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Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
TJ0113 attenuates fibrosis in metabolic dysfunction-associated steatohepatitis by inducing mitophagy
Chun-Lian Huang1, Shen Qi-En2, Xu-Feng Cen3
1Department of Infectious Diseases, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Linhai, Zhejiang 317000, China.
Background:
Metabolic dysfunction-associated steatohepatitis (MASH) fibrosis is a liver disease accompanied by inflammatory cell infiltration. There is growing evidence that insufficient mitophagy can exacerbate inflammation and liver fibrosis (LF). TJ0113 is a novel mitophagy inducer. The study aimed to explore the role of TJ0113 in ameliorating fibrosis in MASH and its mechanisms.
Methods:
A high-fat diet (HFD)-induced MASH mice model and a transforming growth factor (TGF)-β1-induced LX-2 cells model were used, and then they were treated with TJ0113. Changes in hepatocyte damage were observed using electron microscopy. Expression of key molecules related to mitophagy, mitochondrial damage and inflammation in liver was detected by immunofluorescence staining (IF), immunohistochemistry (IHC) and western blotting (WB).
Result:
TJ0113 induces mitophagy through parkin/PINK1 and ATG5 signaling pathways and reduces lipid accumulation, inflammation and fibrosis in the liver of MASH mice. TJ0113 attenuated hepatic injury and lowered serum ALT, AST, TC and TG levels. TJ0113 reduced pro-inflammatory factors (IL-1β, IL-6, TNF-α), TGF-β1/Smad pathway activation and typical fibrosis-related molecules (α-SMA, Collagen-1) expression. In addition, NF-κB/NLRP3 signaling pathway activation after MASH was significantly attenuated by enhanced Mitophagy. We found that TJ0113 was able to effectively and safely induce mitophagy in vitro and reduce TGF-β1/Smad signaling and downstream pro-fibrotic responses in TGF-β1-treated LX-2 cells.
Conclusion:
TJ0113 enhances mitophagy to inhibit lipid accumulation, inflammation and fibrosis formation in MASH, and is a candidate for MASH treatment.
Insights
TJ0113, a mitophagy inducer, effectively reduces liver fibrosis, inflammation, and lipid accumulation in metabolic dysfunction-associated steatohepatitis (MASH) models. This novel compound shows promise as a potential therapeutic agent for MASH treatment.
Area of Science:
- Hepatology and metabolic disease research
- Cellular biology and molecular mechanisms of liver disease
- Drug discovery and therapeutic development
Background:
- Metabolic dysfunction-associated steatohepatitis (MASH) fibrosis involves inflammation and is linked to impaired mitophagy.
- Insufficient mitophagy can worsen liver inflammation and fibrosis (LF).
- TJ0113 is a novel compound designed to induce mitophagy.
Purpose of the Study:
- To investigate the efficacy of TJ0113 in ameliorating MASH-related fibrosis.
- To elucidate the underlying mechanisms by which TJ0113 impacts MASH.
- To evaluate TJ0113's role in mitophagy, inflammation, and fibrogenesis.
Main Methods:
- Utilized a high-fat diet (HFD)-induced MASH mouse model and TGF-β1-induced LX-2 cell model.
- Administered TJ0113 to models and assessed hepatocyte damage via electron microscopy.
- Analyzed mitophagy, mitochondrial damage, and inflammation markers using immunofluorescence, immunohistochemistry, and western blotting.
Main Results:
- TJ0113 induced mitophagy via parkin/PINK1 and ATG5 pathways, reducing liver lipid accumulation, inflammation, and fibrosis in MASH mice.
- TJ0113 treatment attenuated hepatic injury, lowered serum ALT, AST, TC, and TG levels.
- Reduced pro-inflammatory factors, TGF-β1/Smad pathway activation, and fibrosis markers (α-SMA, Collagen-1); inhibited NF-κB/NLRP3 pathway.
Conclusions:
- TJ0113 enhances mitophagy, thereby inhibiting lipid accumulation, inflammation, and fibrosis in MASH.
- TJ0113 demonstrates a therapeutic potential for treating MASH.
- The compound effectively reduces TGF-β1/Smad signaling and pro-fibrotic responses in liver cells.
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