RGD Reference Report - Curative effect of arjunolic acid from Terminalia arjuna in non-alcoholic fatty liver disease models. - Rat Genome Database
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Curative effect of arjunolic acid from Terminalia arjuna in non-alcoholic fatty liver disease models.

Authors: Toppo, Erenius  Sylvester Darvin, S  Esakkimuthu, S  Buvanesvaragurunathan, K  Ajeesh Krishna, T P  Antony Caesar, S  Stalin, A  Balakrishna, K  Pandikumar, P  Ignacimuthu, S  Al-Dhabi, N A 
Citation: Toppo E, etal., Biomed Pharmacother. 2018 Nov;107:979-988. doi: 10.1016/j.biopha.2018.08.019. Epub 2018 Aug 23.
RGD ID: 15090799
Pubmed: (View Article at PubMed) PMID:30257410
DOI: Full-text: DOI:10.1016/j.biopha.2018.08.019

The prevalence of Non Alcoholic Fatty Liver Disease (NAFLD) is increasing globally. Terminalia arjuna W. & Arn. (Combretaceae) is an endemic tree found in India and Sri Lanka and used traditionally for its cardioprotective and hepatoprotective effects. Arjunolic acid (AA) is an oleanane triterpenoid found mainly in the heartwood of T. arjuna. This study was aimed to evaluate the hepatoprotective effect of AA using cellular and rodent models of NAFLD. AA was isolated from the ethyl acetate extract of the heartwood of T. arjuna. The structure of AA was confirmed by physical and spectroscopic data. Steatosis was induced in HepG2 cells using palmitate-oleate mixture and the effects of AA on triglyceride accumulation and lipotoxicity were assessed. In vivo effect of AA on NAFLD was assessed using HFD fed rats. The treatment with AA did not affect the cell viability upto 100 μM and showed GI25 value of 379.9 μM in HepG2 cells. The treatment with AA significantly lowered the ORO concentration by 35.98% and triglyceride accumulation by 66.36% at 50 μM concentration (P < 0.005) compared to the vehicle treated group. The treatment with AA also reduced the leakage of ALT and AST by 61.11 and 48.29% in a significant manner (P < 0.005). The in vivo findings clearly demonstrated that the animals treated with AA at 25 and 50 mg/kg concentrations showed a significant decrease in the levels of transaminases, phosphatase and GGT (P < 0.005). In the liver, the expression of PPARα and FXRα expressions were upregulated, while PPARγ expression was downregulated by the treatment with AA. The liver histology of the animals showed reduction in steatosis and MNC infiltration. These preliminary evidences suggested that AA might be a promising lead to treat NAFLD. Future robust scientific studies on AA will lead to tailoring it for the treatment of NAFLD.


Disease Annotations    

Gene-Chemical Interaction Annotations    
arjunolic acid  (EXP,ISO)
fenofibrate  (EXP,ISO)

Gene Ontology Annotations    

Biological Process

Objects Annotated

Genes (Rattus norvegicus)
Nr1h4  (nuclear receptor subfamily 1, group H, member 4)

Genes (Mus musculus)
Nr1h4  (nuclear receptor subfamily 1, group H, member 4)

Genes (Homo sapiens)
NR1H4  (nuclear receptor subfamily 1 group H member 4)

Additional Information