Neuroprotective properties of aucubin in diabetic rats and diabetic encephalopathy rats

Abstract

In this study, we determined the neuroprotective effect of aucubin on diabetes and diabetic encephalopathy. With the exception of the control group, all rats received intraperitoneal injections of streptozotocin (STZ; 60 mg/kg) to induce type 1 diabetes mellitus (DM). Aucubin (1, 5, 10 mg/kg ip) was used after induction of DM (immediately) and diabetic encephalopathy (65 days after the induction of diabetes). The diabetic encephalopathy treatment groups were divided into short-term and long-term treatment groups. Treatment responses to all parameters were examined (body weight, plasma glucose, Y-maze error rates and proportion of apoptotic cells). In diabetic rats, aucubin controlled blood glucose levels effectively, prevented complications, and improved the quality of life of diabetic rats. In diabetic encephalopathy, aucubin significantly rescued neurons in the hippocampal CA1 subfield and reduced working errors during behavioral testing. The significant neuroprotective effect of aucubin could be seen not only in the short term (15 days) but also in the long term (45 days), which was a highly encouraging finding. These data suggest that aucubin may be a potential neuroprotective agent.

Quantitative profiling of neurotransmitter abnormalities in brain, cerebrospinal fluid, and serum of experimental diabetic encephalopathy male rat

“…Diabetes mellitus (DM), a metabolic disease caused by the deficiency of insulin or the weak response to insulin produced by the body (Xue et al, ), is associated with the occurrence of well‐described microvascular complications, including retinopathy, nephropathy, cardiomyopathy, and peripheral neuropathy. Emerging evidence suggests that diabetes may also have negative effects on the central nervous system (CNS), including a series of neurochemical, neurophysiological, and structural abnormalities (Biessels, Staekenborg, Brunner, Brayne, & Scheltens, ; Chuiko, Bodykhov, & Skvortsova, ), which cumulatively contribute to the prevalence of diabetic encephalopathy (DE).…”

Endoplasmic reticulum stress-induced neuronal inflammatory response and apoptosis likely plays a key role in the development of diabetic encephalopathy

“…Therefore, we hypothesize that ER stress may play a key role in the pathogenesis of DEP. However, most of previous studies have mainly used T1DM animal models [20, 21]. Since two types of diabetes have significant difference for the pathogenic factors to the peripheral tissues, whether the ER stress plays the universal role in the development of DEP, and what is the mechanisms by which ER stress initiates the development of DEP all remain incompletely understood.…”

Encefalopatia Diabética E Depressão: Dano Oxidativo No Cérebro

“…Dados de estudos experimentais anteriores demonstram que a acubina pode evitar a apoptose modulando a expressão de genes relacionados a apoptose Bcl-2 e Bax 85 . O efeito neuroprotetor, a melhora da cognição e proteção contra a perda de neurônios ocorre tanto em curto quanto em longo prazo no tratamento experimental com acubina 86 .…”