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Papain exerts an anti-atherosclerosis effect with suppressed MPA-mediated foam cell formation by regulating the MAPK
Xianming Fei1, Lianlian Pan2, Wufen Yuan1
1Laboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, China.
Background:
Papain possesses a potential anti-atherosclerosis (AS) effect. This study aimed to explore the inhibitory effects of papain on the monocyte-platelet aggregates (MPAs)-mediated production of foam cells in vitro and AS in vivo.
Research Design And Methods:
THP-1 cells were treated by platelet, papain, nuclear factor-κB (NF-κB) inhibitor or activator. An AS rat model was treated with papain. The THP-1 cells, macrophages, and foam cells were detected, and CD36, CD11b and CCR2 (macrophages) and CD14 and CD41 (MPAs) were measured. The levels of inflammatory factors, lipoprotein, and MAPK and PI3K/Akt -NF-κB pathways proteins were determined. Finally, injury of the thoracic aorta of AS rats was observed.
Results:
Papain reduced macrophage production, lipid accumulation, and foam cell formation in vitro and downregulated the expression of monocyte chemoattractant protein 1 (MCP-1), prostaglandin E2 (PGE2), and cyclooxygenase 2 (COX2), and that of p38, JNK, Akt, and p65. Moreover, NF-κB activator could reversed the inhibitory effects of papain. Similarly, papain alleviated aortic smooth muscle hyperplasia, lipid droplet accumulation, and collagen diffusion and inhibited the expression of inflammatory factors and p38, JNK, Akt, and p65 in vivo.
Conclusions:
Papain inhibited MPA-induced foam cell formation by inactivating the MAPK and PI3K/Akt-NF-κB pathways, thereby exerting an anti-AS effect.
Insights
Papain effectively inhibits foam cell formation by targeting monocyte-platelet aggregates, offering a potential treatment for atherosclerosis. This study reveals papain
Area of Science:
- Biochemistry
- Pharmacology
- Cardiovascular Research
Background:
- Atherosclerosis (AS) involves foam cell formation mediated by monocyte-platelet aggregates (MPAs).
- Papain, an enzyme, shows potential in mitigating AS progression.
Purpose of the Study:
- To investigate papain's inhibitory effects on MPA-induced foam cell production.
- To evaluate papain's therapeutic potential in an in vitro and in vivo atherosclerosis model.
Main Methods:
- THP-1 cells and an AS rat model were treated with papain.
- Key cellular markers (CD36, CD11b, CCR2, CD14, CD41) and inflammatory factors were measured.
- MAPK and PI3K/Akt-NF-κB signaling pathways were analyzed.
Main Results:
- Papain reduced foam cell formation, lipid accumulation, and inflammatory markers in vitro.
- Papain alleviated aortic lesions, smooth muscle hyperplasia, and lipid deposition in vivo.
- Papain inactivated the MAPK and PI3K/Akt-NF-κB pathways.
Conclusions:
- Papain inhibits MPA-induced foam cell formation by deactivating MAPK and PI3K/Akt-NF-κB pathways.
- Papain demonstrates significant anti-atherosclerosis effects both in vitro and in vivo.
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