Effects of simultaneous administration of G-CSF and ILE following ischemia-reperfusion in the rat kidney. A histomorphometric study.

Document Type : Original Article

Authors

1 DVM Student, Faculty of Veterinary Medicine, Semnan University, Semnan, Iran

2 Department of Basic Sciences, Faculty of Veterinary Medicine, Semnan University, Semnan, Iran.

10.30466/vrf.2026.2085763.5066
Abstract
Ischemia-reperfusion injury (IRI) is one of the leading causes of cellular necrosis, inflammation, and kidney failure. This study aimed to investigate the combined effects of granulocyte colony-stimulating factor (G-CSF) and intravenous lipid emulsion (ILE) in mitigating kidney damage caused by IRI in rats. Twenty-five male Sprague-Dawley rats were divided into five groups: ILE+GCSF, ILE, GCSF, ISC, and Sham. Ischemia was induced by clamping the renal pedicle for 45 minutes. G-CSF (20 mg/kg) was administered intraperitoneally on days 0, 3, and 7, while ILE (5 mg/kg) was given intravenously for seven days. After the two-week treatment period, the left kidneys of the rats were excised via nephrectomy. The kidney samples were immediately preserved in 10% formalin, processed using standard histological methods, and paraffin-embedded. Sections were prepared, and after H&E staining, histomorphometric analyses were conducted. TUNEL staining was used to quantify apoptotic cells. The ISC group showed the highest increase in urinary space (33.5±0.49), cellular necrosis (score: 3.4), and apoptosis (score: 29.64). The ILE+GCSF group significantly reduced these parameters (urinary space: 15.3±0.47, necrosis: 1.8, apoptosis: 5.24%). Additionally, inflammation levels, renal tubular dilation, and protein cast formation were significantly lower in the ILE+GCSF group compared to the ISC group. The combination of G-CSF and ILE significantly reduced damage-related parameters. G-CSF's protective effect in reducing tissue damage and cell apoptosis following ischemia/reperfusion (I/R) is further enhanced by ILE, which provides a synergistic effect.

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Articles in Press, Accepted Manuscript
Available Online from 03 October 2026

  • Receive Date 21 February 2026
  • Revise Date 24 May 2026
  • Accept Date 11 July 2026