Abstract
The study aimed to develop the finasteride-loaded proniosome (FLP) to enhance the transfollicular delivery of finasteride (FN). The response surface methodology (RSM) combined with central composite design (CCD) with three independent variables (FN concentrations, total lipid content, and cholesterol content) was used to optimize the FLP preparation. The particles size, zeta potential, entrapment efficiency, and drug loading capacity of the FLP were analyzed. The transfollicular delivery of the optimum formulation was investigated in vitro. In vivo hair growth stimulation study was performed on C57BL/6Mlac mice dorsal areas. The Draize primary skin irritation test for erythema and edema was performed in the New Zealand white rabbit skin. The optimum FLP consists of 5.0 mM of FN, 10.1 mM of total lipid content, and 50.0% of the cholesterol in the total lipid. The prepared proniosome delivered the FN significantly (p < 0.05), compared to the naked finasteride solution in a dose- and time-dependent manner. The FLP treatment significantly increases the number and size of hair follicles in a dose-dependent manner. The efficiency of 1% FLP was comparable to the 2% minoxidil solution. The FLP exhibited no skin irritation after 72 h. Therefore, the results demonstrated that the FLP could stimulate hair growth via a transfollicular delivery system.
Highlights
Finasteride (FN) is approved as the first specific competitive inhibitor of 5α-reductase for the treatment of benign prostatic hyperplasia (BPH) and androgenic alopecia (AA) [1,2,3].Several reports suggest that male pattern hair loss or AA are linked to dihydrotestosterone (DHT) [4,5]
finasteride-loaded proniosome (FLP) was developed using response surface methodology (RSM) combined with central composite design (CCD)
The size of the particle was in the range of 220–346 nm in diameter, and the encapsulation efficacy (EE) was about
Summary
Finasteride (FN) is approved as the first specific competitive inhibitor of 5α-reductase for the treatment of benign prostatic hyperplasia (BPH) and androgenic alopecia (AA) [1,2,3]. Several reports suggest that male pattern hair loss or AA are linked to dihydrotestosterone (DHT) [4,5]. DHT on the hair follicles was metabolized from testosterone by 5αreductase [6]. Two isoforms of 5α-reductase are Type I and Type II, the former present in the skin and outer root sheath of the hair follicles, and the latter most evident in the prostate, seminal vesicles, and inner epithelial root sheath of hair follicles. Type II 5α-reductase activity in the dermal papillae of hair follicles has been reported as the major cause of AA. FN is a 5α-reductase inhibitor with a higher affinity to the Type II isoenzyme.
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