Protective effects of bendazac lysine on diabetic peripheral neuropathy in streptozotocin-induced diabetic rats

Jun-Xian Yu1, Xiao-Xing Yin, Jian-Ping Shen

  • 1Department of Pharmacology, Nanjing Medical University, Nangjing, PR China.

Insights

Bendazac lysine (BDL) shows promise in treating diabetic peripheral neuropathy (DPN). This anticataract drug improved nerve function and reduced diabetes-related complications in rats, suggesting a potential therapeutic role.

Area of Science:

  • Neuroscience
  • Endocrinology
  • Pharmacology

Background:

  • Diabetic peripheral neuropathy (DPN) is a significant complication of type I and II diabetes.
  • Existing treatments for DPN have limitations, necessitating the exploration of novel therapeutic agents.

Purpose of the Study:

  • To investigate the efficacy of bendazac lysine (BDL), an anticataract drug, in ameliorating experimental diabetic peripheral neuropathy (DPN) in a rat model.
  • To explore the underlying mechanisms by which BDL may exert protective effects against DPN progression.

Main Methods:

  • Diabetes was induced in rats using streptozotocin (STZ).
  • Bendazac lysine (BDL) was administered at varying doses (50, 100, 200 mg/kg) twice daily for 12 weeks.
  • Neurological, biochemical, and pathological parameters were assessed to evaluate treatment effects.

Main Results:

  • BDL treatment significantly ameliorated symptoms of DPN, including improved nerve conduction velocity and reduced nerve fiber damage in STZ-diabetic rats.
  • BDL administration normalized blood glucose, glycosylated hemoglobin, and insulin levels, while reducing aldose reductase activity and advanced glycation end-products.
  • The drug increased the activity of protective enzymes like glutathione peroxidase and Na(+)/K(+)-ATPase in nerve tissues and erythrocytes.

Conclusions:

  • Bendazac lysine (BDL) demonstrates significant protective effects against the progression of diabetic peripheral neuropathy in a rat model.
  • BDL acts through multiple mechanisms, including antioxidant and anti-glycation pathways, to prevent nerve damage.
  • BDL is a potential therapeutic agent for preventing the deterioration of DPN in diabetic patients.