Analytical cellular pathology (Amsterdam) · 2026
Ophiopogonin D Alleviates Nonalcoholic Steatohepatitis via Ferroptosis Through AKT1/STAT3/HIF-1α Axis.
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Li Dong, Shi Meina, Fang Zhike, Wang Xiaoqing, Huang Linshi, Dong Mingguo
Аннотация
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.
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.