Download the Free Unbound MEDLINE PubMed App to your smartphone or tablet.
Available for iPhone, iPad, iPod touch, and Android.
J Asian Nat Prod Res [journal]
- New cytotoxic sesquiterpene lactones from Anthemis scrobicularis. [JOURNAL ARTICLE]
- J Asian Nat Prod Res 2014 Sep 17.:1-8.
Four new sesquiterpene lactones, 4α-hydroxy-guaia-10(14),11(13)-diene-12,6α-olide (1), 4α-hydroxy-9α-acetoxy-guaia-1(10),2-diene-12,6α-olide (4), 4α-hydroxy-9β-acetoxy-guaia-1(10),2-diene-12,6α-olide (5), and 1α,4α-dihydroxy-9α-acetoxy-guaia-10(14),2-diene-12,6α-olide (6), were isolated from the aerial parts of Anthemis scrobicularis. Their structures were elucidated on the basis of their IR, NMR, and MS spectroscopic data. In addition, two known sesquiterpene lactones micheliolide (2) and achillin (3) were also isolated. The cytotoxicity of some of the isolated compounds was tested against HCT 116, HepG-2, and MCF-7 cell lines. Micheliolide and 4α-hydroxy-guaia-10(14),11(13)-diene-12,6α-olide showed pronounced inhibitory activity while 4α-hydroxy-9α-acetoxy-guaia-1(10),2-diene-12,6α-olide showed weak activity.
- New steroidal glycosides from the rhizome of Anemarrhena asphodeloides. [JOURNAL ARTICLE]
- J Asian Nat Prod Res 2014 Sep 16.:1-9.
Two new steroidal saponins, timosaponin X (1) and timosaponin Y (2), and one new pregnane glycoside, timopregnane B (3), were isolated from the rhizomes of Anemarrhena asphodeloides, as well as three known compounds 25S-timosaponin BII (4), protodesgalactotigonin (5), and timosaponin BII-a (6) isolated from this plant for the first time. By the detailed analysis of 1D, 2D NMR, MS spectra, and chemical evidences, the structures of new compounds were elucidated as 26-O-β-d-glucopyranosyl-(25S)-5β-22-methoxy-furost-3β,26-diol 3-O-β-d-glucopyranosyl-(1 → 2)-α-l-arabinopyranoside (1), 5β-pseudo-spirost-3β,15α,23α-triol 3-O-β-d-glucopyranosyl-(1 → 2)-β-d-galactopyranoside (2), (5β,17α)-Δ(16(17))-20-one-pregn-2β,3β-diol 3-O-β-d-glucopyranosyl-(1 → 2)-β-d-galactopyranoside (3).
- l-3-n-Butylphthalide attenuates β-amyloid-induced toxicity in neuroblastoma SH-SY5Y cells through regulating mitochondrion-mediated apoptosis and MAPK signaling. [Journal Article]
- J Asian Nat Prod Res 2014 Aug; 16(8):854-64.
Alzheimer's disease (AD) is a progressive neurodegenerative disease. Amyloid-β protein (Aβ), the hallmark of AD, invokes a cascade of mitochondrial dysfunction and eventually leads to neuronal death. l-3-n-Butylphthalide (l-NBP) has shown the potent neuroprotective effects in stroke and AD animal models. The present study is to evaluate the neuroprotective effect of l-NBP on Aβ25-35-induced neuronal injury and the possible mechanism in the human neuroblastoma SH-SY5Y cells. Our results showed that l-NBP significantly attenuated Aβ25-35-induced cell death and reduced neuronal apoptosis. l-NBP significantly inhibited Aβ25-35-induced mitochondrial dysfunction, including mitochondrial membrane potential reduction, and reactive oxygen species production. Furthermore, l-NBP could partially reverse the elevations of Aβ25-35-induced active caspase-3, caspase-9, and cytochrome c expressions, and the downregulation of anti-apoptosis protein Bcl-2. Moreover, l-NBP markedly inhibited the activations of p38 mitogen-activated protein kinase and c-Jun N-terminal kinase/stress-activated protein kinase signaling pathway. These results demonstrated that l-NBP was capable of protecting neuronal cells from Aβ25-35-induced toxicity through a mitochondrial-dependent apoptotic pathway. Thus, l-NBP shows promising candidate of multi-target neuronal protective agent for the treatment of AD.
