Biological Activity of a Gallic Acid-Gelatin Conjugate

被引：70

作者：

Cirillo, Giuseppe ^{[1
]}

Kraemer, Kai ^{[2
]}

Fuessel, Susanne ^{[2
]}

Puoci, Francesco ^{[1
]}

Curcio, Manuela ^{[1
]}

Spizzirri, Umile Gianfranco ^{[1
]}

Altimari, Ilaria ^{[1
]}

Iemma, Francesca ^{[1
]}

机构：

[1] Univ Calabria, Dipartimento Sci Farmaceut, I-87036 Arcavacata Di Rende, CS, Italy

[2] Tech Univ Dresden, Dept Urol, Univ Hosp Carl Gustav Carus, D-01307 Dresden, Germany

来源：

BIOMACROMOLECULES | 2010年 / 11卷 / 12期

关键词：

IN-VITRO; ALPHA-GLUCOSIDASE; ANTIOXIDANT; COPOLYMERS; POLYMERS; INHIBITION; APOPTOSIS; PHENOLICS; AMYLASE; SYSTEM;

D O I：

10.1021/bm100760x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Goal of the present study was the characterization of the biological properties of a gelatin-gallic acid conjugate (Gel-GA) to evaluate its applicability in biomedicine and pharmacy. The macromolecular conjugate was synthesized by free radical grafting reaction between gelatin and gallic acid (GA) to form a covalent conjugate that was found to retain the antioxidant and enzymatic activities of free GA. In particular, the peroxynitrite scavenging power was found to be consistent with a IC50 value of 2.17 +/- 0.4 mg mL(-1). The enzymatic capacities of GA, which are regarded beneficial for cell functions, are partly retained in the Gel-GA conjugate. In particular, acetylcholinesterase inhibition (IC50 of 7.1 +/- 1.3 mg mL(-1)) implies the conjugate's usefulness in the chemoprevention of Alzheimer's disease, while the inhibition of alpha-amylase (IC50 of 9.8 +/- 1.1 mg mL(-1)) suggests that the conjugate can be a preferred alternative for inhibition of carbohydrate breakdown and control of glycemic index of food products. Finally, the anticancer activity of Gel-GA was proven in prostate carcinoma and renal cell carcinoma cell lines, confirming the potential of the proposed protein-polyphenol conjugate in medicine.

引用

页码：3309 / 3315

页数：7

共 49 条

[1] Gallic acid causes inactivating phosphorylation of cdc25A/cdc25C-cdc2 via ATM-Chk2 activation, leading to cell cycle arrest, and induces apoptosis in human prostate carcinoma DU145 cells [J].