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Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry
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Pyxinol Fatty Acid Ester Derivatives J16 against AKI by Selectively Promoting M1 Transition to M2c Macrophages
Yaru Wang1, Changcheng Li1, Jingyi Chen2
1Department of Pharmacology, College of Basic Medicine of Jilin University, Changchun, Jilin 130012, China.
Abstract:
Acute kidney injury (AKI) is a common, multicause clinical condition that, if ignored, often progresses to chronic kidney disease (CKD) and end-stage kidney disease, with a mortality rate of 40-50%. However, there is a lack of universal treatment for AKI. Inflammation is the basic pathological change of early kidney injury, and inflammation can exacerbate AKI. Macrophages are the primary immune cells involved in the inflammatory microenvironment of kidney disease. Therefore, regulating the function of macrophages is a crucial breakthrough for the AKI intervention. Our team chemically modified pyxinol, an ocotillol-type ginsenoside, to prepare PJ16 with higher solubility and bioavailability. In vitro, using a model of macrophages stimulated by LPS, it was found that PJ16 could regulate macrophage function, including inhibiting the secretion of inflammatory factors, promoting phagocytosis, inhibiting M1 macrophages, and promoting M1 transition to the M2c macrophage. Further investigation revealed that PJ16 may shield renal tubular epithelial cells (HK-2) damaged by LPS in vitro. Based on this, PJ16 was validated in the animal model of unilateral ureteral obstruction, which showed that it improves renal function and inhibits renal tissue fibrosis by decreasing inflammatory responses, reducing macrophage inflammatory infiltration, and preferentially upregulating M2c macrophages. In conclusion, our study is the first to show that PJ16 resists AKI and fibrosis by mechanistically regulating macrophage function by modulating the phenotypic transition from M1 to M2 macrophages, mainly M2c macrophages.
Insights
PJ16, a modified ginsenoside, effectively treats acute kidney injury (AKI) and fibrosis. It works by regulating macrophage function, shifting them from inflammatory M1 to protective M2c phenotypes, improving kidney outcomes.
Area of Science:
- Nephrology
- Immunology
- Pharmacology
Background:
- Acute kidney injury (AKI) is a prevalent condition with high mortality and limited treatment options.
- Inflammation, driven by macrophages, is a key factor exacerbating AKI and potentially leading to chronic kidney disease.
- Targeting macrophage function presents a promising therapeutic strategy for AKI intervention.
Purpose of the Study:
- To investigate the therapeutic potential of PJ16, a novel chemically modified ginsenoside, in treating AKI.
- To elucidate the mechanisms by which PJ16 modulates macrophage function and impacts kidney injury and fibrosis.
- To evaluate PJ16's efficacy in both in vitro and in vivo models of kidney disease.
Main Methods:
- PJ16 was synthesized by chemically modifying pyxinol for improved solubility and bioavailability.
- In vitro studies involved LPS-stimulated macrophages to assess PJ16's effects on inflammatory factor secretion, phagocytosis, and M1/M2 macrophage polarization.
- In vivo studies utilized a unilateral ureteral obstruction (UUO) mouse model to evaluate PJ16's impact on renal function, fibrosis, and macrophage infiltration.
Main Results:
- PJ16 inhibited inflammatory factor secretion and promoted phagocytosis in LPS-stimulated macrophages.
- PJ16 treatment shifted macrophages from the M1 to the M2c phenotype and protected renal tubular cells in vitro.
- In the UUO model, PJ16 improved renal function, reduced renal tissue fibrosis, decreased inflammatory responses, and upregulated M2c macrophages.
Conclusions:
- This study demonstrates that PJ16 possesses significant therapeutic potential against AKI and renal fibrosis.
- PJ16 exerts its protective effects by mechanistically regulating macrophage polarization, specifically promoting the M1 to M2c transition.
- PJ16 represents a novel therapeutic agent for AKI, offering a new approach by targeting macrophage-mediated inflammation and fibrosis.
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