ABSTRACT
This study examined the effectiveness of niosomes loaded with levofloxacin in treating Pseudomonas aeruginosa (American Type Culture Collection-ATCC 27853) infections in Sprague Dawley rats since these infections are becoming more common and resistant to treatment. Levofloxacin entrapped in niosomes was prepared using the thin-film hydration method and was assessed for in vitro release and stability. Three groups of six (6) animals were infected with a lethal dose of Pseudomonas aeruginosa via the intraperitoneal (Ip) route. At six (6) hours postinfection, the animals were treated with either drug-free niosomes (control), free levofloxacin (conventional), or levofloxacin trapped in niosomes (Ip) at a dose of 7.5 mg/kg/once daily. Blood was collected via tail snips on days 0, 1, 3, 5, 7, and 10 for complete blood counts and viable bacterial counts (CFU/µl). At day 10, the animals were sacrificed, and the kidney, liver, and spleen were harvested for bacterial counts. The niosomes showed a sustained drug release profile and were most stable at 4°C. All animals in the control group succumbed to the infection; one animal from the conventional group died, and all niosome treated animals survived at day 10. The mean lymphocyte count (×109) was lower for the niosome (7.258 ± 1.773) versus conventional group (17.684 ± 10.008) (p < 0.03) at day ten (10). Neutrophil counts (×109) were lower for the niosome (2.563 ± 1.609) versus conventional (6.2 ± 6.548) (p < 0.02) groups. Though CFUs in the bloodstream were comparable for both treatment groups, the niosome treated group showed a significant reduction of CFUs in the liver, kidney, and spleen versus the conventional group (1.33 ± 2.074) vs (5.8 ± 3.74) (p < 0.043), (1.5 ± 2.35) vs (9.6 ± 8.65) (p < 0.038) and (3.8 4.71) vs (25.6 14.66) (p < 0.007), respectively. These findings indicate that niosome is promising as a drug delivery system in treating systemic infections, but further work using niosomes with surface modification is recommended.
ABSTRACT
In order to achieve sustained antiplatelet effect from indomethacin, it was incorporated in a non-ionic surfactant vesicle (niosome). The objective was to study the effect of niosomal-encapsulated indomethacin on platelet function such as inhibition of aggrregation and ATP release induced by a variety of agonists (adenosine 5'-diphosphate (ADP)epinephrine, and arachidonic acid, ristocetine) and to explore the feasibilty of carrier-mediated drug delivery to the platelets. Multilamellar vesicles (niosomes) were prepared from Tween-60 by the lipid hydration method. Freshly prepared human platelet rich plasma (PRP) was used for aggregation/inhibition studies, the extent of which was observed as a change in light transmission measured by the Chronolog Aggregometer. The percent inhibition induced by the agonist ADP ranged from 28.21 ñ 0.28 at the æmol. level to 92.6 ñ 1.20 at 12.7 æmol. of the encapsulated drug while the same concentrations of the drug inhibited aggregation only to the extent of 13.75 ñ 0.13 and 36.82 ñ 0.57 percent respectively. A 100 percent inhibition of aggregation induced by arachidonic acid was achieved by niosomal indomethacin while inhibition by the free drug was 41.9 percent at equimolar concentrations. ATP release study showed that 100 percent inhibition was achieved by 8 æmol. of the encapsulated drug while inhibition by the free drug was 40.00 ñ 1.82 percent. Therefore, at equimolar doses, the niosomal drug proved to be more efficient in inhibiting platelet aggregation than the free drug, probably due to greater quantity of the drug reaching the specific site of inhibition in the interior of the platelets and acting directly on the cyclo-oxygenase system to prevent thromboxane formation(AU)