liver injury and hepatic fibrosis. Activation of hepatic stellate cells (HSCs) is a key feature of liver fibrosis. Salvia miltiorrhiza is a traditional Chinese herb used in the treatment of cardiovascular and liver diseases to resolve stasis. The effects of salvianolic acid B (Sal B), a major component of Salvia miltiorrhiza, on oxidative damage include free radical DPPH scavenging, malondialdehyde (MDA) formation and ROS generation in primary rat hepatocytes and HSCs, and on alpha-SMA, and collagen expression in transforming growth factor-beta1 (TGF-beta1)-stimulated HSCs were examined. Results indicated that Sal B scavenged DPPH potently with an IC50 2.2+/-0.2 microg/ml (3.06+/-0.3 microM), inhibited lipid peroxidation and eliminated ROS accumulation in a concentration-dependent manner on primary rat hepatocytes and HSCs. Sal B also reduced alpha-SMA and collagen synthesis and deposition in HSCs, and had no direct cytotoxicity on both hepatocytes and HSCs. Our results suggest that Sal B ameliorated oxidative damage and eliminated ROS accumulation in hepatocytes, and attenuated HSC activation, potentially conferring hepatoprotective and anti-fibrogenic effects.

Actins↗

PubMed2005

Herpes simplex virus type 1 propagation in HeLa cells interrupted by Nelumbo nucifera.

Inhibitory effects of ethanolic extracts from 10 Chinese herbs on herpes simplex virus type 1 (HSV-1) replication were investigated. By a bioassay-guided fractionation procedure, NN-B-5 was identified from seeds of N. nucifera. NN-B-5 significantly blocked HSV-1 multiplication in HeLa cells without apparent cytotoxicity. To elucidate the point in HSV-1 replication where arrest occurred, a set of key regulatory events leading to the viral multiplication was examined, including HSV-1 DNA synthesis and viral immediate early gene expressions. Data from polymerase chain reaction and Southern blotting showed that there were impairments of HSV-1 DNA replication in HeLa cells treated with NN-B-5. Results indicated that the production and mRNA transcription of infected cell protein (ICP) 0 and ICP4 were decreased in NN-B-5 treated HeLa cells. Results of an electrophoretic mobility shift assay demonstrated that NN-B-5 interrupted the formation of alpha-trans-induction factor/C1/Oct-1/GARAT multiprotein/DNA complexes. The mechanisms of antiviral action of NN-B-5 seem to be mediated, at least in part, through inhibition of immediate early transcripts, such as ICP0 and ICP4 mRNA and then blocking of all downstream viral products accumulation and progeny HSV-1 production.

Antiviral Agents↗

PubMed2005

Antifibrotic effects of Salvia miltiorrhiza on dimethylnitrosamine-intoxicated rats.

Excessive oxidative stress is implicated in hepatic fibrogenesis. Extracts of Salvia miltiorrhiza (Sm) have been shown to protect cells against oxidative stress. In this study we investigated the in vitro and in vivo effects of Sm on hepatic fibrosis. A cell line of rat hepatic stellate cells (HSC-T6) was stimulated with transforming growth factor-beta1 (TGF-beta1). The inhibitory effects of Sm (50-400 microg/ml) on TGF-beta1-induced alpha-smooth muscle actin (alpha-SMA) secretion and the mRNA expressions of fibrosis-related genes, including alpha-SMA, connective tissue growth factor (CTGF), and tissue inhibitor of metalloproteinase-1 (TIMP-1), were assessed. Fibrosis was induced by dimethylnitrosamine (DMN) administration in rats. DMN-treated rats were randomly assigned to 1 of 4 groups: saline, Sm (20 mg/kg), Sm (100 mg/kg), or silymarin (100 mg/kg), each given by gavage twice daily for 5 weeks starting from the onset of DMN administration. Sm (200 and 400 microg/ml) significantly inhibited TGF-beta1-stimulated alpha-SMA secretion and the mRNA expressions of alpha-SMA, CTGF, and TIMP-1 in HSC-T6 cells. Fibrosis scores of livers from DMN-treated rats with either a low (1.8 +/- 0.2) or high (1.8 +/- 0.1) dose of Sm, or silymarin (1.4 +/- 0.2) were significantly reduced in comparison with DMN-treated rats receiving saline (3.1 +/- 0.1). Hepatic collagen contents were also significantly reduced by either Sm or silymarin treatment. The mRNA expression levels of alpha-SMA, TGF-beta1, and procollagen I were all attenuated in Sm- and silymarin-treated rats. Moreover, levels of plasma aspartate transaminase activities were reduced by Sm and silymarin treatment. In conclusion, our results show that Sm exerted antifibrotic effects in both HSC-T6 cells and in rats with DMN-induced fibrosis.

