Tissue distribution study:

In case of Taxol®, plasma absorption
of paclitaxel was nearly negligible at 6 h, and it was readily uptake and clean
by the liver, spleen and lung.Though , when paclitaxel was encapsulated in
liposomes, the plasma concentration was sustained for up to 24 h.

Furthermore , PEGylated
liposomes gave  greater plasma level than
that of conventional liposomes, which is consistent with the results from the
pharmacokinetic study in rats. In tumor tissue, paclitaxel concentration in
PEGylated liposomes was significantly higher than that in conventional
liposomes and in Taxol® at 6 and 24 h. Also, in the case of PEGylated
liposomes, the paclitaxel concentration in tumor was higher than that in
spleen, lung, heart, kidney and brain tissues from 6 h. These results proposed
that PEGylated liposomes were noticeably localized in the tumor tissues.

It look like that
long-circulating time and slow discharge of PEGylated liposomes might offer sufficient
chance for paclitaxel to be achieved at the tumor site through the EPR effect
and preserve the effective therapeutic concentration for a long period of time
through the depot effect.

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Therefore, these results designate
that our PEGylated liposomal formulation successfully increased the antitumor effectiveness
while declining the potential side-effects.

Inhibition of tumor

Since the paclitaxel loaded
classical liposomes and PEGylated liposomes were highly stored in the tumor
tissues of MDA-MB-231 human breast cancer xenograft model, the tumor growth
inhibition effect was further estimated. The study on the control (saline) group
ended on the 35th day reason is that the tumor capacity was extremely enlarged
(about 2000 mm3), while other groups lasted until the 60th day.

PEGylated liposomes inhibited tumor growth most efficiently, followed by the
conventional liposomes and Taxol® (p < 0.05). This improved anti-tumor activity of the PEGylated liposomes can be clarified by the increased local concentration of pacltiaxel near the tumor via EPR effect


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