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Efficient delivery of ursolic acid by poly(N-vinylpyrrolidone)-block-poly (ε-caprolactone) nanoparticles for inhibiting the growth of hepatocellular carcinoma in vitro and in vivo.

Zhang H, Zheng D, Ding J, Xu H, Li X, Sun W - Int J Nanomedicine (2015)

Bottom Line: Moreover, UA-NPs significantly delayed tumor growth and localized to the tumor site when compared with the equivalent dose of UA.In addition, both Western blotting and immunohistochemistry suggested that the possible mechanism of the superior efficiency of UA-NPs is mediation by the regulation of apoptosis-related proteins.Therefore, UA-NPs show potential as a promising nanosized drug system for liver cancer therapy.

View Article: PubMed Central - PubMed

Affiliation: Department of Geriatric Gastroenterology, First Affiliated Hospital with Nanjing Medical University, Nanjing, People's Republic of China.

ABSTRACT
Previous reports have shown that ursolic acid (UA), a pentacyclic triterpenoid derived from Catharanthus trichophyllus roots, could inhibit the growth of a series of cancer cells. However, the potential for clinical application of UA is greatly hampered by its poor solubility, whereas the hydrophobicity of UA renders it a promising model drug for nanosized delivery systems. In the current study, we loaded UA into amphiphilic poly(N-vinylpyrrolidone)-block-poly (ε-caprolactone) nanoparticles and performed physiochemical characterization as well as analysis of the releasing capacity. In vitro experiments indicated that UA-NPs inhibited the growth of liver cancer cells and induced cellular apoptosis more efficiently than did free UA. Moreover, UA-NPs significantly delayed tumor growth and localized to the tumor site when compared with the equivalent dose of UA. In addition, both Western blotting and immunohistochemistry suggested that the possible mechanism of the superior efficiency of UA-NPs is mediation by the regulation of apoptosis-related proteins. Therefore, UA-NPs show potential as a promising nanosized drug system for liver cancer therapy.

No MeSH data available.


Related in: MedlinePlus

Apoptotic induction in H22 cells treated with equivalent doses of UA or UA-NPs.Notes: (A) Flow cytometry-based annexin V-FITC/PI labeling of apoptotic cells. (B) The histogram represents apoptosis rates. #P<0.01 versus control group. *P<0.01 versus the group exposed to UA 20 μM. **P<0.01 versus the group exposed to UA 40 μM. Data are presented as mean ± SD (n=3).Abbreviations: FITC, fluorescein isothiocyanate; PI, propidium iodide; SD, standard deviation; NP, nanoparticle; UA, ursolic acid; UA-NPs, UA-loaded poly(N-vinylpyrrolidone)-block-poly (ε-caprolactone) nanoparticles; A, annexin.
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f5-ijn-10-1909: Apoptotic induction in H22 cells treated with equivalent doses of UA or UA-NPs.Notes: (A) Flow cytometry-based annexin V-FITC/PI labeling of apoptotic cells. (B) The histogram represents apoptosis rates. #P<0.01 versus control group. *P<0.01 versus the group exposed to UA 20 μM. **P<0.01 versus the group exposed to UA 40 μM. Data are presented as mean ± SD (n=3).Abbreviations: FITC, fluorescein isothiocyanate; PI, propidium iodide; SD, standard deviation; NP, nanoparticle; UA, ursolic acid; UA-NPs, UA-loaded poly(N-vinylpyrrolidone)-block-poly (ε-caprolactone) nanoparticles; A, annexin.

Mentions: We examined apoptotic rates of H22 cells caused by UA and UA-NPs, using fluorescent annexin V-FITC/PI double staining with flow cytometry. Annexin V and PI were applied to discriminate cellular apoptosis from necrosis, due to the difference in penetrative ability of the two dyes into the apoptotic and necrotic cells.24 As shown in Figure 5, a significant increase of early and late apoptotic cells was detected in H22 following the treatment. Moreover, both UA and UA-NPs induced apoptosis in H22 cells in a dose-dependent manner. Notably, the number of either early or late apoptotic cells induced by UA-NPs was significantly larger than that of cells treated with the equivalent dose of free UA.


