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Fluvastatin-Loaded Emulsomes Exhibit Improved Cytotoxic and Apoptosis in Prostate Cancer Cells
Nabil A Alhakamy1,2,3, Shaimaa M Badr-Eldin1,4, Hibah M Aldawsari1,2,3
1Department of Pharmaceutics, Faculty of Pharmacy, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.
Abstract:
Fluvastatin (FLV) is known to inhibit the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA), which is over-expressed in various cancers. FLV has been reported to decrease cancer development and metastasis. However, because of low bioavailability, extensive first-pass metabolism and short half-life of FLV (1.2 h), it is not appropriate for clinical application. Therefore, FLV-loaded emulsomes were formulated and optimized using Box-Behnken experimental design to achieve higher efficiency of formulation. Antitumor activity of optimized FLV-loaded emulsomes was evaluated in prostate cancer cells using cell cytotoxicity, apoptotic activity, cell cycle analysis, and enzyme-linked immunosorbent assay. The FLV-loaded emulsomes exhibited a monodispersed size distribution with a mean particle size less than 100 nm as measured by zetasizer. The entrapment efficiency was found to be 93.74% with controlled drug release profile. FLV-EMLs showed a significant inhibitory effect on the viability of PC3 cells when compared to the free FLV (P < 0.0025). Furthermore, FLV-EMLs showed significant arrest in G2/M and increase in percentage of apoptotic cells as compared to free FLV. FLV-EMLs were more effective than free FLV in reducing mitochondrial membrane potential and increase in caspase-3 activity. These results suggesting that FLV-EMLs caused cell cycle arrest which clarifies its significant antiproliferative effect compared to the free drug. Therefore, optimized FLV-EMLs may be an effective carrier for FLV in prostate cancer treatment.
Insights
New emulsome formulations enhance the effectiveness of Fluvastatin (FLV) for prostate cancer treatment by improving its bioavailability and targeting capabilities. These optimized FLV-emulsomes demonstrate significant antiproliferative effects, offering a promising drug delivery system.
Area of Science:
- Pharmacology
- Nanotechnology
- Oncology
Background:
- Fluvastatin (FLV) inhibits HMG-CoA reductase, an enzyme overexpressed in cancers, showing potential in decreasing cancer development and metastasis.
- FLV's clinical application is limited by low bioavailability, extensive first-pass metabolism, and a short half-life (1.2 hours).
Purpose of the Study:
- To formulate and optimize Fluvastatin-loaded emulsomes (FLV-EMLs) for enhanced prostate cancer treatment.
- To evaluate the antitumor activity of optimized FLV-EMLs in prostate cancer cells.
Main Methods:
- Formulation and optimization of FLV-loaded emulsomes using Box-Behnken experimental design.
- Evaluation of antitumor activity through cell cytotoxicity, apoptosis assays, cell cycle analysis, and ELISA.
- Characterization of emulsome particle size and drug release profile.
Main Results:
- Optimized FLV-EMLs achieved high entrapment efficiency (93.74%) and controlled drug release, with particle size under 100 nm.
- FLV-EMLs significantly inhibited PC3 prostate cancer cell viability compared to free FLV (P < 0.0025).
- FLV-EMLs induced G2/M cell cycle arrest, increased apoptosis, reduced mitochondrial membrane potential, and elevated caspase-3 activity.
Conclusions:
- Optimized FLV-loaded emulsomes demonstrate superior efficacy over free FLV in prostate cancer cells.
- FLV-EMLs effectively induce cell cycle arrest and apoptosis, clarifying their significant antiproliferative effect.
- Optimized FLV-EMLs represent a promising drug delivery system for enhancing Fluvastatin's role in prostate cancer therapy.
