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Published on: March 11, 2017
Ophiopogonin D Alleviates Nonalcoholic Steatohepatitis via Ferroptosis Through AKT1/STAT3/HIF-1α Axis
Dong Li1, Meina Shi2, Zhike Fang3
1Institute of Traditional Chinese Medicine, Dongguan TCM Hospital, Dongguan, 523005, China, itmonline.org.
Background:
Not enough is known about how ophiopogonin D (OP-D) works and the molecular mechanisms involved in nonalcoholic steatohepatitis (NASH). This study aimed to investigate the antifibrosis effect and underlying mechanism of OP-D in NAFLD.
Methods:
The rats were fed a high-fat diet (HFD) to simulate NAFLD. After OP-D treatment or not, the rat serum lipid levels and inflammatory and ferroptosis-related factors were detected. Online databases and network pharmacology were used to collect the targets of OP-D against NASH. The effect of OP-D on AKT1, STAT3, ferroptotic markers, and fibrotic markers was determined using western blot or PCR assays.
Results:
OP-D inhibited abnormal liver function, fibrotic markers (α-SMA/Col1α1), and ferroptosis-related factor (GPX4) in NASH rats. Network pharmacology proposed AKT1 and STAT3 as targets for OP-D against NASH. OP-D reduced the p-AKT and p-STAT3 in liver tissues. OP-D reduced the levels of AKT1, STAT3, and HIF-1α in model hepatic stellate cells. AKT1 and STAT3 overexpression reversed the antifibrosis and ferroptosis-induced effects of OP-D in model hepatic stellate cells.
Conclusion:
OP-D may alleviate fibrosis in NASH by regulating ferroptosis via the AKT1/STAT3/HIF-1α axis.
Insights
Ophiopogonin D (OP-D) shows potential in treating nonalcoholic steatohepatitis (NASH) by reducing liver fibrosis. It works by regulating ferroptosis through the AKT1/STAT3/HIF-1α pathway, offering a new therapeutic avenue for NASH.
Area of Science:
- * Pharmacology
- * Molecular Biology
- * Gastroenterology
Background:
- * Nonalcoholic steatohepatitis (NASH) pathogenesis and molecular mechanisms remain incompletely understood.
- * Ophiopogonin D (OP-D) is a compound with potential therapeutic applications.
- * Investigating OP-D's antifibrotic effects in NASH is crucial.
Purpose of the Study:
- * To investigate the antifibrotic effect of OP-D in a nonalcoholic fatty liver disease (NAFLD) model.
- * To elucidate the underlying molecular mechanisms of OP-D's action in NASH.
- * To identify key molecular targets of OP-D in NASH treatment.
Main Methods:
- * A high-fat diet (HFD) induced NAFLD in rats.
- * OP-D treatment effects on liver function, lipid levels, and inflammatory/ferroptosis markers were assessed.
- * Network pharmacology identified OP-D targets; Western blot and PCR analyzed protein and gene expression (AKT1, STAT3, HIF-1α, fibrotic markers).
Main Results:
- * OP-D treatment improved liver function and reduced fibrotic markers (α-SMA/Col1α1) and ferroptosis (GPX4) in NASH rats.
- * Network pharmacology identified AKT1 and STAT3 as key targets for OP-D in NASH.
- * OP-D decreased p-AKT, p-STAT3, AKT1, STAT3, and HIF-1α levels in liver tissues and hepatic stellate cells; overexpression of AKT1/STAT3 reversed OP-D's effects.
Conclusions:
- * OP-D demonstrates significant antifibrotic effects in NASH.
- * The mechanism involves regulating ferroptosis via the AKT1/STAT3/HIF-1α signaling axis.
- * OP-D presents a promising therapeutic candidate for NASH treatment.
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