- Three new compounds from the stem bark of Juglans mandshurica. [Journal Article]
- J Asian Nat Prod Res 2014 Aug; 16(8):819-24.
Three new compounds, 3,6-dihydroxy-4,5-dimethoxy-1,8-naphalic anhydride (1), 3,4,5,6-tetrahydroxy-1,8-naphalic anhydride (2), and methyl (7E,9E)-6,11-dioxononadeca-7,9-dienoate (3), were isolated from the stem bark of Juglans mandshurica. Their structures were elucidated on the basis of spectroscopic evidence, including 1D and 2D NMR, HR-TOF-MS, and by comparison with the literature data.
- Effect of ligustrazine on levels of amino acid neurotransmitters in rat striatum after cerebral ischemia-reperfusion injury. [JOURNAL ARTICLE]
- J Asian Nat Prod Res 2014 Aug 27.:1-8.
This study aimed to evaluate the effect of ligustrazine on levels of amino acid transmitters in the extracellular fluid of striatum following cerebral ischemia/reperfusion (I/R) in male Sprague-Dawley rats. A microdialysis cannula guide was implanted into the right striatum. After recovery, animals underwent a sham operation or middle cerebral artery occlusion (MCAO). Those that developed cerebral ischemia after MCAO were randomized to receive propylene glycol salt water and ligustrazine respectively. Striatal fluid samples were collected from all animals at 15-min intervals after treatment and were subjected to HPLC analysis of aspartic acid, glutamic acid, taurine, and γ-amino butyric acid. Upon the last sample collection, animals were sacrificed and brain tissue specimens were collected for triphenyltetrazolium chloride staining and NeuN staining. Compared with the sham operation, MCAO induced significant neurological deficits and increased striatal concentrations of the four neurotransmitters assessed in a time-dependent manner (P < 0.01). Ligustrazine effectively attenuated the detrimental effects of MCAO on the brain. These observations suggest that ligustrazine as a novel cerebral infarction-protective agent may have potential clinical implications for I/R-related brain damage.
- Aromatic acid derivatives from the lateral roots of Aconitum carmichaelii. [JOURNAL ARTICLE]
- J Asian Nat Prod Res 2014 Aug 27.:1-10.
Seven new aromatic acid derivatives (1-7), together with five known analogs, were isolated from the lateral roots of Aconitum carmichaelii. Structures of the new compounds were determined by spectroscopic and chemical methods as 4-methyl ( - )-(R)-hydroxyeucomate (1), 4-butyl ( - )-(R)-hydroxyeucomate (2), 4-butyl-1-methyl (+)-(R)-2-O-(4'-hydroxy-3'-methoxybenzoyl)malate (3), 1-butyl-4-methyl (+)-(R)-2-O-(4'-hydroxy-3'-methoxybenzoyl)malate (4), dimethyl (+)-(R)-2-O-(4'-hydroxy-3'-methoxybenzoyl)malate (5), dimethyl (+)-(R)-2-O-(4'-hydroxybenzoyl)malate (6), and methyl ( ± )-3-(4'-hydroxy-3'-methoxyphenyl)-3-sulfopropionate (7), respectively. Compounds 1 and 2 are 2-benzylmalates (eucomate derivatives), 3-6 belong to 2-O-benzoylmalates, and 7 is a rare phenylpropionate containing a sulfonic acid group. The absolute configurations of eucomate derivatives were confirmed by X-ray crystallographic analysis of 4-methyl eucomate (11).
- Sodium tanshinone IIA sulfonate attenuates radiation-induced fibrosis damage in cardiac fibroblasts. [JOURNAL ARTICLE]
- J Asian Nat Prod Res 2014 Aug 19.:1-12.