Actins↗

PubMed2005

Homoflavonoids from Ophioglossum petiolatum.

Six homoflavonoids, ophioglonin (1), ophioglonin 7-O-beta-D-glucopyranoside (2), ophioglonol (3), ophioglonol prenyl ether (4), ophioglonol 4'-O-beta-D-glucopyranoside (5), and isoophioglonin 7-O-beta-D-glucopyranoside (6), together with five known compounds, quercetin, luteolin, kaempferol, 3,5,7,3',4'-pentahydroxy-8-prenylflavone, and quercetin 3-O-methyl ether, were isolated from Ophioglossum petiolatum. Their structures were elucidated by analysis of spectroscopic data and chemical evidence. Compounds 1 and quercetin 3-O-methyl ether showed slight anti-HBV surface antigen activity at 25 microM.

Flavonoids↗

PubMed2005

Nitrogen-containing compounds from Salvia miltiorrhiza.

Five new N-containing compounds, neosalvianen (1), salvianen (2), salvianan (3), salviadione (4), and 5-(methoxymethyl)-1H-pyrrole-2-carbaldehyde (5), were isolated from Salvia miltiorrhiza. Their structures were mainly established by spectroscopic methods. Neosalvianen (1) and its analogues (6a, 6b) were synthesized for spectroscopic data comparison. Compounds 1, 2, 4, and 6a were evaluated for their cytotoxic activities against selected cancer cell lines. Among these components, salvianen (2) exhibited the most potent cytotoxicity with a CD50 range of 30.4-39.5 microM against HeLa (cervical epitheloid carcinoma), HepG2 (hepatocellular carcinoma), and OVCAR-3 (ovarian adenocarcinoma) cell lines in a dose-dependent manner. The cytotoxicities of the tested compounds were not specific and showed similar activities to the selected cancer cell lines.

Antineoplastic Agents, Phytogenic↗

PubMed2005

Falcarindiol impairs the expression of inducible nitric oxide synthase by abrogating the activation of IKK and JAK in rat primary astrocytes.

The effects of falcarindiol on the expression of inducible nitric oxide synthase (iNOS) induced by lipopolysaccharide/interferon-gamma (LPS/IFN-gamma) in rat primary astrocytes were investigated. The molecular mechanisms underlying falcarindiol that confers its effect on iNOS expression were also elucidated. Falcarindiol abrogated the LPS/IFN-gamma-mediated induction of iNOS by about 80%. Falcarindiol attenuated the induction of iNOS in a concentration-dependent manner. The inhibitory effect of falcarindiol on iNOS induction was attributable to decrease in the protein content and the mRNA level of iNOS. Treatment with 50 microM of falcarindiol for 30 min decreased LPS/IFN-gamma-induced nuclear factor-kappaB (NF-kappaB) activation by 32%. Treatment with 50 microM of falcarindiol for 60 min diminished the LPS/IFN-gamma-mediated activation of IkappaB kinase-alpha (IKK-alpha) and IKK-beta by 28.2 and 29.7%, respectively. Falcarindiol modulated the nuclear translocation of signal transducer and activator of transcription 1 (Stat1) in a time-dependent manner. Falcarindiol (50 microM) decreased the tyrosine phosphorylation of janus kinase 1 (JAK1) by 84.8% at 5 min. Falcarindiol also abrogated the tyrosine phoshorylation of JAK2 by 82.3% at 10 min.The present study demonstrates that falcarindiol attenuated the activation of IKK and JAK contributing to the blockade of activation of NF-kappaB and Stat1, thereby leading to the suppression of iNOS expression.

