ABSTRACT
Aim: To produce and analyze mupirocin nanomicelle (MP-NM) in insulin-based gel. Procedures: MP-NM was prepared using solvent evaporation with Tween 80 as a surfactant. HPMC polymer prepared gel. MP-NM was characterized by globular diameter, polydispersity index (PDI), pH, entrapment efficiency (EE), and transmission electron microscopy (TEM). NM MP release was studied in vitro. Results: The revolutionary MP-NM in insulin-based gel dissolves MP completely without precipitation due to its unique physical and chemical properties. MP had 8.64 ± 0.2 nm globular diameter, high EE (98.85 ± 0.01%), and normal homogeneous dispersion (PDI, 0.143 ± 0.003) in NM. MP's formula showed rapid first-order kinetics release. Conclusion: To our knowledge, this is the first MP-NM nano-drug delivery system employing insulin-based gel. It has promising pre-clinical and clinical uses.
ABSTRACT
OBJECTIVES: To evaluate hepatoprotective potential of carvedilol, prazosin, metoprolol and prazosin plus metoprolol in paracetamol-induced hepatotoxicity. MATERIALS AND METHODS: Thirty-six male rabbits were divided into six groups, six in each, group 1 received distilled water, group 2 were treated with paracetamol (1 g/kg/day, orally), group 3, 4,5 and 6 were treated at a dose in (mg/kg/day) of the following: Carvedilol (10 mg), prazosin (0.5 mg), metoprolol (10 mg), and a combination of metoprolol (10 mg) and prazosin (0.5 mg) respectively 1 h before paracetamol treatment. All treatments were given for 9 days; animals were sacrificed at day 10. Liver function tests, malondialdehyde (MDA) and glutathione (GSH) in serum and liver homogenates were estimated. Histopathological examinations of liver were performed. RESULTS: Histopathological changes of hepatotoxicity were found in all paracetamol-treated rabbits. The histopathological findings of paracetamol toxicity disappeared in five rabbits on prazosin, very mild in one. In carvedilol group paracetamol toxicity completely disappeared in three, while mild in three rabbits. Paracetamol hepatotoxicity was not changed by metoprolol. In metoprolol plus prazosin treated rabbits, moderate histopathological changes were observed. Serum liver function tests and MDA in serum and in liver homogenate were elevated; GSH was depleted after paracetamol treatment and returned back to the control value on prior treatment with prazosin. MDA in serum and liver homogenate, alkaline phosphatase, total bilirubin were significantly decreased after carvedilol and prazosin plus metoprolol treatments. CONCLUSION: Carvedilol and prazosin are hepatoprotective in paracetamol hepatotoxicity, combination of prazosin and metoprolol have moderate, and metoprolol has a little hepatoprotection.
