Albumin is a versatile drug carrier in anti-cancer drug delivery system and it also has an actively targeting capacity to tumors. Recently, nanoparticle albumin-bound (nab) paclitaxel (nab-paclitaxel; Abraxane) has been approved in 2006 for use in patients with metastatic breast cancer who have failed in the combination chemotherapy, and so the nab-technology has attracted much interest in the anti-cancer drug delivery system. The details about the preparation, characterization and evaluation of nab-paclitaxel (ABI-007) are discussed. The pharmacokinetics, pharmacodynamics and the clinical trials of ABI-007 are also reviewed. Furthermore, the recent applications of nab-technology in the anti-cancer drug delivery systems are summarized by virtue of the patents pertaining to nab-technology. To sum up, nab-technology has a great potential of being applied extensively in the field of anti-cancer agents delivery in the future in order to acquire the good safety and better therapeutical effect.

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Downregulation of P-glycoprotein (P-gp) is implicated in the pathophysiology of inflammatory bowel disease (IBD). Berberine, a principal isoquinoline alkaloid extracted from species, has been reported to exhibit therapeutic potential in IBD. In this study, we used a dextran sulfate sodium (DSS)-induced colitis rat model to evaluate the effect of berberine on P-gp and explore its mechanism of action. Berberine treatment improved DSS-induced colitis symptoms, attenuated inflammatory markers (myeloperoxidase, tumor necrosis factor-, and interleukin-1 and -6), and enhanced P-gp expression in a dose-dependent manner. Although colonic expression of the P-gp-related nuclear receptor pregnane X receptor and transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) were downregulated in the colitis model, gene and protein expression analysis revealed that berberine treatment reversed only the downregulation of Nrf2. In vitro studies using Caco-2 cells showed that the multidrug resistance 1 () gene and P-gp protein were upregulated by berberine in a dose- and time-dependent manner. Significant upregulation of the gene by berberine was abrogated by Nrf2 silencing, indicating that the Nrf2-mediated pathway was responsible for this activation. Luciferase assays showed a dose-dependent increase in Nrf2 reporter gene activity after berberine treatment in Caco-2 cells, with a significant 2-fold elevation at 2.5M berberine, suggesting that berberine is a strong Nrf2 activator. These results indicate the possible involvement of Nrf2-mediated upregulation of P-gp in the therapeutic effect of berberine on colitis and highlight the potential of P-gp and/or Nrf2 as new therapeutic targets for IBD.