Protective effect of rutin against diabetes-associated cognitive decline in rats.

Diabetes is a well-known risk factor for cognitive deficit. Rutin (RUT) possesses diverse pharmacological activities and is widely used in diabetic complication. The aim of this study is to assess the improvement of RUT on diabetes-associated cognitive decline (DACD). In our study, Morris water maze was examined to estimate cognitive function. In hippocampus tissue, spectrophotometer was performed to evaluate super oxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), malondialdehyde (MDA), acetyl cholinesterase (AChE) and choline acetyl transferase (ChAT) levels. Quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) were utilized to analyze Tumor necrosis factor-a (TNF-a) and interleukin-1ß (IL-1ß) contents. Western blot was used to detect the protein expressions of brain derived neurotrophic factor (BDNF), glial fibrillary acidic protein (GFAP), nuclear factor erythroid-2-related factor-2 (Nrf-2) and heme oxygenase-1 (HO-1). Our data revealed that RUT markedly improved learning and memory capacities in Morris water maze test. In hippocampus, RUT markedly inhibited AChE, GFAP MDA, TNF-a and IL-1ß levels and augmented ChAT and BDNF, SOD, CAT, GSH, Nrf-2 and HO-1 levels. In conclusion, RUT may be involved in protection efficacy against STZ-induced cognitive deficits via improvement of oxidative stress, inflammatory response and Nrf-2/HO-1 pathway.

Sinapic acid attenuates muscle atrophy in streptozotocin-induced diabetic mice.

Objectives: Diabetes is fundamentally connected with the inability of skeletal muscle. Sinapic acid (SA) has multiple biologic functions and is diffusely utilized in diabetic complications. The purpose of this study was to explore the potential improvement effect and mechanisms of SA in streptozotocin (STZ)-induced diabetic muscle atrophy. Materials and Methods: The model of diabetic mice was established by intraperitoneal STZ (200 mg/kg) to evaluate the treatment effect of SA (40 mg/kg/d for 8 weeks) on muscle atrophy. Muscle fiber size was assessed by Hematoxylin and Eosin (HE) staining. Muscle force was measured by a dynamometer. Biochemical parameters were tested by using corresponding commercial kits. The expressions of Atrogin-1, MuRF-1, nuclear respiratory factor 1 (NRF-1), peroxisome proliferative activated receptor gamma coactivator 1 alpha (PGC-1α), CHOP, GRP-78, BAX, and BCL-2 were detected by Western blot. Results: Our data demonstrated that SA increased fiber size and weight of gastrocnemius, and enhanced grip strength to alleviate diabetes-induced muscle atrophy. In serum, SA restrained creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), tumor necrosis factor (TNF-a), and interleukin 6 (IL-6) levels, while enhancing total anti-oxidant capacity (T-AOC), superoxide dismutase (SOD) and catalase (CAT) levels to improve muscle injury. In gastrocnemius, SA promoted NRF-1, PGC-1α, and BCL-2 expressions, while inhibiting Atrogin-1, MuRF-1, CHOP, GRP-87, and BAX expressions. Conclusion: SA protected against diabetes-induced gastrocnemius injury via improvement of mitochondrial function, endoplasmic reticulum (ER) stress, and apoptosis, and could be developed to prevent and treat diabetic muscle atrophy.