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Lixisenatide protects doxorubicin-induced renal fibrosis by activating wNF-κB/TNF-α and TGF-β/Smad pathways

N-F Guo1, Y-J Cao, X Chen

  • 1Department of Nephrology, the Affiliated Hospital of Nantong University, Nantong, China. chenxl8448@sina.com.

European Review for Medical and Pharmacological Sciences
|May 23, 2019
PubMed
Abstract

Insights

Lixisenatide treatment effectively protected against doxorubicin-induced renal fibrosis in rats by inhibiting key inflammatory pathways, including NF-kB/TNF-α and TGF-β/Smad.

Area of Science:

  • Nephrology
  • Pharmacology
  • Molecular Biology

Background:

  • Doxorubicin (DOX) is a potent chemotherapy agent with known nephrotoxic effects, often leading to renal fibrosis.
  • The precise molecular mechanisms underlying DOX-induced renal fibrosis, particularly the roles of NF-kB/TNF-α and TGF-β/Smad pathways, require further elucidation.

Purpose of the Study:

  • To investigate the protective effects of Lixisenatide against doxorubicin-induced renal fibrosis in a rat model.
  • To determine whether Lixisenatide modulates the NF-kB/TNF-α and TGF-β/Smad signaling pathways in the context of DOX-induced kidney injury.

Main Methods:

  • A rat model of doxorubicin-induced renal fibrosis was established, with animals randomized into sham, DOX, and Lixisenatide treatment groups.
  • Kidney function markers (Cr, BUN), oxidative stress indicators (MDA, T-AOC, CAT, GSH, SOD), and renal histopathology were assessed.
  • Protein expression levels of key genes within the NF-kB/TNF-α and TGF-β/Smad pathways were quantified using immunohistochemistry and Western blot.

Main Results:

  • Lixisenatide treatment significantly improved renal function, evidenced by reduced serum creatinine (Cr) and blood urea nitrogen (BUN) levels.
  • Lixisenatide administration attenuated oxidative stress and reduced kidney tissue damage and apoptosis induced by doxorubicin.
  • The expression of proteins involved in the NF-kB/TNF-α and TGF-β/Smad pathways was significantly downregulated in the Lixisenatide-treated group compared to the DOX group.

Conclusions:

  • Lixisenatide demonstrates significant renoprotective effects against doxorubicin-induced renal fibrosis in rats.
  • These protective effects are mediated through the inhibition of the NF-kB/TNF-α and TGF-β/Smad signaling pathways.
  • Lixisenatide represents a potential therapeutic agent for mitigating chemotherapy-induced kidney damage.

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