Sinapic acid attenuates muscle atrophy in streptozotocin-induced diabetic mice

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.

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.

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.

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.