Investigating the Effect of Dose-Dependent Administration of Magnesium Sulfate on the Serum Level of the Inflammatory Cytokine TNF-α as a Treatment for Diabetic Nephropathy and Peripheral Neuropathy in an Animal Model

Diabetic nephropathy and peripheral neuropathy complications are attributed to the elevated concentration of the pro-inflammatory cytokine TNF-α. This cytokine, recognized as a crucial biomarker, plays a pivotal role in investigating the pathogenesis of diabetes due to its level fluctuations in glomerular, tubular damage, and fibrosis. This study explores the dose-dependent effect of magnesium sulfate on the serum concentration of TNF-α in an animal model induced with paclitaxel.

Twenty-four male Wistar rats with a mean weight of 200±40 g were randomly divided into four groups: three experimental groups (E1, E2, and E3) and a control group, each comprising six mice. To induce neuropathy, paclitaxel (10 mg/kg) was intraperitoneally administered every other day. To prevent neuropathy occurrence, magnesium sulfate (doses of 75, 150, and 300 mg/kg) was intraperitoneally prescribed daily. Sampling was conducted after 10 days, and serums were separated to measure TNF-α concentration using the ELISA method.

The mean±SD serum level of TNF-α in the E1 group (2.31±0.26 pg/ml) significantly increased compared to the control group (1.46±0.21) (P<0.05). In the E3 group, the mean±SD serum level of TNF-α (4.54±1.32) also significantly increased compared to the control group. However, there was an insignificant increase in TNF-α serum level in the E2 group (3.34±1.08) compared to the control group (P>0.05).

This study, confirming the rise in TNF-α serum level induced by paclitaxel, demonstrates that the dose-dependent administration of magnesium sulfate (300 and 150 mg/kg) reduces the potential incidence of nephropathy and peripheral neuropathy by lowering TNF-α serum levels