The effects of N-acetyl cysteine on the expression of MMP9 and TIMP2 genes in the liver tissue of cadmium exposed rats

Document Type : (original research)

Authors

1 Department of Biology, Faculty of Sciences, Rasht Branch, Islamic Azad University, Rasht, Iran

2 Department of Biology, Faculty of Sciences, Rasht Branch, Islamic Azad University, Rasht, Iran.

3 Department of Pharmaceutics, School of Pharmacy, Guilan University of Medical Sciences, Rasht, Iran

10.22034/AEJ.2021.280495.2495

Abstract

The aim of this experimental study was to investigate the effect of cadmium (Cd) on the expression of matrix metalloproteinase 9 (MMP9) and tissue inhibitor of metalloproteinase 2 (TIMP2) genes and to investigate the protective role of N-acetylcysteine ​​(NAC) on cadmium toxicity in the liver tissue of rats. In this study, male Wistar rats were randomly divided into 5 groups: control (G1), single dose of cadmium (80 mg/kg) (G2), continuous dose of cadmium (2.5 mg/kg) (G3), Single dose of cadmium (80 mg/kg) and continuous dose of NAC (50 mg/kg) (G4) and continuous dose of cadmium (2.5 mg/kg) and continuous dose of NAC (50 mg/kg) (G5). Hematoxylin and eosin (H&E) staining was used to study histopathological changes. Cadmium concentration was measured by graphite furnace spectroscopy in the liver samples. The expression of MMP9 and TIMP2 genes was evaluated using RT-PCR. Cadmium exposure, especially at continuous dose, was associated with severe tissue damage and increased inflammatory cells in the liver. The mean tissue of cadmium concentration was significantly increased by 27% (P<0.05) in the G2 group and 60% (P<0.01) in G3 group. NAC treatment in G4 group (P<0.01) and G5 group (P<0.01) significantly reduced the tissue concentration of cadmium. Cadmium also increased the expression of MMP9 gene (P<0.001) and TIMP2 gene (P<0.01) in G2 and G3 groups. NAC treatment significantly reversed these effects. Our results suggested that NAC protects liver cells by decreasing the accumulation of cadmium and reducing the expression of TIMP2 and MMP9 genes.

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