Brown algae phlorotannins enhance the tumoricidal effect of cisplatin and ameliorate cisplatin nephrotoxicity

Gynecol Oncol. 2015 Feb;136(2):355-64. doi: 10.1016/j.ygyno.2014.11.015. Epub 2014 Nov 20.

Abstract

Objective: The clinical application of cisplatin is limited due to its drug resistance and side effects. We investigated the effect of a phlorotannin-rich extract from the edible brown alga Ecklonia cava (PREC) and its major phlorotannin (dieckol) on cisplatin responsiveness and side effects.

Methods: The A2780 and SKOV3 ovarian cancer cell lines and the SKOV3-bearing mouse model were used. The MTT assay was applied to assess cell viability, and the annexin V assay was employed for apoptosis analysis. Reactive oxygen species (ROS) production and protein expression were assessed by H2DCFDA staining and Western blotting, respectively.

Results: We found that PREC enhanced the tumor growth-inhibitory effect of cisplatin and diminished cisplatin-induced nephrotoxicity and weight loss in SKOV3-bearing mice. PREC augmented cisplatin-induced apoptosis by activating caspases in SKOV3 and A2780 ovarian cancer cells. In addition, a combination of PREC and cisplatin-induced ovarian cancer cell apoptosis by downregulating the Akt and NFκB pathways. We further demonstrated that PREC increased intracellular ROS and that antioxidants significantly attenuated Akt-NFκB activation and apoptosis in ovarian cancer cells. In contrast, PREC inhibited cisplatin-induced ROS production and cell death in normal HEK293 kidney cells. Dieckol, a major compound in PREC, significantly enhanced the inhibition of tumor growth by cisplatin with less weight loss and kidney damage in a mouse model.

Conclusion: These data suggest that brown algae phlorotannins may improve the efficacy of platinum drugs for ovarian cancer by enhancing cancer cell apoptosis via the ROS/Akt/NFκB pathway and reduce nephrotoxicity by protecting against normal kidney cell damage.

Keywords: Cisplatin; Ecklonia cava; Nephrotoxicity; Ovarian cancer; Phlorotannins; ROS/Akt/NFκB pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology*
  • Apoptosis / drug effects
  • Cell Line, Tumor
  • Cisplatin / administration & dosage
  • Cisplatin / pharmacology*
  • Cisplatin / toxicity
  • Drug Synergism
  • Female
  • Humans
  • Kidney Diseases / chemically induced
  • Kidney Diseases / prevention & control
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Ovarian Neoplasms / drug therapy*
  • Ovarian Neoplasms / metabolism
  • Phaeophyceae / chemistry*
  • Random Allocation
  • Reactive Oxygen Species / metabolism
  • Signal Transduction
  • Tannins / administration & dosage
  • Tannins / pharmacology*
  • Xenograft Model Antitumor Assays

Substances

  • Reactive Oxygen Species
  • Tannins
  • Cisplatin