Abstract
Ophiopogonin D (OP-D) is the principal pharmacologically active ingredient from Ophiopogon japonicas, which has been demonstrated to have numerous pharmacological activities. However, its protective effect against renal damage in streptozotocin (STZ)-induced diabetic nephropathy (DN) rats remains unclear. The present study was performed to investigate the protective effect of OP-D in the STZ-induced DN rat model. DN rats showed renal dysfunction, as evidenced by decreased serum albumin and creatinine clearance, along with increases in serum creatinine, blood urea nitrogen, TGF-β1, and kidney hypertrophy, and these were reversed by OP-D. In addition, STZ induced oxidative damage and inflammatory response in diabetic kidney tissue. These abnormalities were reversed by OP-D treatment. The findings obtained in the present study indicated that OP-D might possess the potential to be a therapeutic agent against DN via inhibiting renal inflammation and oxidative stress.
Highlights
Diabetes mellitus is a chronic metabolic disorder, primarily characterized by hyperglycemia arising from insulin insensitivity, damaged secretion of insulin, and inflammatory response [1]
Effect of Ophiopogonin D (OP-D) on renal hypertrophy The renal size of the diabetic nephropathy (DN) rats was increased compared to the control rats, indicating that renal hypertrophy occurred in the DN rats
Previous research indicates that diabetes-evoked metabolites, such as inflammatory markers, glucose, oxidative stress, and others, are involved in the progression and development of DN [9,23]
Summary
Diabetes mellitus is a chronic metabolic disorder, primarily characterized by hyperglycemia arising from insulin insensitivity, damaged secretion of insulin, and inflammatory response [1]. Diabetic nephropathy (DN) is a progressive diabetic complication, which might initially lead to nephrotic syndrome and eventually develop into chronic kidney disease and end-stage renal disease [3]. The full molecular mechanisms involved in the pathogenesis and development of DN is still insufficiently understood, increasing evidence indicates that inflammation and oxidative stress induced by hyperglycemia play a vital role in the progression of DN [4]. Hyperglycemia usually promotes oxidative stress either by altering the redox balance or by excessive generation of reactive oxygen species [5]. Increased oxidative stress and excessive production of reactive oxygen species result in enzyme inactivation, alteration in antioxidant gene expression, and cell membrane injury [6]. The excessive generation of reactive oxygen species causes renal failure, resulting in increased albumin excretion and glomerular barrier dysfunction [7]. Chemically synthesized drugs are unable to effectively slow the progression of DN, the need for developing more effective and novel therapeutic agents to treat DN is urgent
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