Inflammation-Responsive Cell Membrane-Camouflaged Nanoparticles against Liver Fibrosis via Regulating Endoplasmic Reticulum Stress and Oxidative Stress.
Yang BaiJiaqi ChenSitong ZhangGuangyu XuZhengwei MaoYuan DingWei-Lin WangPublished in: Advanced materials (Deerfield Beach, Fla.) (2024)
Liver fibrosis represents a reversible stage of various chronic liver diseases that progresses to cirrhosis. This condition is characterized by an imbalance between tissue damage and repair, and the production of fibers in the liver exceeds their degradation. Oxidative stress (OS) resulting from tissue injury and endoplasmic reticulum stress (ERS) triggered by the overproduction of proteins are pivotal factors in liver fibrosis. Melatonin demonstrates the capability to neutralize free radicals, shielding cells from oxidative harm. It is also a specific inhibitor of the ERS receptor transcription activating factor 6 (ATF6), indicating its great potential in ameliorating liver fibrosis. However, its limited water solubility and oral bioavailability of under 15% present hurdles in achieving therapeutic blood concentrations for treating liver fibrosis. The PLGA@Melatonin is constructed by loading melatonin with poly (lactic-co-glycolic acid) (PLGA). Platelet membranes (PM) and activated hepatic stellate cell membranes (HSCM) with high expression of the platelet-derived growth factor receptor (PDGFR) are extracted to successfully construct PM@PLGA@Melatonin and HSCM@PLGA@Melatonin, which are subsequently utilized to treat mice with liver fibrosis. The results illustrated the remarkable therapeutic effects of the two nanoparticles on liver fibrosis, along with their excellent targeting and biosafety properties.
Keyphrases
- liver fibrosis
- endoplasmic reticulum stress
- oxidative stress
- induced apoptosis
- growth factor
- drug delivery
- dna damage
- drug release
- air pollution
- particulate matter
- signaling pathway
- ischemia reperfusion injury
- type diabetes
- transcription factor
- stem cells
- binding protein
- metabolic syndrome
- insulin resistance
- adipose tissue
- diabetic rats
- skeletal muscle
- cell therapy
- long non coding rna
- wild type