Bruceine E attenuates hepatic steatosis through modulation of PI3K/AKT/NFκB signalling pathway.

IF 2.8 4区医学 Q2 PHARMACOLOGY & PHARMACY

Journal of Pharmacy and Pharmacology Pub Date : 2025-05-07 DOI:10.1093/jpp/rgaf016

Farahdina Man, Neti Eka Jayanti, Chiuan Yee Leow, Chee-Yan Choo

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引用次数: 0

Abstract

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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麻菜碱E通过调节PI3K/AKT/NFκB信号通路减轻肝脂肪变性。

目的：本研究旨在通过PI3K/AKT/NFκB通路确定马三氨酸E在减轻非酒精性脂肪性肝炎（NASH）中的作用。方法：高脂饮食（HFD）雄性Wistar大鼠口服格列本脲（20 mg/kg）或马尾氨酸E(400、800或1600µg/kg) 4周。治疗4周后，分析血清肝脏标志物。肝脏组织学用于确定炎症程度。检测肝组织中磷酸肌苷3-激酶/蛋白激酶B （PI3K/AKT）及炎症基因（核因子κB [NFκB]、肿瘤坏死因子α [TNFα]、白细胞介素6 [IL6]、白细胞介素10 [IL10]）及蛋白表达。主要发现：口服马钱子碱e的HFD大鼠的丙氨酸转移酶和天冬氨酸转移酶降低。在肝脏组织学上，马钱子碱e治疗的HFD大鼠的脂肪变性、水肿和小叶炎症得到缓解。在麻豆碱e处理的HFD大鼠中，PI3K/AKT基因和蛋白被激活，炎症基因和蛋白表达被抑制，表现出胰岛素抵抗（IR）、肝脏脂肪变性和炎症的改善。结论：综上所述，马毒苷E通过激活PI3K/AKT/NFκB炎症通路减轻NASH，并可能进一步延缓NASH向肝细胞癌的进展。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Pharmacy and Pharmacology 医学-药学

CiteScore

6.60

自引率

0.00%

发文量

审稿时长

3 months

期刊介绍： JPP keeps pace with new research on how drug action may be optimized by new technologies, and attention is given to understanding and improving drug interactions in the body. At the same time, the journal maintains its established and well-respected core strengths in areas such as pharmaceutics and drug delivery, experimental and clinical pharmacology, biopharmaceutics and drug disposition, and drugs from natural sources. JPP publishes at least one special issue on a topical theme each year.