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Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis
Published on: November 28, 2015
Paeoniflorin suppresses kidney inflammation by regulating macrophage polarization via KLF4-mediated mitophagy
Yiwen Cao1, Jingli Xiong1, Xueping Guan1
1Department of Pharmacology, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510006, Guangdong, China.
Background:
Macrophages M1 polarization involved in the process of renal inflammatory injury, is a well-established hallmark of chronic kidney disease (CKD). Paeoniflorin (PF), a water-soluble monoterpene glycoside extracted from Paeonia lactiflora, revealed renal anti-inflammatory activities in our previous study. However, the potential molecular mechanism of PF on CKD remains unknown.
Purpose:
The present study aims to investigate the regulation of PF on macrophage polarization in CKD.
Methods:
A CKD model was established by cationic bovine serum albumin and a murine macrophage cell line RAW264.7 induced with lipopolysaccharide (LPS) were used to clarify the underlying mechanisms of PF in CKD.
Results:
Results showed that PF exhibited favorable protective effects on CKD model mice by promoting renal function, ameliorating renal pathological injury and podocyte damage. Furthermore, PF inhibited the infiltration of M1 macrophage marker CD68 and iNOS in kidney tissue, but increased the proportion of M2 macrophage marker CD206. In RAW264.7 cells stimulated with LPS, the levels of cytokines including IL-6, IL-1β, TNF-α, MCP-1 were lessened under PF treatment, while the levels of Arg1, Fizz1, IL-10 and Ym-1 were augmented. These results indicated that PF promoted macrophage polarization from M1 to M2 in vivo and in vitro. More importantly, PF repaired the damaged mitochondria through increasing mitochondrial membrane potential and reducing ROS accumulation. The mitophagy-related proteins PINK1, Parkin, Bnip3, P62 and LC3 were up-regulated by PF, accompanied by the incremental expressions of Krüppel-like transcription factor 4 (KLF4). Moreover, the promotion of mitophagy and inhibition of M1 macrophage polarization owing to PF were reversed by mitophagy inhibitor Mdivi-1 or silencing KLF4.
Conclusion:
Overall, PF suppressed renal inflammation by promoting macrophage polarization from M1 to M2 and inducing mitophagy via regulating KLF4. It is expected to provide a new strategy for exploring the effects of PF in treating CKD.
Insights
Paeoniflorin (PF) suppresses kidney inflammation in chronic kidney disease (CKD) by shifting M1 macrophages to M2 and enhancing mitophagy through KLF4 regulation. This offers a potential new therapeutic strategy for CKD treatment.
Area of Science:
- Nephrology
- Immunology
- Pharmacology
Background:
- Macrophage M1 polarization is a key factor in renal inflammatory injury and chronic kidney disease (CKD).
- Paeoniflorin (PF), derived from Paeonia lactiflora, has demonstrated renal anti-inflammatory properties, but its mechanism in CKD is unclear.
Purpose of the Study:
- To investigate the regulatory effects of Paeoniflorin (PF) on macrophage polarization in the context of chronic kidney disease (CKD).
Main Methods:
- A CKD mouse model was induced using cationic bovine serum albumin.
- Murine macrophage cell line RAW264.7 was stimulated with lipopolysaccharide (LPS) to mimic inflammatory conditions.
- The effects of PF on macrophage polarization, renal function, pathological injury, mitochondrial function, and mitophagy-related proteins were analyzed.
Main Results:
- PF improved renal function and reduced pathological damage in CKD mice by inhibiting M1 macrophage markers (CD68, iNOS) and increasing M2 markers (CD206).
- In vitro, PF reduced pro-inflammatory cytokines (IL-6, IL-1β, TNF-α, MCP-1) and increased anti-inflammatory markers (Arg1, Fizz1, IL-10, Ym-1), indicating M1 to M2 polarization.
- PF enhanced mitochondrial function, reduced oxidative stress, and upregulated mitophagy-related proteins (PINK1, Parkin, Bnip3, P62, LC3) by regulating Krüppel-like factor 4 (KLF4).
Conclusions:
- Paeoniflorin (PF) suppresses renal inflammation in CKD by promoting M1 to M2 macrophage polarization and inducing mitophagy via KLF4.
- PF demonstrates potential as a novel therapeutic strategy for treating chronic kidney disease (CKD).
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