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Functionalized selenium nanoparticles with nephroprotective activity, the important roles of ROS-mediated signaling

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Selenium nanoparticles functionalized with trolox (Se@Trolox) show promise in preventing kidney damage caused by cisplatin chemotherapy. Se@Trolox effectively reduced oxidative stress and protected kidney cells from chemotherapy-induced toxicity.

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Area of Science:

  • Nanomedicine
  • Biochemistry
  • Toxicology

Background:

  • Cisplatin chemotherapy frequently causes nephrotoxicity, a significant clinical challenge.
  • Oxidative stress is a key mechanism driving cisplatin-induced kidney damage.

Purpose of the Study:

  • To investigate the nephroprotective effects of trolox-functionalized selenium nanoparticles (Se@Trolox).
  • To evaluate Se@Trolox's ability to mitigate cisplatin-induced nephrotoxicity.

Main Methods:

  • Preparation of Se@Trolox nanoparticles via self-assembly.
  • Assessment of cell uptake and in vitro antioxidant activity.
  • Evaluation of Se@Trolox's protective effects against cisplatin in HK-2 cells.
  • Mechanistic studies involving apoptosis markers, reactive oxygen species (ROS), and signaling pathways (AKT, MAPK, p53).

Main Results:

  • Trolox functionalization enhanced nanoparticle cell uptake and antioxidant capacity.
  • Se@Troxtreatment dose-dependently inhibited cisplatin-induced cell death in HK-2 cells.
  • Se@Trolox prevented cisplatin-induced apoptosis by inhibiting DNA fragmentation, PARP cleavage, and caspase-3 activation.
  • Se@Trolox suppressed ROS accumulation, AKT/MAPK signaling activation, and p53 phosphorylation.

Conclusions:

  • Se@Trolox exhibits significant nephroprotective properties against cisplatin toxicity.
  • The protective mechanism involves reducing oxidative stress and inhibiting apoptosis.
  • Se@Trolox represents a promising selenium-based therapeutic strategy for preventing cisplatin-induced renal injury.