Abstract:
:The present study aimed to investigate the antifibrogenic effects of genistein (GEN) on the kidney in streptozotocin (STZ)‑induced diabetic rats and to determine the associated mechanisms. Rats were randomized into four groups: Normal control (N), STZ (S), L (STZ + low‑dose GEN) and H (STZ + high‑dose GEN). After 8 weeks, the fasting blood glucose (FBG) level, the ratio of kidney weight to body weight (renal index), 24‑h urine protein, blood urea nitrogen (BUN), serum creatinine (SCr), renal total antioxidant capacity (T‑AOC), superoxide dismutase (SOD), lipid peroxidation (LPO), malondialdehyde (MDA) and hydroxyproline (Hyp) contents were measured. The histomorphology and ultrastructure of the kidney were also assessed. In addition, mRNA expression levels of transforming growth factor‑β1 (TGF‑β1) and protein expression levels of nuclear factor erythroid 2‑related factor 2 (Nrf2), heme oxygenase‑1 (HO‑1), NAD(P)H:quinone oxidoreductase 1 (NQO1), TGF‑β1, mothers against decapentaplegic homolog 3 (Smad3), phosphorylated (p)‑Smad3 and collagen IV were estimated. Compared with group N, the levels of FBG, renal index, 24‑h urine protein, BUN, SCr, LPO, MDA and Hyp were increased, whereas the levels of T‑AOC and SOD were decreased in group S. The structure of renal tissue was damaged, and the expression of Nrf2, HO‑1 and NQO1 were reduced, whereas the expression of TGF‑β1, Smad3, p‑Smad3 and collagen IV were increased in group S. Compared with group S, the aforementioned indices were improved in groups L and H. In conclusion, GEN exhibited reno‑protective effects in diabetic rats and its mechanisms may be associated with the inhibition of oxidative stress by activating the Nrf2‑HO‑1/NQO1 pathway, and the alleviation of renal fibrosis by suppressing the TGF‑β1/Smad3 pathway.
journal_name
Mol Med Repjournal_title
Molecular medicine reportsauthors
Jia Q,Yang R,Liu XF,Ma SF,Wang Ldoi
10.3892/mmr.2018.9635subject
Has Abstractpub_date
2019-01-01 00:00:00pages
423-431issue
1eissn
1791-2997issn
1791-3004journal_volume
19pub_type
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