15-Methoxypinusolidic acid
15-Methoxypinusolidic acid has anti-inflammatory effects, it
inhibits LPS-induced iNOS expression and NO production, independent on MAPK and NF-kappaB. 15-Methoxypinusolidic acid suppresses adipocyte differentiation through the inhibition of PPARgamma-dependent adipogenic gene expression.15-Methoxypinusolidic acid attenuates glutamate-induced excitotoxicity via stabilization of [Ca2+]i homeostasis and suppression of oxidative stress possibly through the actions on the NMDA receptors.15-Methoxypinusolidic acid induced apoptosis in murine microglial cells, presumably via inhibition of the cell cycle progression.
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Arch Pharm Res. 2010 Jul;33(7):1035-41.
Suppression of adipocyte differentiation by 15-methoxypinusolidic acid through inhibition of PPARĪ³ activity.[Pubmed:
20661713]
Pinusolide and its derivative, 15-Methoxypinusolidic acid (15-MPA) are diterpenoid compounds isolated from Biota orientalis, which has been used as a Korean folk medicine for treating inflammatory disorders. Pinusolide and 15-Methoxypinusolidic acid suppress nitric oxide generation by suppressing inducible nitric oxide synthase and exerted anti-inflammatory functions, whereas other functions and regulatory mechanisms are largely unknown.
METHODS AND RESULTS:
In this study, we investigated whether pinusolide and 15-Methoxypinusolidic acid modulate adipocyte differentiation from pre-adipocytes 3T3-L1 cells. We found that 15-Methoxypinusolidic acid, not pinusolide, suppressed adipocyte differentiation in a dose-dependent manner, as revealed by lipid droplet formation and expression of adipogenic genes such as adiponectin and aP2. 15-Methoxypinusolidic acid did not affect mRNA and protein levels of PPARgamma, a key adipogenic transcription factor, whereas transcriptional activity of PPARgamma was significantly attenuated by 15-Methoxypinusolidic acid. While aP2 promoter activity was increased by ectopic overexpression of PPARgamma or by rosiglitazone-induced endogenous PPARgamma activation, PPARgamma-induced aP2 promoter activity was inhibited in the presence of 15-Methoxypinusolidic acid.
CONCLUSIONS:
These results suggest that 15-Methoxypinusolidic acid suppresses adipocyte differentiation through the inhibition of PPARgamma-dependent adipogenic gene expression.
Toxicol In Vitro. 2006 Sep;20(6):936-41.
15-Methoxypinusolidic acid from Biota orientalis attenuates glutamate-induced neurotoxicity in primary cultured rat cortical cells.[Pubmed:
16564156]
METHODS AND RESULTS:
15-Methoxypinusolidic acid (15-MPA), a pinusolide derivative isolated from Biota orientalis (Cupressaceae) leaves prevented glutamate-induced excitotoxicity in primary cultured rat cortical cells in vitro.
15-Methoxypinusolidic acid had more selectivity in protecting neurons against N-methyl-D-aspartate (NMDA)-induced neurotoxicity than that induced by kainic acid (KA). The glutamate-induced increase of intracellular calcium ([Ca2+]i) in cortical cells was effectively reduced by 15-Methoxypinusolidic acid . Moreover, 15-Methoxypinusolidic acid could successfully reduce the subsequent overproduction of nitric oxide (NO) and the level of cellular peroxide, and inhibit glutathione (GSH) depletion and lipid peroxidation induced by glutamate in our cultures.
CONCLUSIONS:
Collectively, these results suggested that 15-Methoxypinusolidic acid attenuated glutamate-induced excitotoxicity via stabilization of [Ca2+]i homeostasis and suppression of oxidative stress possibly through the actions on the NMDA receptors.
Int Immunopharmacol. 2008 Apr;8(4):548-55.
A pinusolide derivative, 15-methoxypinusolidic acid from Biota orientalis inhibits inducible nitric oxide synthase in microglial cells: implication for a potential anti-inflammatory effect.[Pubmed:
18328446]
The inhibitory effect of 15-Methoxypinusolidic acid (15-MPA) isolated from Biota orientalis (Cupressaceae) on lipopolysaccharide (LPS)-induced inflammation in microglial BV2 cells was investigated.
METHODS AND RESULTS:
15-Methoxypinusolidic acid significantly reduced the expression of inducible nitric oxide synthase (iNOS), the activity of iNOS, and the production of nitric oxide (NO) in LPS-stimulated BV2 cells. In addition, 15-Methoxypinusolidic acid significantly suppressed the expressions of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and cyclooxygenase (COX)-2. However, 15-Methoxypinusolidic acid did not affect LPS-induced degradation of inhibitor kappaB-alpha (IkappaB-alpha) and translocation of nuclear factor-kappaB (NF-kappaB) into the nucleus. LPS-activated p38 MAPK, extracellular signal-regulated kinase (ERK)-1/2, and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) were not affected by 15-Methoxypinusolidic acid.
CONCLUSIONS:
Taken together, this study demonstrates that 15-Methoxypinusolidic acid inhibits LPS-induced iNOS expression and NO production, independent on MAPK and NF-kappaB, suggesting a potential anti-inflammatory effect of the compound on microglial cells.
Br J Pharmacol. 2009 Jul;157(6):1053-64.
Oligonucleotide microarray analysis of apoptosis induced by 15-methoxypinusolidic acid in microglial BV2 cells.[Pubmed:
19466985]
We conducted a genome wide gene expression analysis to explore the biological aspects of 15-Methoxypinusolidic acid (15-MPA) isolated from Biota orientalis and tried to confirm the suitability of 15-MPA as a therapeutic candidate for CNS injuries focusing on microglia.
METHODS AND RESULTS:
Murine microglial BV2 cells were treated with 15-Methoxypinusolidic acid, and their transcriptome was analysed by using oligonucleotide microarrays. Genes differentially expressed upon 15-Methoxypinusolidic acid treatment were selected for RT-PCR (reverse transcription-polymerase chain reaction) analysis to confirm the gene expression. Inhibition of cell proliferation and induction of apoptosis by 15-Methoxypinusolidic acid were examined by bromodeoxyuridine assay, Western blot analysis of poly-ADP-ribose polymerase and flow cytometry. A total of 514 genes were differentially expressed by 15-Methoxypinusolidic acid treatment. Biological pathway analysis revealed that 15-Methoxypinusolidic acid induced significant changes in expression of genes in the cell cycle pathway. 15-Methoxypinusolidic acid significantly reduced bromodeoxyuridine incorporation, increased poly-ADP-ribose polymerase cleavage and the number of apoptotic cells, indicating that 15-Methoxypinusolidic acid induces apoptosis in BV2 cells.
CONCLUSIONS:
15-Methoxypinusolidic acid induced apoptosis in murine microglial cells, presumably via inhibition of the cell cycle progression. As microglial activation is detrimental in CNS injuries, these data suggest a strong therapeutic potential of 15-Methoxypinusolidic acid.
