Liposomes protected EGCG from degradation, resulting in the induction of greater BCC death compared to that by free EGCG at lower concentrations.
These results suggest that the intratumor injection of liposomes containing EGCG with moderate modification is an effective approach for increasing EGCG deposition in BCCs.
EGCG encapsulated in liposomes with deoxycholic acid (DA) and ethanol increased drug deposition by 20-fold as compared to the free form.
The liposomes without ethanol showed low or negligible enhancement on EGCG uptake in BCCs.
In order to clarify the sealing effect of EGCG, we prepared liposomes and examined inhibition of PKC activation by various concentrations of EGCG dispersed in the liposome.
The potency of inhibitory effect of EGCG on PKC activation was dependent on the nature of liposomes, indicating that interaction of EGCG with phospholipid bilayer membrane affects PKC activation.
The proportion of EGCG incorporated into liposomes treated with the mixture of EGCG and Zn2+ at the ratio of 1:1 was 90.57%, which was significantly higher than that treated with EGCG alone (30.33%).
The intranasal quercetinliposomes are effective in the delivery of quercetin to the central nervous system.
A lower dose and a faster rate were observed with intranasal quercetinliposomes when compared with oral quercetin, conventional and liposomal.
Oral quercetin (300 mg/kg body weight/day) was compared with oral and intranasal quercetinliposomes (20 microg/day).
Anxiolytic and cognitive-enhancing effects of quercetin, conventional and liposomal, were subjected to elevated plus maze and Morris water maze tests, respectively.
Spectrophotometric analysis of brain tissue with the TTC-technique showed that liposomalquercetin reduced ischemic damage and infarct volume after permanent occlusion of the middle cerebral artery (ischemic: 41.3 mm3 vs liposomalquercetin: 17 mm3).
Aqueous and liposomal preparations of quercetin, fisetin and catechin were administered IP in a single dose and assessed in the brain by HPLC at 30 min, 1 h, 2 h and 4 h.
Cerebral concentrations of catechin (10.5 ng/g), fisetin (8.23 ng/g) and quercetin (509 ng/g) were detected in the brain only after IP injection of the liposomal preparations.
In conclusion, early administration of liposomal preparations of quercetin and structurally related flavonoids are beneficial and neuroprotective in experimental focal ischemia.
Our results showed that liposomalquercetin diminished the increase of total cell counts and macrophage counts in bronchoalveolar lavage fluid.
Thus, our results suggested that liposomalquercetin could attenuate the bleomycin-induced pulmonary fibrosis in vivo by the suppression of inflammatory cytokines.
Histopathological assessment revealed that treatment with liposomalquercetin apparently lessened the lung fibrosis areas and collagen deposition accompanied with decreased expression of TGF-beta1.
The levels of TNF-alpha, IL-1beta, and IL-6 in bronchoalveolar lavage fluid at day 7 were strikingly reduced in liposomalquercetin treated group compared with bleomycin-induced group (TNF-alpha: 56.21+/-3.16 pg/ml vs.79.85+/-6.91 pg/ml; IL-1beta: 37.64+/-2.10 pg/ml vs. 73.29+/-5.78 pg/ml; IL-6: 88.52+/-5.96 pg/ml vs. 128.56+/-8.72 pg/ml; P<0.05).
To explore the effect of cell proliferation, c-met and vascular endothelial growth factor (VEGF) expression by liposomalquercetin in the Eca109/9706 cells induced by liposomalquercetin.
The liposomalquercetin could suppress the proliferation of culture Eca109/9706 cells, which was about to be related with the suppression high expression of c-met and VEGF.
After 48-hour-exposure to liposomalquercetin, the expression and cellular localization of c-met and VEGF in Eca109/9706 cells were examined by using immunohistochemistry assay and Western blotting.
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