Key result
Catalpol reduces urinary protein excretion ~47% in diabetic mice, correlating with down-regulated Grb10 expression.
Why the study?
It is unknown whether Grb10 expression is up-regulated and plays a role in diabetic nephropathy and whether catalpol has therapeutic effects on this condition.
Does catalpol treatment improve renal function and pathology in a mouse model of diabetic nephropathy?
Does catalpol treatment improve renal function and pathology in a mouse model of diabetic nephropathy?
Absolute Event Rate: 0.4939% vs 0.9362%
p-value: p=<0.05
Catalpol ameliorates diabetic nephropathy in mice, potentially by down-regulating Grb10 and activating the IGF-1/IGF-1R signaling pathway.
Hypothesis-generating for catalpol in diabetic nephropathy; leaves open translation to human therapy.
Growth factor receptor-bound protein 10 (Grb10) is an adaptor protein that can negatively regulate the insulin-like growth factor 1 receptor (IGF-1R). The IGF1-1R pathway is critical for cell growth and apoptosis and has been implicated in kidney diseases; however, it is still unknown whether Grb10 expression is up-regulated and plays a role in diabetic nephropathy. Catalpol, a major active ingredient of a traditional Chinese medicine, Rehmannia, has been reported to possess anti-inflammatory and anti-aging activities and then used to treat diabetes. Herein, we aimed to assess the therapeutic effect of catalpol on a mouse model diabetic nephropathy and the potential role of Grb10 in the pathogenesis of this diabetes-associated complication. Our results showed that catalpol treatment improved diabetes-associated impaired renal functions and ameliorated pathological changes in kidneys of diabetic mice. We also found that Grb10 expression was significantly elevated in kidneys of diabetic mice as compared with that in non-diabetic mice, while treatment with catalpol significantly abrogated the elevated Grb10 expression in diabetic kidneys. On the contrary, IGF-1 mRNA levels and IGF-1R phosphorylation were significantly higher in kidneys of catalpol-treated diabetic mice than those in non-treated diabetic mice. Our results suggest that elevated Grb10 expression may play an important role in the pathogenesis of diabetic nephropathy through suppressing IGF-1/IGF-1R signaling pathway, which might be a potential molecular target of catalpol for the treatment of this diabetic complication.
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Yang et al. (2016) studied Diabetic nephropathy (n=35). Catalpol vs. Normal saline was evaluated on 24h urinary protein excretion (mg/24h) (p=<0.05). Catalpol treatment significantly reduced 24-hour urinary protein excretion, blood urea nitrogen, and serum creatinine in diabetic mice compared to untreated diabetic controls, correlating with down-regulated Grb10 expression.
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