Histopathological, biochemical and molecular studies on a model of systemic autoimmune disease induced by sodium...

Sodium silicate (Na2SiO₃) is an inorganic silica salt used in many products. Few studies reported autoimmune diseases (AIDs) due to Na2SiO₃ exposure. This study investigates the role of Na2SiO₃ exposure by different routes and doses in AID development in rats. We assigned 40 female rats to four groups: G1 control group, G2 rats were subcutaneously injected with 5 mg Na2SiO₃ suspension, and G3 and G4 rats were orally administered 5 mg and 7 mg Na2SiO₃ suspension, respectively. Na2SiO₃ was administered weekly for 20 weeks. Serum anti-nuclear antibodies (ANA) detection, histopathology of kidney, brain, lung, liver, and heart, oxidative stress biomarkers (MDA and GSH) in tissues, Matrix metalloproteinase activity in serum, TNF-α, and Bcl-2 expression in tissues were performed. ANA was significantly increased in silicate groups, especially G2. Creatinine was significantly increased in silicate groups. Histopathology revealed vasculitis and fibrinoid degeneration of blood vessels, a picture of immune-mediated glomerulonephritis in the kidneys, and chronic interstitial pneumonia with medial hypertrophy of pulmonary blood vessels. The activity of gelatinases (MMP-2 and MMP-9) and collagenase (MMP-13), which play role in inflammation, remodeling, and immune complex degradation, were significantly increased in the silicate-exposed groups. Bcl-2 was significantly decreased, indicating apoptosis. Therefore, oral administration and subcutaneous injection of Na2SiO₃ induced immune-mediated glomerulonephritis with elevated ANA levels and overexpression of TNF-α in rats.