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Updated: Jul 31, 2026
Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry
Published on: October 18, 2016
Lovastatin reduces glomerular macrophage influx and expression of monocyte chemoattractant protein-1 mRNA in
1Department of Medicine, Hennepin County Medical Center, Minneapolis, MN 55404, USA.
Abstract:
Glomerular expression of monocyte chemoattractant protein-1 (MCP-1) and subsequent glomerular macrophage infiltration may play an important role in the development of glomerulosclerosis. Previous studies have shown that lovastatin ameliorates experimental renal disease and reduces MCP-1 expression in serum-stimulated, cultured mesangial cells. We investigated the effects of lovastatin on glomerular MCP-1 expression and macrophage infiltration in rats with puromycin aminonucleoside (PA) nephrosis, an experimental model of renal disease characterized by early macrophage infiltration. Male Sprague-Dawley rats were pretreated for 5 days with either lovastatin (4 mg/kg) or vehicle. At the end of pretreatment, the lovastatin-pretreated rats received a single i.v. injection of PA (50 mg/kg) and continued to receive daily lovastatin thereafter. The vehicle-pretreated rats received i.v. injections of either PA or saline, and continued to receive daily vehicle treatment thereafter. Ten days after PA injection, the vehicle-treated PA rats showed increased (P < 0.05) serum cholesterol (359 +/- 25 mg/100 mL) and urine albumin excretion (343 +/- 95 mg/24 hr), compared with the vehicle-treated control rats (61 +/- 3 mg/100 mL and 2.5 +/- 0.6 mg/24 hr, respectively). Serum cholesterol (193 +/- 22 mg/dL) and urine albumin excretion (255 +/- 68 mg/24 hr) were less in the lovastatin-treated PA rats than in the vehicle-treated PA rats. The number of glomerular macrophages, assessed as ED-1-positive cells, per glomerular profile was increased 77% in the vehicle-treated PA rats (3.3 +/- 0.2) compared with the vehicle-treated control rats (1.8 +/- 0.2) (P < 0.05). By contrast, the number of glomerular macrophages was not elevated in the lovastatin-treated PA rats (2.3 +/- 0.2). Thus, lovastatin in vivo can attenuate glomerular macrophage infiltration. This may represent one mechanism by which lovastatin ameliorates experimental glomerular disease.
Insights
Lovastatin treatment reduced glomerular macrophage infiltration in rats with puromycin aminonucleoside (PA) nephrosis. This finding suggests lovastatin may ameliorate experimental glomerular disease by inhibiting MCP-1-driven inflammation.
Area of Science:
- Nephrology
- Immunology
- Pharmacology
Background:
- Glomerular monocyte chemoattractant protein-1 (MCP-1) and macrophage infiltration are implicated in glomerulosclerosis.
- Lovastatin has previously shown potential in ameliorating experimental renal disease and reducing MCP-1 expression in cultured cells.
Purpose of the Study:
- To investigate the in vivo effects of lovastatin on glomerular MCP-1 expression and macrophage infiltration in a rat model of puromycin aminonucleoside (PA) nephrosis.
Main Methods:
- Male Sprague-Dawley rats were pretreated with lovastatin or vehicle, followed by PA injection.
- Glomerular macrophage infiltration was assessed by counting ED-1-positive cells 10 days post-injection.
Main Results:
- PA-induced nephrosis significantly increased serum cholesterol and urine albumin excretion compared to controls.
- Lovastatin treatment significantly reduced serum cholesterol and urine albumin excretion in PA-treated rats.
- Vehicle-treated PA rats showed a 77% increase in glomerular macrophages, while lovastatin-treated rats did not exhibit this elevation.
Conclusions:
- Lovastatin administration in vivo attenuates glomerular macrophage infiltration in experimental renal disease.
- Inhibition of macrophage infiltration may be a key mechanism by which lovastatin exerts its protective effects in glomerular diseases.
