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Asiatic acid

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-A1009

  • Specification : 98%

  • CAS number : 464-92-6

  • Formula : C30H48O5

  • Molecular Weight : 488.7

  • PUBCHEM ID : 119034

  • Volume : 20mg

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Catalogue Number

BF-A1009

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

488.7

Appearance

White crystalline powder

Botanical Source

Centella asiatica,Forsythia suspensa,Ilex cornuta,Cissus repens,Clematoclethra scandens

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1CCC2(CCC3(C(=CCC4C3(CCC5C4(CC(C(C5(C)CO)O)O)C)C)C2C1C)C)C(=O)O

Synonyms

2,3,23-TRIHYDROXY-12-URSEN-28-OIC ACID/(2α,3β)-2,3,23-Trihydroxyurs-12-en-28-oic acid/Asiatic acid/Urs-12-en-28-oic acid, 2,3,23-trihydroxy-, (2α,3β)-/Asiantic acid/Asiaticacid/Dammarolic acid

IUPAC Name

(1S,2R,4aS,6aR,6aS,6bR,8aR,9R,10R,11R,12aR,14bS)-10,11-dihydroxy-9-(hydroxymethyl)-1,2,6a,6b,9,12a-hexamethyl-2,3,4,5,6,6a,7,8,8a,10,11,12,13,14b-tetradecahydro-1H-picene-4a-carboxylic acid

Applications

Asiatic acid, a pentacyclic triterpene found in Centella asiatica, induces apoptosis in melanoma cells. Asiatic acid can be used to treat skin cancer[1]. Asiatic acid also has anti-inflammatory activities[2].

Density

1.2±0.1 g/cm3

Solubility

Methanol

Flash Point

336.4±28.0 °C

Boiling Point

609.4±55.0 °C at 760 mmHg

Melting Point

325-330 °C(lit.)

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2918190000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:464-92-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

28738247

Abstract

antioxidative and anti-inflammatory activities. In this study, we aimed to investigate the anti-inflammatory effects of asiatic acid both in vivo and in vitro. HGFs or RAW264.7 cells were treated with asiatic acid 1h before LPS treatment. Cell viability was measured by MTT assay. The levels of PGE2, NO, IL-6, and IL-8 were detected by ELISA. Protein expression levels were detected by western blot analysis. In vivo, asiatic acid significantly inhibited LPS-induced IL-6 and IL-8 expression levels in gingival tissues. In vitro, LPS-induced PGE2, NO, IL-6, and IL-8 production was significantly attenuated by asiatic acid. Asiatic acid also inhibited p65 NF-κB phosphorylation induced by LPS in HGFs. The expression of PPAR-γ was up-regulated by asiatic acid. Furthermore, GW9662, a PPAR-γ inhibitor, attenuated the inhibitory effect of asiatic acid on PGE2, NO, IL-6, and IL-8 production. Our results suggest that asiatic acid activates PPAR-γ, which subsequently inhibits LPS-induced NF-κB activation and inflammatory mediators production. Asiatic acid may offer therapeutic potential for the treatment of periodontitis.

KEYWORDS

Asiatic acid; Human gingival fibroblasts; LPS; PPAR-γ.

Title

Asiatic Acid Inhibits LPS-induced Inflammatory Response in Human Gingival Fibroblasts

Author

Chunbo Hao 1 , Buling Wu 2 , Zhiming Hou 3 , Qi Xie 4 , Tianan Liao 3 , Tao Wang 4 , Dandan Ma 5 Affiliations Expand

Publish date

2017 Sep

PMID

30498333

Abstract

Background: Asiatic acid is a reported glycogen phosphorylase inhibitor derived from the tropical medicinal plant Centella asiatica and exhibits myocardial protection both in vivo and in vitro. The purpose of this study was to evaluate the effects of asiatic acid on myocardial ischemia/reperfusion (MI/R) injury and investigate the underlying mechanisms associated with the modulation of glycometabolism in cardiomyocyte.
Materials and methods: The rats were subjected to MI/R with or without asiatic acid pretreatment. The cardiac function indexes, the size of myocardial infarction, and plasma lactate dehydrogenase (LDH) and creatine kinase (CK) activities were detected. Cardiomyocyte apoptosis was analyzed by TUNEL assay. The Akt/GSK-3β activation was measured by Western blot. The glycogen content, plasma glucose and lactate concentrations were determined following MI/R. The mRNA and protein levels of PPARγ and GLUT4 were determined by real-time PCR and Western blot, respectively.
Results: Asiatic acid pretreatment significantly improved the cardiac function indexes, attenuated the size of myocardial infarction, reduced LDH and CK activities, and suppressed cardiomyocyte apoptosis after MI/R. Asiatic acid activated Akt/GSK-3β signal pathway in the myocardium following MI/R injury. In addition, asiatic acid effectively suppressed MI/R-induced glycogen breakdown and inhibited the elevation of plasma glucose and lactate concentrations. Asiatic acid treatment increased PPARγ expression at both mRNA and protein levels, and promoted the translocation of GLUT4 to plasma membrane after MI/R insult. However, the effects mediated by asiatic acid on glycometabolism and GLUT4 translocation were reversed by the administration of LY294002, the Akt inhibitor.
Conclusion: These findings demonstrated that asiatic acid exerts beneficial effects on MI/R injury in rats. This protection may be related to the modulation of glycometabolism via Akt-dependent GLUT4 translocation and PPARγ activation in ischemic cardiomyocyte.

KEYWORDS

Asiatic acid; Human gingival fibroblasts; LPS; PPAR-γ.

Title

Asiatic Acid Protests Against Myocardial Ischemia/Reperfusion Injury via Modulation of Glycometabolism in Rat Cardiomyocyte

Author

Yang Dai 1 , Ziwei Wang 1 , Minxue Quan 1 , Yanni Lv 2 , Yunman Li 3 , Hong-Bo Xin 1 , Yisong Qian 1

Publish date

2018 Oct 25

PMID

29086235

Abstract

Increased accumulation of endogenous neurotoxin quinolinic acid has been found in various neurodegenerative diseases. Oxidative stress caused by quinolinic acid is considered as imperative factor for its toxicity. Asiatic acid, a natural triterpene is widely studied for its various medicinal values. In the present study the effects of asiatic acid in preventing the cognitive impairment and oxidative stress caused by quinolinic acid was investigated. Male Spraque-Dawley rats were orally administered asiatic acid (30 mg/kg/day) for 28 days, while quinolinic acid toxicity-induced animals received quinolinic acid (1.5 mmol/kg/day) from day 15 to day 28 for 14 days. Asiatic acid administration prevented the loss of spatial memory caused due to quinolinic acid-induced toxicity as determined using the novel object location test. In addition, asiatic acid administration alleviated the deleterious effect of quinolinic acid in brain such as increased oxidative stress, decreased antioxidant status and mitochondrial oxidative phosphorylation dysfunction. These data demonstrate that asiatic acid through its potent antioxidant and cognition enhancement property prevented the neuronal impairments caused by quinolinic acid.

KEYWORDS

Asiatic acid; Cognition; Neurodegenerative diseases; Oxidative stress; Quinolinic acid; Spatial working memory.

Title

Asiatic Acid Prevents the Quinolinic Acid-Induced Oxidative Stress and Cognitive Impairment

Author

Chitra Loganathan 1 , Palvannan Thayumanavan 2

Publish date

2018 Feb