Maslinic acid has been shown to control the phosphorylation of IκB-α and the LPS-induced translocation of NF-κB from cells to the nucleus. According to reports, maslinic acid reduces TNF-α-induced NF-κB activity and the expression of its downstream genes in the pancreas and regulates NF-κB-regulated osteoclastogenesis in scaffold monocytes. An experimental dose determination of the effective concentration of maslinic acid at 10 -20 μM is required to confirm if the anti-inflammatory activity of olive pomace extract (OPE) in RAW264.7 cells can ultimately eradicate maslinic acid. In RAW 264.7 cells, 20 μM maslinic acid markedly reduced the expression of COX-2, IL-1, and IL-6 mRNA as well as the generation of TNF-α. In RAW 264.7 cells, the DNA binding activity of NF-κB p65 was dramatically reduced by mastinic acid (10 and 20 μM) caused by LPS. Maslinic acid has the ability to dramatically lower LPS-induced phosphorylation of IκB-α [1].

When animals were given 200 mg/kg of maslinic acid four hours after receiving an injection of λ-carrageenan, their paw swelling decreased in comparison to the carrageenan-induced scaffold (0.91 ± 0.51 mm and 1.79 ± 0.4 mm, respectively [1]).

[1]. Anti-inflammatory and anti-arthritic effects of pentacyclic triterpenoids maslinic acid through NF-κB inactivation. Mol Nutr Food Res. 2016 Feb;60(2):399-409.

Maslinic acid is a pentacyclic triterpenoid that is olean-12-ene substituted by hydroxy groups at positions 2 and 3 and a carboxy group at position 28 (the 2alpha,3beta stereoisomer). It is isolated from Olea europaea and Salvia canariensis and exhibits anti-inflammatory, antioxidant and antineoplastic activity. It has a role as an antioxidant, an antineoplastic agent, an anti-inflammatory agent and a plant metabolite. It is a pentacyclic triterpenoid and a dihydroxy monocarboxylic acid. It derives from a hydride of an oleanane.
Maslinic acid has been reported in Salvia miltiorrhiza, Sideritis candicans, and other organisms with data available.
See also: Centaurium erythraea whole (part of).