Efficient delivery of ursolic acid by poly(N-vinylpyrrolidone)-block-poly (ε-caprolactone) nanoparticles for inhibiting the growth of hepatocellular carcinoma in vitro and in vivo.

Zhang H, Zheng D, Ding J, Xu H, Li X, Sun W - Int J Nanomedicine (2015)

Apoptotic induction in H22 cells treated with equivalent doses of UA or UA-NPs.Notes: (A) Flow cytometry-based annexin V-FITC/PI labeling of apoptotic cells. (B) The histogram represents apoptosis rates. #P<0.01 versus control group. *P<0.01 versus the group exposed to UA 20 μM. **P<0.01 versus the group exposed to UA 40 μM. Data are presented as mean ± SD (n=3).Abbreviations: FITC, fluorescein isothiocyanate; PI, propidium iodide; SD, standard deviation; NP, nanoparticle; UA, ursolic acid; UA-NPs, UA-loaded poly(N-vinylpyrrolidone)-block-poly (ε-caprolactone) nanoparticles; A, annexin.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4362907&req=5

f5-ijn-10-1909: Apoptotic induction in H22 cells treated with equivalent doses of UA or UA-NPs.Notes: (A) Flow cytometry-based annexin V-FITC/PI labeling of apoptotic cells. (B) The histogram represents apoptosis rates. #P<0.01 versus control group. *P<0.01 versus the group exposed to UA 20 μM. **P<0.01 versus the group exposed to UA 40 μM. Data are presented as mean ± SD (n=3).Abbreviations: FITC, fluorescein isothiocyanate; PI, propidium iodide; SD, standard deviation; NP, nanoparticle; UA, ursolic acid; UA-NPs, UA-loaded poly(N-vinylpyrrolidone)-block-poly (ε-caprolactone) nanoparticles; A, annexin.
Mentions: We examined apoptotic rates of H22 cells caused by UA and UA-NPs, using fluorescent annexin V-FITC/PI double staining with flow cytometry. Annexin V and PI were applied to discriminate cellular apoptosis from necrosis, due to the difference in penetrative ability of the two dyes into the apoptotic and necrotic cells.24 As shown in Figure 5, a significant increase of early and late apoptotic cells was detected in H22 following the treatment. Moreover, both UA and UA-NPs induced apoptosis in H22 cells in a dose-dependent manner. Notably, the number of either early or late apoptotic cells induced by UA-NPs was significantly larger than that of cells treated with the equivalent dose of free UA.

Bottom Line: Moreover, UA-NPs significantly delayed tumor growth and localized to the tumor site when compared with the equivalent dose of UA.In addition, both Western blotting and immunohistochemistry suggested that the possible mechanism of the superior efficiency of UA-NPs is mediation by the regulation of apoptosis-related proteins.Therefore, UA-NPs show potential as a promising nanosized drug system for liver cancer therapy.

View Article: PubMed Central - PubMed

Affiliation: Department of Geriatric Gastroenterology, First Affiliated Hospital with Nanjing Medical University, Nanjing, People's Republic of China.

ABSTRACT
Previous reports have shown that ursolic acid (UA), a pentacyclic triterpenoid derived from Catharanthus trichophyllus roots, could inhibit the growth of a series of cancer cells. However, the potential for clinical application of UA is greatly hampered by its poor solubility, whereas the hydrophobicity of UA renders it a promising model drug for nanosized delivery systems. In the current study, we loaded UA into amphiphilic poly(N-vinylpyrrolidone)-block-poly (ε-caprolactone) nanoparticles and performed physiochemical characterization as well as analysis of the releasing capacity. In vitro experiments indicated that UA-NPs inhibited the growth of liver cancer cells and induced cellular apoptosis more efficiently than did free UA. Moreover, UA-NPs significantly delayed tumor growth and localized to the tumor site when compared with the equivalent dose of UA. In addition, both Western blotting and immunohistochemistry suggested that the possible mechanism of the superior efficiency of UA-NPs is mediation by the regulation of apoptosis-related proteins. Therefore, UA-NPs show potential as a promising nanosized drug system for liver cancer therapy.

No MeSH data available.


Related in: MedlinePlus