Arthrospira platensis has
been the
subject of plentiful studies due to its purported health advantages;
nevertheless, additional investigation is required to determine whether
several chronic diseases may be treated or avoided with its nanoform.
Therefore, we set out to examine A. platensis nanoparticles (SNPs) to protect against kidney impairment caused
by Streptozotocin (STZ) in diabetic rats, precisely focusing on its
effect and the cellular intracellular pathways involved. Male Wistar
rats were assigned into four groups: Group 1 was set as control, comprising
the normal rats; group 2 was administered SNPs (0.5 mg/kg BW, once/day)
orally for 84 consecutive days; group 3, STZ-diabetic rats were injected
with STZ (65 mg/kg BW); and group 4, in which the diabetic rats were
treated with SNPs. After inducing diabetes in rats for 84 days, the
animals were euthanized. The results disclosed that SNP treatment
substantially (P < 0.05) improved the glucose
and glycated hemoglobin levels (HbA1c %), insulin, C-peptide, and
cystatin C deterioration in diabetic rats. Furthermore, SNP administration
significantly lowered (P < 0.05) nitric oxide
(NO) and malondialdehyde (MDA) levels in renal tissue and enhanced
kidney function metrics, as well as improved the antioxidant capacity
of the renal tissue. In addition, oral SNPs overcame the diabetic
complications concerning diabetic nephropathy, indicated by downregulation
and upregulation of apoptotic and antiapoptotic genes, respectively,
along with prominent modulation of the antiangiogenic marker countenance
level, improving kidney function. SNP modulated the nuclear factor
erythroid 2-related factor 2 and heme oxygenase-1 (NRF2/HO-1) pathways
and inhibited the nuclear factor-κB (NF-κB) expression,
strengthening the SNP pathways in alleviating diabetic nephropathy.
The histopathology results corroborated the obtained biochemical and
molecular observations, suggesting the therapeutic potential of SNPs
in diabetic nephropathy via mechanisms other than its significant
antioxidant and hypoglycemic effects, including modulation of antiangiogenic
and inflammatory mediators and the NRF2/HO-1 pathways.