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Mechanism of Action
Maslinic acid, a pentacyclic triterpene found in the protective wax-like coating of the leaves and fruit of Olea europaea L., is a promising agent for the prevention of colon cancer. Investigators have shown /previously/ that maslinic acid inhibits cell proliferation to a significant extent and activates mitochondrial apoptosis in colon cancer cells. /This study/ investigated... this compound's apoptotic molecular mechanism. /Investigators/ used HT29 adenocarcinoma cells. Changes /in/ genotoxicity were analyzed by single-cell gel electrophoresis (comet assay). The cell cycle was determined by flow cytometry. Finally, changes in protein expression were examined by western blotting. Student's t-test was used for statistical comparison. HT29 cells treated with maslinic acid showed significant increases in genotoxicity and cell-cycle arrest during the G0/G1 phase after 72 hours treatment and an apoptotic sub-G0/G1 peak after 96 hours... the anti-tumoral activity of maslinic acid might proceed via p53-mediated apoptosis by acting upon the main signaling components that lead to an increase in p53 activity and the induction of the rest of the factors that participate in the apoptotic pathway. /Investigators/ found that in HT29 cells maslinic acid activated the expression of c-Jun NH2-terminal kinase (JNK), thus inducing p53. Treatment of tumor cells with maslinic acid also resulted in an increase in the expression of Bid and Bax, repression of Bcl-2, release of cytochrome-c and an increase in the expression of caspases -9, -3, and -7. Moreover, maslinic acid produced belated caspase-8 activity, thus amplifying the initial mitochondrial apoptotic signaling. All these results suggest that maslinic acid induces apoptosis in human HT29 colon-cancer cells through the JNK-Bid-mediated mitochondrial apoptotic pathway via the activation of p53...
Maslinic acid (2-alpha, 3-beta-dihydroxyolean-12-en-28-oic acid) is a natural triterpenoid compound from Olea europaea. This compound prevents oxidative stress and pro-inflammatory cytokine generation in vitro. This study ...investigated the anti-inflammatory effects of maslinic acid in central nervous system by using rat astrocyte cultures stimulated with lipopolysaccharide (LPS). /It/ evaluated different proteins implicated in the nuclear factor kappa B (NF-kappa B) signal transducer pathway employing Western blot and quantitative real time PCR techniques. Results demonstrated that maslinic acid treatment exerted potent anti-inflammatory action by inhibiting the production of Nitric Oxide and tumor necrosis factor alpha (TNF-alpha). Western blot analysis showed that maslinic acid treatment attenuated LPS-induced translocation of NF-kappa B p65 subunit to the nucleus and prevented LPS-induced I kappa B alpha phosphorylation in a concentration-dependent manner, Moreover, maslinic acid significantly suppressed the expression of cyclooxygenase 2 (COX-2) and inducible nitric oxide synthase (iNOS) at protein and mRNA levels. These results suggest that maslinic acid can potentially reduce neuroinflammation by inhibiting NF-kappa B signal transducer pathway in cultured cortical astrocytes.
Activation of NF-kappaB and MAPK/activator protein 1 (AP-1) signaling pathways by receptor activator NF-kappaB ligand (RANKL) is essential for osteoclast activity. Targeting NF-kappaB and MAPK/AP-1 signaling to modulate osteoclast activity has been a promising strategy for osteoclast-related diseases. /This study/ examined the effects of maslinic acid (MA), a pentacyclic triterpene acid that is widely present in dietary plants, on RANKL-induced osteoclastogenesis, osteoclast function, and signaling pathways by in vitro and in vivo assay systems. In mouse bone marrow monocytes (BMMs) and RAW264.7 cells, MA inhibited RANKL-induced osteoclastogenesis in a dose-dependent manner within nongrowth inhibitory concentration, and MA decreased osteoclastogenesis-related marker gene expression, including TRACP, MMP9, c-Src, CTR, and cathepsin K. Specifically, MA suppressed osteoclastogenesis and actin ring formation at early stage. In ovariectomized mice, administration of MA prevented ovariectomy-induced bone loss by inhibiting osteoclast activity. At molecular levels, MA abrogated the phosphorylation of MAPKs and AP-1 activity, inhibited the Ikappa Balpha phosphorylation and degradation, blocked NF-kappaB/p65 phosphorylation, nuclear translocation, and DNA-binding activity by downregulating RANK expression and blocking RANK interaction with TRAF6. Together /this/ data demonstrate that MA suppresses RANKL-induced osteoclastogenesis through NF-kappa B and MAPK/AP-1 signaling pathways and that MA is a promising agent in the treatment of osteoclast-related diseases such as osteoporosis.

C30H48O4

472.6997

472.355

4373-41-5

73659

White to off-white solid powder

1.1±0.1 g/cm3

570.0±50.0 °C at 760 mmHg

249 - 250 °C

312.6±26.6 °C

0.0±3.6 mmHg at 25°C

1.568

7.87

3

4

1

34

919

9

C[C@@]12CC[C@@H]3[C@@]([C@H]1CC=C4[C@]2(CC[C@@]5([C@H]4CC(CC5)(C)C)C(=O)O)C)(C[C@H]([C@@H](C3(C)C)O)O)C

MDZKJHQSJHYOHJ-LLICELPBSA-N

InChI=1S/C30H48O4/c1-25(2)12-14-30(24(33)34)15-13-28(6)18(19(30)16-25)8-9-22-27(5)17-20(31)23(32)26(3,4)21(27)10-11-29(22,28)7/h8,19-23,31-32H,9-17H2,1-7H3,(H,33,34)/t19-,20+,21-,22+,23-,27-,28+,29+,30-/m0/s1

(4aS,6aR,6aS,6bR,8aR,10R,11R,12aR,14bS)-10,11-dihydroxy-2,2,6a,6b,9,9,12a-heptamethyl-1,3,4,5,6,6a,7,8,8a,10,11,12,13,14b-tetradecahydropicene-4a-carboxylic acid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~211.55 mM)

Solubility in Formulation 1: 2.5 mg/mL (5.29 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (5.29 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)