| Description: |
Euscaphic acid has anti-diabetic, and anti-inflammatory activities, it
inhibits LPS-induced inflammatory responses by interference with the clustering of TRAF6 with IRAK1 and TAK1, resulting in blocking the activation of IKK and MAPKs signal transduction to downregulate NF-κB activations. Euscaphic acid induces death by activation of caspase-3, dependent apoptotic pathway. Euscaphic acid and tormentic acid have inhibitory effect on high fat diet-induced obesity in the rat. Euscaphic acid also has anti-contraction effects on rat’s aortic smooth muscle. |
| Targets: |
LDL | NO | PGE | TNF-α | NOS | COX | NF-kB | JNK | ERK | p38MAPK | Calcium Channel | Sodium Channel | ATPase | Potassium Channel | IkB | IKK |
| In vitro: |
| Adv Life Sci. Technol., 2015, 33. | | Anti-Contraction Effects of Euscaphic Acid Isolated from Crataegus azarolus var. aronia L on Rat’s Aortic Smooth Muscle.[Reference: WebLink] |
The current study represents the first attempt to investigate the effect of the Euscaphic acid (EA) on Rats isolated thoracic aortic smooth muscle cells.
METHODS AND RESULTS:
Isolated aorta was used to test the anti-contraction effects and the possible mode of action(s) of the EA (1*10 -7 M) and (3*10 -7 M) isolated from Crataegus azarolus var. aronia L. Euscaphic acid showed high anti-contraction effects on norepinephrin (NE), (1*10 -9 -10 -4 M) induced contraction in aortic smooth muscle cells in endothelium-intact, endothelium-denuded, and aortic rings pre-incubated with potassium (K + )-channels blocker (tetraethylammonium, TEA), prostaglandin I 2 (PGI ) inhibitor (indomethacin) and cyclic guanosine monophosphate (cGMP) inhibitor ( methylene blue). On the other hand, other K 2 channels subtype blockers glibenclamide (GLIB); barium chloride (BaCl ) and 4-aminopyridine (4-AP) demonstrated that adenosine triphosphate sensitive K + (K ATP ), inwardly rectifying K 2 + (K ir ) and voltage-dependent K ) channels played no role in anti-contraction induced by EA. Furthermore, the role of L-types calcium (Ca ) channels in EA anti-contractile effects on aortic smooth muscle cells was proved, by using the Ca -channel blocker verapamil, as indicated by the production of a potent anti-contraction effect . The results of the current study indicate that the anti-contraction effects of EA may be due to the activation of calcium dependent, K ) channels and blocking of L-type Ca ++ channels.
CONCLUSIONS:
Thus, from these results it can be concluded that both K and Ca ++ channels play an important role in anti-contraction effects of EA, which are mediated possibly through opening of K channels and blockade of voltage-dependent calcium channels, which may justify the use of medicinal plant C. azarolus in cardiovascular disease. | | Am J Transl Res . 2019 Apr 15;11(4):2090-2098. eCollection 2019. | | Euscaphic acid inhibits proliferation and promotes apoptosis of nasopharyngeal carcinoma cells by silencing the PI3K/AKT/mTOR signaling pathway[Pubmed: 31105820] | | Abstract
Rubus alceaefolius Poir. has been used for the treatment of nasopharyngeal carcinoma (NPC) in China for many years. Euscaphic acid is an active component of Rubus alceaefolius Poir. However, the mechanism of action of Euscaphic acid in NPC remains unclear. In this study, Euscaphic acid inhibited the proliferation of NPC cells, induced apoptosis, and led to cell cycle arrest in the G1/S phase. In addition, Euscaphic acid inhibited the expression of phosphatidylinositide 3-kinases (PI3K), phosphorylated protein kinase B (p-AKT), and phosphorylated mammalian target of rapamycin (p-mTOR) p-mTOR in NPC cells. The activation of the PI3K/AKT/mTOR signaling pathway by IGF-1 promoted cell proliferation, inhibited apoptosis, and cell cycle arrest in NPC cells. In conclusion, we demonstrated that Euscaphic acid reduced cell proliferation and induced apoptosis and cell cycle arrest in NPC cells by suppressing the PI3K/AKT/mTOR signaling pathway.
Keywords: AKT; Euscaphic acid; PI3K; mTOR; nasopharyngeal carcinoma. |
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| In vivo: |
| Korean J. Pharmacogn., 2005, 36(4):324-31. | | Inhibitory effect of euscaphic acid and tormentic acid from the roots of Rosa rugosa on high fat diet-induced obesity in the rat.[Reference: WebLink] | The roots of Rosa rugosa have been used to treat diabetes mellitus in the folkloric society of Korea.
METHODS AND RESULTS:
To demonstrate the active component for the rat obesity induced by high fat diet for 6 weeks, the phytochemical fractionation and the pharmacological activity test were performed on this crude drug. It was shown that the methanolic extract and its EtOAc fraction inhibited the weight increase of the rat body, abdominal fat pad and hyperlipidemia at 200 mg/kg dose. Further, the triterpenoids, Euscaphic acid and tormentic acid, isolated from R. rugosa roots were active at 30 mg/kg in the same assay. The two components shifted serum total-, HDL, and LDL-cholesterol levels toward the values of the unteated group, suggesting that the active compounds has hypolipidemic effects. The rats fed Euscaphic acid and tormentic acid also reduced thiobarbituric acid-reactive substance (TBARS) and hydroxyl radical in the rat blood and increased Superoxide dismutase activity compared to the control. TBARS values and carbonyl content of the hepatic protein were reduced by treatment with the two triterpenoids. Antioxidative enzyme (SOD, glutathione peroxidase, and catalase) activities in hepatic tissues were increased by treatment of rats with the triterpenoids, which suggests that triterpenoids inhibited the reduction of hepatic antioxidative activity caused by high fat diet.
CONCLUSIONS:
Taken together, these results support that Euscaphic acid and tormentic acid improve a high fat diet-induced hyperlipidemia via the activation of antioxidative mechanism. |
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Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.IF=36.216(2019)
Cell Metab. 2020 Mar 3;31(3):534-548.e5. doi: 10.1016/j.cmet.2020.01.002.IF=22.415(2019)
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.IF=14.548(2019)
ACS Nano. 2018 Apr 24;12(4): 3385-3396. doi: 10.1021/acsnano.7b08969.IF=13.903(2019)
Nature Plants. 2016 Dec 22;3: 16206. doi: 10.1038/nplants.2016.205.IF=13.297(2019)
Sci Adv. 2018 Oct 24;4(10): eaat6994. doi: 10.1126/sciadv.aat6994.IF=12.804(2019)