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Folic Acid Protects Against Kidney Damage in Mice with Diabetic Nephropathy by Inhibiting M1 Macrophage Polarization
Abstract:
Kidney damage is one of the most common complications of diabetes, and inflammation caused by macrophage infiltration plays an important role. Folic acid (FA), a water-soluble vitamin, was previously found to affect inflammation by regulating macrophage polarization. In our study, we aimed to investigate the effect of FA on renal injury in mice with diabetic nephropathy (DN). We found that FA treatment ameliorated diabetic metabolic parameters in mice with DN, including reducing 24-hour food consumption, 24-hour urine volume and 24-hour water intake and increasing body weight and serum insulin. Of note, FA treatment improved renal functional and structural damage in mice with DN. In addition, FA treatment significantly reduced the number of renal infiltrating M1 macrophages, inflammatory cytokine FA stimulation significantly reduced the increase in F4/80+CD86+ cell ratio, inflammatory factor content and p-p65/p65 protein expression induced by high glucose exposure in RAW264.7 cells. All in all, our results indicated that FA protects against kidney damage in mice with DN by inhibiting M1 macrophage polarization, and its mechanism may be related to the inhibition of nuclear factor-k-gene binding (NF-kB) signaling pathway.
Insights
Folic acid (FA) protects against diabetic kidney disease by reducing inflammation and improving kidney function in mice. FA inhibits M1 macrophage polarization, a key factor in diabetic nephropathy (DN) pathogenesis.
Area of Science:
- Nephrology
- Immunology
- Endocrinology
Background:
- Diabetic nephropathy (DN) is a major complication of diabetes, characterized by kidney damage and inflammation.
- Macrophage infiltration and polarization are critical in DN pathogenesis.
- Folic acid (FA) is known to modulate inflammatory responses by regulating macrophage polarization.
Purpose of the Study:
- To investigate the protective effects of folic acid (FA) on kidney injury in a mouse model of diabetic nephropathy (DN).
- To elucidate the underlying mechanisms of FA's action, particularly concerning macrophage polarization and inflammatory pathways.
Main Methods:
- Diabetic nephropathy was induced in mice, followed by treatment with folic acid (FA).
- Renal function, metabolic parameters, and kidney structural damage were assessed.
- Macrophage infiltration (M1 phenotype) and inflammatory markers were analyzed in renal tissues and in vitro cell models (RAW264.7 cells) exposed to high glucose.
- NF-kB signaling pathway activation was evaluated.
Main Results:
- FA treatment improved metabolic parameters (food/water intake, urine volume, body weight, serum insulin) and ameliorated renal functional and structural damage in DN mice.
- FA significantly reduced M1 macrophage infiltration and inflammatory cytokine levels in the kidneys.
- In vitro, FA inhibited high glucose-induced M1 macrophage polarization and inflammatory factor production, including p-p65/p65 expression, suggesting NF-kB pathway involvement.
Conclusions:
- Folic acid (FA) demonstrates protective effects against kidney damage in diabetic nephropathy (DN).
- FA exerts its renoprotective effects by inhibiting M1 macrophage polarization.
- The mechanism may involve the suppression of the nuclear factor-kappa B (NF-kB) signaling pathway.
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