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Doxorubicin chemotherapy causes neurotoxicity known as chemobrain. Dapagliflozin, an SGLT2 inhibitor, protected against doxorubicin-induced chemobrain by improving neurogenesis and synaptic integrity in rats.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Oncology

Background:

  • Doxorubicin chemotherapy can induce neurological deficits, termed chemobrain, characterized by impaired neurogenesis and synaptic plasticity.
  • Sodium-glucose co-transporter 2 (SGLT2) inhibitors, such as dapagliflozin, possess neuroprotective properties independent of their glucose-lowering effects.

Purpose of the Study:

  • To investigate the potential neuroprotective effects of dapagliflozin in a rat model of doxorubicin-induced chemobrain.

Main Methods:

  • Adult male Wistar rats were administered doxorubicin (DOX) or doxorubicin plus dapagliflozin (DOX-DAPA) for 30 days.
  • Control rats received normal saline (NSS).
  • Hippocampal tissue was analyzed for molecular markers of neurogenesis and synaptic plasticity.

Main Results:

  • Doxorubicin treatment led to chemobrain, evidenced by reduced BDNF, SOX2, DCX, NeuN, and PSD-95 protein expression, and decreased dendritic spine density in the hippocampus.
  • Dapagliflozin co-treatment significantly increased DCX and PSD-95 protein levels and restored dendritic spine density compared to doxorubicin-only treated rats.

Conclusions:

  • Doxorubicin induces chemobrain through impaired adult neurogenesis and synaptic integrity.
  • Dapagliflozin demonstrates neuroprotective effects, mitigating doxorubicin-induced chemobrain.
  • Dapagliflozin presents a potential therapeutic strategy for managing doxorubicin-related neurotoxicity.