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Curcumin analogue C66 attenuates hypertensive nephropathy by inhibiting JNK-mediated inflammation

Yudie Yang1, Hanghui He2, Leiming Jin3

  • 1Department of Endocrinology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.; Medical Research Center, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325035, China; Chemical Biology Research Center, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.

International Immunopharmacology
|June 26, 2026
PubMed

Insights

C66, an anti-inflammatory compound, effectively treats hypertensive nephropathy (HTN) by inhibiting JNK-mediated inflammation and reversing kidney damage. This offers a potential new therapy for this disabling condition.

Area of Science:

  • Nephrology
  • Pharmacology
  • Inflammation research

Background:

  • Hypertensive nephropathy (HTN) is a severe complication of hypertension, marked by fibrosis, oxidative stress, and chronic inflammation.
  • Chronic inflammation persists in HTN pathogenesis, even with renin-angiotensin-aldosterone system (RAAS) blockade.
  • C66, a curcumin derivative, previously prevented metabolic diseases by inhibiting c-Jun N-terminal kinase (JNK), a key inflammatory target.

Purpose of the Study:

  • To investigate the potential of C66 in preventing hypertensive nephropathy (HTN) by suppressing JNK-mediated inflammation.
  • To elucidate the role of JNK activation in renal tubular epithelial cells during HTN.

Main Methods:

  • Mice were treated with Angiotensin II (Ang II) to induce nephropathy and RAAS overactivity.
  • C66 was administered to a subset of Ang II-treated mice.
  • Renal pathology, fibrosis, inflammation, and JNK activation were assessed in vivo and in vitro using rat renal tubular epithelial cells (NRK52E).

Main Results:

  • Ang II-induced nephropathy in mice showed significant renal tubular injuries, fibrosis, and inflammation with increased pro-inflammatory cytokines.
  • C66 treatment remarkably reversed these pathological changes by inhibiting JNK-mediated inflammation.
  • JNK activation was specifically observed in renal tubular epithelial cells in HTN models.
  • C66 attenuated Ang II-induced fibrosis and inflammation in rat renal tubular epithelial cells.

Conclusions:

  • C66 effectively inhibits JNK-mediated chronic inflammation in hypertensive nephropathy (HTN).
  • C66 demonstrates potential as a therapeutic agent for HTN by targeting JNK pathways in renal tubular epithelial cells.
  • The findings highlight C66's efficacy in reversing kidney damage associated with hypertension.

Keywords:
C66Curcumin derivativeHypertensive nephropathyInflammationJNK

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