Lepidium sativum alleviates diabetic nephropathy in a rat model by attenuating glucose levels, oxidative stress, and inflammation with concomitant suppression of TGF-β1

In this research, the treatment of diabetic nephropathy in rats induced by streptozotocin with L. sativium whole-plant aqueous extract was examined, and the mechanism of action was proposed. Adult male rats were grouped into: control, L. sativum, T1DM, and T1DM + L. sativum-treated groups. For 8 weeks, L. sativum S was given to rats at a final dose of 250 mg/kg. Treatment with L. sativum reduced the amount of fasting glucose, increased the amount of fasting insulin, and diminished the increase in hepatic and serum cholesterol, free fatty acid, and triglyceride levels. The level of serum LDL-c was reduced. At the level of the kidney, L. sativum reduced urine volume and albumin excretion and spiked creatinine excretion. It also attenuated the tubular damage in the rats’ kidneys and reduced the amounts of major inflammatory markers, including nuclear factor-kappaα (NF-κB), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6). Interestingly, L. sativium reduced the amount of mRNA transforming growth factor-β1 (TGF-β1), stimulated mRNA superoxide dismutase (SOD) and catalase (CAT), reduced lipid peroxide levels (MDA), and increased the glutathione (GSH), SOD, and CAT in the rat kidneys of the control and T1DM-treated group. In conclusion, L. sativum is a novel therapy against DN owing to its hypoglycemic effect, insulin-releasing, and antioxidant potential.