The main pathological change in radiation-induced heart disease is fibrosis. Emerging evidence has indicated that sodium tanshinone IIA sulfonate (STS) was used for treating ﬁbrosis diseases. The present study was undertaken to characterize the effect of STS on radiation-induced cardiac fibrosis (RICF) on cultured cardiac fibroblasts (CFs). CFs were irradiated with 1 or 2 Gy X-rays, and the expression of TGF-β1 and collagen I (Col-1) increased, indicating that low-dose X-rays promoted fibrosis damage effect. The fibrosis damage was accompanied by morphologic changes in the endoplasmic reticulum (ER), as well as an increase in the expression of the ER stress-related molecules, GRP78 and CHOP. Administration of STS reduced ROS production and decreased the expression of Col-1, TGF-β1, p-Smad2/3, GRP78, and CHOP in irradiated CFs, thus weakening the radiation-induced fibrosis damage and ER stress. Radiation-induced fibrosis damage was observed on a cellular level. The involvement of ER stress in radiation-induced fibrosis damage was demonstrated for the first time. STS attenuated the fibrosis damage effect in CFs and this effect may be related to its antioxidant action, and also related to its inhibition of ER stress and TGF-β1-Smad pathway. These results suggest that STS shows a good prospect in clinical prevention and treatment of RICF.
- Evodiamine activates AMPK and promotes adiponectin multimerization in 3T3-L1 adipocytes. [JOURNAL ARTICLE]
- J Asian Nat Prod Res 2014 Aug 1.:1-10.
Adiponectin, an adipokine with insulin-sensitizing effect, is secreted from adipocytes into circulation as high, medium, and low molecular weight (HMW, MMW, and LMW) forms. The HMW adiponectin is more metabolically active and the ratio of HMW adiponectin to total adiponectin directly correlates with insulin sensitivity. Evodiamine is an indole alkaloid found in the traditional Chinese medicinal plant Evodia rutaecarpa. In this study, evodiamine was found to activate AMP-activated protein kinase (AMPK) in both 3T3-L1 adipocytes and 293T cells. Activation of AMPK by evodiamine promoted the assembly of HMW adiponectin and increased the HMW/total ratio of adiponectin in 3T3-L1 adipocytes. The Ca(2+)-dependent PI3K/Akt/CaMKII-signaling pathway was demonstrated to be involved in evodiamine-induced AMPK activation. This study revealed a novel role of this Ca(2+)-mediated signaling pathway in promoting the multimerization of adiponectin.
- Studies on chemical constituents of Ophiopogon japonicus. [JOURNAL ARTICLE]
- J Asian Nat Prod Res 2014 Aug 1.:1-9.
Two new and six known steroidal glucosides were isolated from the tuber of Ophiopogon japonicus. The new steroidal glucosides were established as (20R,25R)-26-O-β-d-glucopyranosyl-3β,26-dihydroxycholest-5-en-16,22-dioxo-3-O-α-l-rhamnopyranosyl-(1 → 2)-β-d-glucopyranoside (1) and 26-O-β-d-glucopyranosyl-(25R)-furost-5-en-3β,14α,17α,22α,26-pentaol-3-O-α-l-rhamnopyranosyl-(1 → 2)-β-d-glucopyranoside (3) on the basis of spectroscopic data as well as chemical evidence.
- Polygalasaponin F inhibits secretion of inflammatory cytokines via NF-κB pathway regulation. [Journal Article]
- J Asian Nat Prod Res 2014 Aug; 16(8):865-75.
To study the anti-neuroinflammatory mechanisms of polygalasaponin F (PS-F), ELISA method was used to detect the secretion of inflammatory cytokines. Western blot was used to detect the protein expression and phosphorylation levels. Immunofluorescence assay was used to observe the NF-κB nuclear translocation. PS-F could inhibit the release of inflammatory cytokines TNF-α and NO induced by lipopolysaccharides (LPS) and reduce the expression of inducible nitric oxide synthases (iNOS). As for MAPK-signaling pathway, PS-F could only inhibit the phosphorylation levels of p38 MAPK, but did not significantly affect the phosphorylation levels of JNK and ERK1/2 protein kinases. PS-F could inhibit NF-κB nuclear translocation in a dose-dependent manner. The results of Western blot assay were consistent with immunofluorescence assays. Meanwhile, p38-specific inhibitor SB203580 (20 μM) and p65-specific inhibitor PDTC (100 μM) were, respectively, administered as a positive control. In addition, PS-F could significantly inhibit the cytotoxicity of conditioned medium prepared by LPS-stimulated BV-2 microglia (LPS conditioned media) to neuronal PC12 cells and improve cell viability. PS-F inhibits the secretions of neuroinflammatory cytokines by the regulation of NF-κB-signaling pathway.