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Morin hydrate attenuates adenine-induced renal fibrosis via targeting cathepsin D signaling

Mahendra Pal Singh1, Chanchal Sharma2, Sun Chul Kang2

  • 1Department of Biotechnology, Daegu University, Gyeongsan, Gyeongbuk 38453, Republic of Korea; Department of Immunology, Mayo Clinic, Rochester MN55905, USA.

International Immunopharmacology
|December 14, 2020
PubMed

Insights

Morin hydrate (MH) effectively modulated cathepsin D (CATD) to reduce kidney fibrosis and inflammation in a mouse model of chronic kidney disease (CKD). This intervention improved kidney function and survival rates.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Pharmacology

Background:

  • Lysosomal proteases, including cathepsins, are implicated in organ fibrosis.
  • The specific role of cathepsin D (CATD) in kidney fibrosis and chronic kidney disease (CKD) remains unclear.
  • Investigating therapeutic strategies to target CATD in kidney fibrosis is crucial.

Purpose of the Study:

  • To investigate the potential of morin hydrate (MH) in modulating cathepsin D (CATD) to attenuate kidney fibrosis in a mouse model of CKD.
  • To elucidate the mechanisms by which MH affects fibrosis, inflammation, and kidney function.

Main Methods:

  • Chronic kidney disease (CKD) was induced in mice using adenine (AD) administration.
  • Histopathological analysis (H&E, Oil-Red-O), serum biochemistry (creatinine, albumin, BUN), and molecular analyses (MMP-2, MMP-9, MCP-1, COX-2) were performed.
  • Molecular docking was used to predict the binding interaction between MH and CATD.

Main Results:

  • MH treatment significantly reduced kidney fibrosis, evidenced by decreased collagen fragmentation and lower levels of MMP-2 and MMP-9.
  • MH modulated CATD expression and reduced inflammation markers (MCP-1, COX-2).
  • MH treatment improved kidney function, increased body weight, and enhanced survival rates by approximately 150% in AD-treated mice.

Conclusions:

  • Morin hydrate (MH) effectively attenuates kidney fibrosis and inflammation in a mouse model of chronic kidney disease (CKD) by modulating cathepsin D (CATD).
  • MH treatment improves renal function and survival, suggesting its therapeutic potential for CKD.
  • Targeting CATD with MH offers a promising strategy for managing kidney fibrosis.
Keywords:
Cathepsin DChronic kidney diseaseExtracellular matrixInflammationKidney fibrosisMatrix metalloproteinases

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