Abstract
Salvianolic acid A (SalA) is one of the main efficacious, water-soluble constituents of Salvia miltiorrhiza Bunge. This study investigated the protective effects of SalA on peripheral nerve in diabetic rats. Administration of SalA (0.3, 1 and 3 mg/kg, ig) was started from the 5th week after strepotozotocin (STZ60 mg/kg) intraperitoneal injection and continued for 8 weeks. Paw withdrawal mechanical threshold (PWMT) and motor nerve conduction velocity (MNCV) were used to assess peripheral nerve function. The western blot methods were employed to test the expression levels of serine-threonine liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1α), silent information regulator protein3 (sirtuin 3/Sirt3) and neuronal nitric oxide synthase (nNOS) in sciatic nerve. Results showed that SalA administration could increase PWMT and MNCV in diabetic rats; reduce the deterioration of sciatic nerve pathology; increase AMPK phosphorylation level, up-regulate PGC-1α, Sirt3 and nNOS expression, but had no influence on LKB1. These results suggest that SalA has protective effects against diabetic neuropathy. The beneficial effects of SalA on peripheral nerve function in diabetic rats might be attributed to improvements in glucose metabolism through regulation of the AMPK-PGC1α-Sirt3 axis.
Highlights
The World Health Organization (WHO) predicts that by 2025 there will be 300 million people with diabetes
The paw withdrawal threshold decreased by 22.4% in diabetic rats compared with that in normal control rats (p < 0.05)
The alleviation of motor nerve conduction velocity (MNCV) deficits were observed in Salvianolic acid A (SalA)-treated groups, of which only
Summary
The World Health Organization (WHO) predicts that by 2025 there will be 300 million people with diabetes. Long-lasting hyperglycaemia is thought to trigger the energy metabolism disorders and generate more reactive oxygen species (ROS), resulting in metabolic stress and excessive oxidative stress, which could promote the development of diabetic complications [3]. It is reported that nutrient excess associated with prolonged diabetes may trigger a switching off of AMPK and/or silence information regulator T1 (Sirt1) signaling, which leads to impaired peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) activity and diminished mitochondrial activity [8]. Sirtuins are attractive targets for drug discovery, and determination of specific sirtuin inhibitors and activators may provide treatments for metabolic disorders and many age-related neurodegenerative diseases [10]. We have demonstrated that SalA could restore vascular reactivity in diabetic rats, and could prevent the development of diabetic foot problems [12,13]. We evaluated the effects of SalA on peripheral nerve dysfunction in streptozotocin (STZ)-induced type 1 diabetic rats, and investigated the potential mechanisms
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