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Updated: May 3, 2026

Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
Bruceine E attenuates hepatic steatosis through modulation of PI3K/AKT/NFκB signalling pathway
Farahdina Man1,2, Neti Eka Jayanti3, Chiuan Yee Leow4
1MedChem Herbal Research Group, Faculty of Pharmacy, Universiti Teknologi MARA, Selangor Branch, Puncak Alam Campus, 42300 Bandar Puncak Alam, Selangor, Malaysia.
Objectives:
This study aims to establish the effect of bruceine E in attenuating nonalcoholic steatohepatitis (NASH) through the PI3K/AKT/NFκB pathway.
Methods:
High-fat-diet (HFD) male Wistar rats were orally administered with glibenclamide (20 mg/kg) or bruceine E (400, 800, or 1600 µg/kg) for 4 weeks. After 4 weeks of treatment, blood serum was analysed for liver markers. Liver histology was used to identify the degree of inflammation. The liver tissue was evaluated on the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) and inflammatory genes (nuclear factor-kappa B [NFκB], tumor necrosis factor alpha [TNFα], interleukin-6 [IL6], and interleukin-10 [IL10]) and protein expressions.
Key Findings:
The alanine transferase and aspartate transferase were reduced in HFD rats administered orally with bruceine E. In liver histology, steatosis, ballooning, and lobular inflammation were alleviated in bruceine E-treated HFD rats. The PI3K/AKT genes and proteins were activated while the inflammatory genes and protein expressions were suppressed in the bruceine E-treated HFD rats showing improvement towards insulin resistance (IR), liver steatosis, and inflammation.
Conclusions:
In conclusion, bruceine E attenuated NASH through activation of the PI3K/AKT/NFκB inflammation pathway and may further delay the progression of NASH to hepatocellular carcinoma .
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