Ethosomal Curcumin Promoted Wound Healing and Reduced Bacterial Flora in Second Degree Burn in Rat.

Background: Curcumin is well known in biomedical investigations with an extensive antimicrobial properties and wound repair effect. However, clinical criteria recommend curcumin should be formulated for topical medication. Material and method: In this study, we prepared Ethosomal curcumin (Etho-cur) formulation for wound healing and bacterial flora assessments in treated rats which were subjected to second degree burn under a standard procedure. Results: Applying once daily of Etho-cur (0.2%) topically on rat's dorsal for 14 days significantly recovered main aspects of wound repair including re-epithelization (P<0.01), neovascularization (P<0.01), collagen synthesis (P<0.001), granulation tissue formation (P<0.001) compared with control. Considerable wound contraction was occurred by Etho-cur treatment sooner than other groups and after 16 days it was completed with a significant (P<0.001) value. Furthermore, ethosomal formulation of curcumin similar to silver sulfadiazine (SSD) cream 1% potentially inhibited (P<0.001) growth of the burn bacterial flora including Pseudomonas aeruginosa as predominant bacteria among experimental isolations during 14 days treatment. Also, antibacterial activity of Etho-cur was estimated approximately 11% more potent than free curcumin in reduction of the burn bacterial flora. Conclusion: Regarding the results, ethosomal curcumin efficiently fights against wound infection and promotes wound repair in burn injuries in rats.

The γ-secretase blocker DAPT impairs recovery from lipopolysaccharide-induced inflammation in rat brain.

γ-Secretase is an important contributing enzyme in Alzheimer's disease and is therefore an important therapeutic target. However, the impact of γ-secretase inhibition is not well studied in acute neuroinflammation induced by systemic infection. In this study the influence of γ-secretase on the expression of some proinflammatory markers was assessed in the acute phase as well as the subsiding phase of neuroinflammation. Cerebral γ-secretase cleavage activity was measured by a fluorometric assay after lipopolysaccharide (LPS) intraperitoneal administration. Time profiles of TNF-α and COX-II expression were then determined to detect the time points relevant to the maximal inflammatory responses and the subsequent recovery phase. γ-Secretase activity coincident with TNF-α protein expression returned to its basal level till 8-12 h after systemic challenge with low dose LPS while COX-II over expression lasted for 48-72 h later. Pharmacological inhibition of γ-secretase with local or systemic administration of DAPT (N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester) was performed to indicate the results on the developmental and sinking phases of inflammatory responses in 6 and 72 h post LPS respectively. Our results demonstrate that both local and systemic modulation of γ-secretase hyper-activity with DAPT increase the duration of TNF-α, COX-II, and NFκB induction. We consistently found mild augmented apoptosis in animals treated with DAPT as determined by measuring cleaved caspase-3 expression and by TUNEL assay 72 h following LPS injection. These results suggest that γ-secretase modulation interferes with certain immune regulatory pathways which may restrict some inflammatory transcription factors such as NFκB.