Animals↗

PubMed2005

Neuroprotective flavonoids from Flemingia macrophylla.

Using an Abeta-induced neurotoxicity blocking assay to direct fractionation, three new flavonoids, fleminginin (1), flemingichromone (2), and flemingichalcone (3), and twenty known compounds were isolated from the active fractions of the aerial parts of Flemingia macrophylla. The structures of 1 - 3 were elucidated on the basis of spectroscopic data. When tested for neuroprotective activity, compound 2, osajin ( 4), 5,7,4'-trihydroxy-6,8-diprenylisoflavone (5), 5,7,4'-trihydroxy-6,3'-diprenylisoflavone (6), and aureole (7) protected neuronal cells from Abeta-induced damage with EC50 values of 31.43 +/- 3.16, 5.01 +/- 1.28, 11.25 +/-1.51, 4.47 +/- 0.65, 12.09 +/- 2.55 microM, respectively.

Alzheimer Disease↗

PubMed2005

Tournefolic acid B methyl ester attenuates glutamate-induced toxicity by blockade of ROS accumulation and abrogating the activation of caspases and JNK in rat cortical neurons.

The effects of nine polyphenolic compounds on glutamate-mediated toxicity were investigated. The underlying mechanisms by which a polyphenolic compound confers its effect were also elucidated. Treatment of cortical neurons with 50 microm glutamate for 24 h decreased cell viability by 45.8 +/- 7.9%, and 50 microm of tournefolic acid B methyl ester attenuated glutamate-induced cell death by 46.8 +/- 17.8%. Glutamate increased the activity of caspase 35.2-fold, and to a similar extent for caspase 2, 6, 8 and 9. Tournefolic acid B methyl ester abrogated glutamate-induced activation of caspase 2, 3, 6 and 9 by about 70%, and to a lesser extent for caspase 8. Treatment with glutamate for 1 h elevated reactive oxygen species (ROS) by 208.3 +/- 21.3%. Tournefolic acid B methyl ester eliminated the glutamate-induced accumulation of ROS. Glutamate increased the phosphorylation of p54-c-jun N-terminal kinase (JNK) concomitantly with activation of the endogenous antioxidant defense system. Tournefolic acid B methyl ester at 50 microm diminished the activity of p54-JNK in control and glutamate-treated cells, coinciding with the abolishment of the glutamate-triggered antioxidant defense system. Therefore, tournefolic acid B methyl ester blocked the activation of the caspase cascade, eliminated ROS accumulation and abrogated the activation of JNK, thereby conferring a neuroprotective effect on glutamate-mediated neurotoxicity.

Animals↗

PubMed2005

Dihydrophenanthrenes from Bletilla formosana.

Three new dihydrophenanthrenes, 4-methoxy-9,10-dihydrophenanthrene-1,2,7-triol (1), 1-(4-hydroxybenzyl)-4,7-dimethoxy-9,10-dihydrophenanthrene-2-ol (2), and 1,3,6-tri(4-hydroxybenzyl)-4-methoxydihydrophenanthrene-2,7-diol (3) together with seven known phenanthrene derivatives, six known flavonoids, a bibenzyl and three phenolic compounds were isolated from the whole plant of Bletilla formosana. Their structures were elucidated by spectroscopic, mainly 2D NMR spectrometry and chemical methods.

Acetylation↗