article · Archives of Pharmacal Research
Alcoholic liver disease involves complex biological mechanisms driven largely by inflammation and oxidative stress resulting from excessive alcohol consumption. Boswellic acids, naturally occurring compounds derived from the plant Boswellia serrata, are recognised for their antioxidant and anti-inflammatory properties, but their specific impact on alcoholic liver disease had not been examined previously. In an experimental study using an alcoholic liver disease mouse model, male mice received boswellic acids across three dosage levels over fourteen days. A dose of 500 milligrams per kilogram produced the strongest hepatoprotective effects. It improved blood alcohol concentration, liver function enzymes, lipid profiles, and liver tissue integrity. These benefits occurred through the suppression of oxidative and inflammatory signalling pathways, including CYP2E1, NOX enzymes, p38 MAPK, and miR-155 expression, alongside an increase in PPARalpha levels, ultimately curbing liver cell death and inflammation.
Excessive alcohol consumption causes severe liver damage driven by ongoing inflammation and oxidative stress. By identifying how natural compounds from Boswellia serrata help protect liver tissue and regulate specific biological pathways in animals, this research provides foundational knowledge that could inform future efforts to address alcohol-related liver injury.
This research is at an early experimental stage, having been evaluated solely in a fourteen-day mouse model. The findings could eventually interest pharmaceutical or nutraceutical developers seeking active plant-derived compounds for liver protection. However, substantial further preclinical testing and clinical trials would be required before any therapeutic formulation or real-world application can be pursued.
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Alcoholic liver disease (ALD) refers to hepatic ailments induced by excessive alcohol intake. The pathogenesis of ALD comprises a complex interplay between various mechanistic pathways, among which inflammation and oxidative stress are key players. Boswellic acids (BAs), found in Boswellia serrata, have shown hepatoprotective effects owing to their antioxidant and anti-inflammatory activities, nevertheless, their therapeutic potential against ALD has not been previously investigated. Hence, this study was performed to depict the possible protective effect of BAs and detect their underlying mechanism of action in an experimentally-induced ALD mouse model. Male BALB/c mice were equally categorized into six groups: control, BAs-treated, ALD, and ALD that received BAs at three-dose levels (125, 250, and 500 mg/kg) by oral gavage for 14 days. Results showed that the high dose of BAs had the most protective impact against ALD according to histopathology examination, blood alcohol concentration (BAC), and liver function enzymes. Mechanistic investigations revealed that BAs (500 mg/kg) caused a significant decrease in cytochrome P450 2E1(CYP2E1), nicotine adenine dinucleotide phosphate oxidase (NOX) 1/2/4, p38 mitogen-activated protein kinase (MAPK), and sterol regulatory element-binding protein-1c (SREBP-1c) levels, and the expression of miR-155, yet increased peroxisome proliferator-activated receptor alpha (PPARα) levels. This led to an improvement in lipid profile and reduced hepatic inflammation, oxidative stress, and apoptosis indices. In summary, our study concludes that BAs can protect against ethanol-induced hepatic injury, via modulating NOX/p38 MAPK/PPARα pathways and miR-155 expression.
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DOI: 10.1007/s12272-023-01441-6
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