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Research on the mechanism of sea buckthorn leaf Fu tea in the treatment of hyperlipidemia

Authors :
Si-Kai Chen
Wen-Xin Wei
Feng-Yu Huang
Jing Wang
Xing-Yu Li
Yu-Ting Yang
Wan-Tao Xing
Feng Gao
Min Li
Feng Miao
Liang-Liang Chen
Pei-Feng Wei
Source :
Heliyon, Vol 10, Iss 12, Pp e32343- (2024)
Publication Year :
2024
Publisher :
Elsevier, 2024.

Abstract

Background: Hyperlipidemia (HLP) presents a significant challenge to global public health. Mounting evidence suggests that statins, the recommended first-line lipid-lowering agents, have significant adverse effects. Consequently, the quest for natural and efficacious alternative therapies is steadily emerging as a research priority for HLP prevention and treatment. Consumption of tea, which is rich in diverse biologically active compounds with the capacity to regulate lipid metabolism and combat obesity, has emerged as a promising alternative therapy. Sea buckthorn leaves are rich in a multitude of biologically active substances, have a hypolipidemic effect, and can be used as a raw material for tea because of their unique flavor. There is a suggestion that combining Aspergillus cristatus with tea could modify or boost the lipid-lowering active compounds present in tea, thereby increasing its efficacy in regulating lipid metabolism. Results: Sea Buckthorn Leaf Fu Tea (SBLFT) was obtained by fermentation when sea buckthorn leaves contained 42 % moisture, inoculated with Aspergillus cristatus 0.2 mL/g, and incubated for 8 d at constant temperature. Animal experiments demonstrated that SBLFT significantly inhibited body weight gain in HLP rats and reduced lipid content and serum oxidative stress. In addition, liver tissue sections and functional indices showed that SBLFT can improve liver morphology and function abnormalities. Reverse transcription-polymerase chain reaction results indicated that the expression of Liver kinase B1 (LKB1), adenosine 5‘-monophosphate (AMP)-activated protein kinase (AMPK), acetyl CoA carboxylase 1 (ACC1), and sterol-regulatory element binding protein-1 (SREBP1c) gene related to lipid metabolism was altered. Conclusion: SBLFT improved HLP, specifically via promoting the expression of LKB1 in the liver of HLP rats, activating AMPK, and inhibiting ACC1 and SREBP1c expression, resulting in the inhibition of fatty acid and triglyceride synthesis-related enzymes at the transcriptional level.

Details

Language :
English
ISSN :
24058440
Volume :
10
Issue :
12
Database :
Directory of Open Access Journals
Journal :
Heliyon
Publication Type :
Academic Journal
Accession number :
edsdoj.20a7d0b615f842df9f9d1d220469df6d
Document Type :
article
Full Text :
https://doi.org/10.1016/j.heliyon.2024.e32343