This study aimed to assess the impact of
allicin on the course of
diabetic nephropathy. Study groups included control, diabetes, and diabetes-treated rats.
Allicin treatment (16 mg/kg day/p.o.) started after 1 month of diabetes onset and was administered for 30 days. In the diabetes group, the systolic blood pressure (SBP) increased, also, the oxidative stress and
hypoxia in the kidney cortex were evidenced by alterations in the total
antioxidant capacity as well as the expression of nuclear factor (erythroid-derived 2)-like 2/Kelch ECH associating
protein 1 (Nrf2/Keap1),
hypoxia-inducible factor 1-alpha (HIF-1α),
vascular endothelial growth factor (
VEGF),
erythropoietin (Epo) and its receptor (Epo-R). Moreover, diabetes increased
nephrin, and kidney injury molecule-1 (KIM-1) expression that correlated with mesangial matrix, the
fibrosis index and with the expression of
connective tissue growth factor (CTGF), transforming growth factor-β1 (TGF-β1), and α-smooth muscle actin (α-SMA). The
insulin levels and
glucose transporter protein type-4 (GLUT4) expression were decreased; otherwise,
insulin receptor substrates 1 and 2 (IRS-1 and IRS-2) expression was increased.
Allicin increased Nrf2 expression and decreased SBP, Keap1, HIF-1α, and
VEGF expression. Concurrently,
nephrin, KIM-1, the mesangial matrix,
fibrosis index, and the fibrotic
proteins were decreased. Additionally,
allicin decreased
hyperglycemia, improved
insulin levels, and prevented changes in (GLUT4) and IRSs expression induced by diabetes. In conclusion, our results demonstrate that
allicin has the potential to help in the treatment of
diabetic nephropathy. The cellular mechanisms underlying its effects mainly rely on the regulation of
antioxidant, antifibrotic, and
antidiabetic mechanisms, which can contribute towards delay in the progression of renal disease.