Molineria recurvata Ameliorates Streptozotocin-Induced Diabetic Nephropathy through Antioxidant and Anti-Inflammatory Pathways.
Prasanta DeyAmit KunduHa Eun LeeBabli KarVineet VishalSuvakanta DashIn Su KimTejendra BhaktaHyung-Sik KimPublished in: Molecules (Basel, Switzerland) (2022)
Molineria recurvata (MR) has been traditionally used to manage diabetes mellitus in India. However, the molecular mechanism of MR on the diabetic-induced nephropathy has not been clearly investigated. Thus, this study investigates the protective effects of the MR extract on nephropathy in streptozotocin (STZ)-induced diabetic rats. Diabetes was instigated by a single intraperitoneal injection of STZ (45 mg/kg) in male Sprague-Dawley rats. Once the diabetes was successfully induced, the MR extract (200 mg/kg/day) or metformin (200 mg/kg/day) was orally administered for 14 days. Renal function, morphology changes and levels of inflammatory cytokines were measured. Blood glucose concentrations were considerably reduced in STZ-induced diabetic rats following treatment with the MR extract. The administration of the MR extract substantially restored the abnormal quantity of the oxidative DNA damage marker 8-hydroxy-2'-deoxy-guanosine (8-OHdG), malondialdehyde, glutathione, oxidized glutathione, superoxide dismutase, catalase, interleukin (IL)-1β, IL-6, IL-10, and transforming growth factor-β (TGF-β). The urinary excretion of kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), selenium binding protein 1 (SBP1), and pyruvate kinase M2 (PKM2) was significantly reduced in diabetes rats after administration of the MR extracts. In the kidneys of STZ-induced diabetic rats, the MR extracts markedly downregulated the expression of fibronectin, collagen-1, and α-smooth muscle actin (α-SMA). In particular, the MR extracts markedly increased the level of SIRT1 and SIRT3 and reduced claudin-1 in the kidney. These results suggest that the MR extracts exhibits therapeutic activity in contrast to renal injury in STZ-induced diabetic rats through repressing inflammation and oxidative stress.
Keyphrases
- diabetic rats
- oxidative stress
- dna damage
- ischemia reperfusion injury
- induced apoptosis
- type diabetes
- contrast enhanced
- magnetic resonance
- transforming growth factor
- anti inflammatory
- blood glucose
- glycemic control
- smooth muscle
- poor prognosis
- blood pressure
- epithelial mesenchymal transition
- heat shock
- nitric oxide
- high resolution
- combination therapy
- skeletal muscle
- adipose tissue
- computed tomography
- signaling pathway
- mouse model
- wound healing
- endothelial cells
- weight loss
- high fat diet
- dna repair
- heat stress