Abstract

Curcumin (Cur) exhibits biological activities that support its candidacy for cancer treatment. However, there are limitations to its pharmacological effects, such as poor solubility and bioavailability. Notably, the use of Cur analogs has potential for addressing these limitations. Dehydrozingerone (DZG) is a representative of the half-chemical structure of Cur, and many reports have indicated that it is anticancer in vitro. We, therefore, have hypothesized that DZG could inhibit prostate cancer progression both in vitro and in vivo. Results revealed that DZG decreased cell proliferation of rat castration-resistant prostate cancer, PLS10 cells, via induction of the cell cycle arrest in the G1 phase in vitro. In the PLS10 xenograft model, DZG significantly decreased the growth of subcutaneous tumors when compared to the control via the inhibition of cell proliferation and angiogenesis. To prove that DZG could improve the limitations of Cur, an in vivo pharmacokinetic was determined. DZG was detected in the serum at higher concentrations and remained up to 3 h after intraperitoneal injections, which was longer than Cur. DZG also showed superior in vivo tissue distribution than Cur. The results suggest that DZG could be a candidate of the Cur analog that can potentially exert anticancer capabilities in vivo and thereby improve its bioavailability.

Highlights

  • Prostate cancer is the second cause of cancer-related deaths among men worldwide [1,2]

  • We investigated the effects of DZG onthe cancer progression progression in vitro against rat castration-resistant and incells vivo incancer vitro against rat castration-resistant prostate cancer, PLS10prostate cells andcancer, in vivoPLS10 usingcells the PLS10 using the

  • The results indicated that the cell population in the G1 phase slightly increased from 38% in the control group to 46% in 20 μM of the Cur treatment (Figure 3a)

Read more

Summary

Introduction

Prostate cancer is the second cause of cancer-related deaths among men worldwide [1,2]. The five-year survival rate of early-stage prostate cancer patients is more than 99%, while in the advanced metastatic stage, it is only 28% [3]. A previous study revealed that DZG could inhibit 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced Epstein-Barr virus early antigen (EBV-EA) activation in EBV genome-carrying human based synthesis procedure [13]. A previous study revealed that DZG could inhibit 12-O-tetradecanoylphorbol-13acetate (TPA)-induced Epstein-Barr virus early antigen (EBV-EA) activation in EBV genome-carrying human lymphoblastoid in amanner similarto manner to Cur [15]. We investigated the effects of DZG onthe cancer progression progression in vitro against rat castration-resistant and incells vivo incancer vitro against rat castration-resistant prostate cancer, PLS10prostate cells andcancer, in vivoPLS10 usingcells the PLS10 using the PLS10 cells xenograft model.

2.2.Results
DZG Induced Cell Cycle Arrest in G1 Phase
In Vivo Antitumor Activity
In vivo Pharmacokinetics and Tissue Distribution
Discussion
Reagents
Cell Culture
Animals
Cell Viability Assay
Cell Cycle Analysis
Western Blot Analysis
Immunohistochemistry
4.11. In Vivo Pharmacokinetics and Tissue Distributions
4.12. Serum and Tissue Concentrations of Cur and DZG
4.13. Statistical Analysis
Conclusions
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call