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The aim of this study was to evaluate the photochemopreventive effects of ferulic acid (FA) against chronic ultraviolet-B (290–320 nm) induced oxidative stress, inflammation and angiogenesis in the skin of Swiss albino mice. Chronic UVB exposure (180 mJ/cm 2 for 30 weeks; thrice in a week) induced tumor formation in the mice skin that showed increased expression of carcinogenic and inflammatory markers when compared with the control animals. The intraperitoneal (FAIP) and topical (FAT) administration of FA significantly reduced the incidence of UVB-induced tumor volume and tumor weight in the mice skin. Histopathological studies revealed that both FAIP and FAT administration prevented the UVB-induced hyperplasia, squamous cell carcinoma (SCC) and dysplastic feature in the mice skin. Further, it has been observed that FA treatment reverted chronic UVB-induced oxidative damage (thiobarbituric acid reactive substances, superoxide dismutase, catalase, glutathione peroxidase) accompanied with modulation of vascular endothelial growth factor ( VEGF ), inducible nitric oxide synthase ( iNOS ), TNF-α and IL-6 in the mice skin tumor. FA treatment also modulates mutated p53 , Bcl-2 and Bax expressions in the UVB-induced mice skin tumor. Thus, the results of the present study indicate ferulic acid has potential against UVB-induced carcinogenesis in the Swiss albino mice. [ABSTRACT FROM AUTHOR]

Abstract: The present study was aimed to explore the antioxidant potential of apigenin and its preventive effect on radiation-induced oxidative damage in human peripheral blood lymphocytes (HPBL). Apigenin (4′, 5, 7-trihydroxy flavone) effectively scavenges hydroxyl (OH•), superoxide anion (O2 •–), 1, 1-diphenyl- 2-picrylhydrazyl (DPPH•) and 2, 2-azino-bis-3-ethylbenzothiazoline-6-sulphonic acid radical cation (ABTS•+) in a concentration-dependent manner (37.2–186μM). Gamma-radiation (3Gy) exposure increased the levels of reactive oxygen species (ROS), % apoptotic cells and decreased the mitochondrial membrane potential (ΔΨm) in HPBL. On the other hand, apigenin treatment (37.2μM) 60min prior to irradiation significantly decreased ROS generation in HPBL. It has also been observed that apigenin treatment significantly reduced γ-radiation-induced apoptotic incidence and modulates loss of ΔΨm in HPBL. Furthermore, apigenin treatment significantly maintains cellular antioxidant status (superoxide dismutase, catalase, glutathione peroxidase activities and reduced glutathione level) and protects cellular milieu from γ-radiation-induced lipid peroxidation and micronuclei formation in irradiated HPBL. Radiation exposure increased p53, p21, Bax and NF-kB expressions and decreased Bcl-2 expression in HPBL. Conversely, an increase in Bcl-2 along with a decrease in p53, p21, Bax and NF-kB expression was observed in apigenin plus irradiated HPBL. Taken together, the present study indicates that apigenin showed strong antioxidant property in free radical scavenging systems and protects HPBL from radiation-induced oxidative damages at cellular and molecular level. [Copyright &y& Elsevier]

Exposure to solar ultraviolet-B (UVB) radiation leads to the formation of cyclobutane pyrimidine dimers (CPDs). We investigated the protective effect of apigenin against UVB-induced CPDs formation in human dermal fibroblasts cells (HDFa). For this purpose, HDFa cells were treated with apigenin (15 μM) prior to UVB irradiation (20 mJ/cm 2 ); DNA damage and subsequent molecular end points were observed. Exposure to UVB radiation increased significant CPDs formation in HDFa cells and the frequencies of CPDs were reduced by treatment with apigenin (15 μM). UVB-induced CPDs downregulates the expression of nucleotide excision repair (NER) genes such as xeroderma pigmentosum complementation group C, B, G and F (XPC, XPB, XPG and XPF), transcription factor II human (TFIIH) and excision repair cross-complementation group 1 (ERCC1) in HDFa cells. Conversely, apigenin treatment restored UVB-induced loss of NER proteins in HDFa cells, which indicates its preventive effect against CPDs formation. Besides, single low dose UVB-exposure induced nuclear fragmentation, apoptotic frequency and apoptotic proteins expression (Bax and Caspase-3) have been prevented by the apigenin pretreatment. Furthermore, apigenin exhibits strong UV absorbance property and showed 10.08 SPF value. Thus, apigenin can protect skin cells against UVB-induced CPDs formation probably through its sunscreen effect. Hence, apigenin can be considered as an effective protective agent against UV induced skin damages. [ABSTRACT FROM AUTHOR]

Multidrug resistance (MDR) remains a major obstacle in cancer chemotherapy. The use of the dietary phytochemicals as chemosensitizing agents to enhance the efficacy of conventional cytostatic drugs has recently gained the attention as a plausible approach for overcoming the drug resistance. The aim of this study was to investigate whether a naturally occurring diet-based phenolic acid, ferulic acid, could sensitize paclitaxel efficacy in ABCB1 overexpressing (P-glycoprotein) colchicine selected KB Ch R 8-5 cell line. In vitro drug efflux assays demonstrated that ferulic acid inhibits P-glycoprotein transport function in drug resistant KB Ch R 8-5 cell lines. However, ferulic acid significantly downregulates ABCB1 expression in a concentration dependent manner. Cytotoxicity assay reveals that ferulic acid decreased paclitaxel resistance in KBCh R 8-5 and HEK293/ABCB1 cells, which indicates its chemosensitizing potential. Clonogenic cell survival assay and apoptotic morphological staining further confirm the chemosensitizing potential of ferulic acid in drug resistant KB Ch R 8-5 cell lines. Ferulic acid treatment enhances paclitaxel mediated cell cycle arrest and upregulates paclitaxel-induced apoptotic signaling in KB resistant cells. Hence, it has been concluded that downregulation of ABCB1 and subsequent induction of paclitaxel-mediated cell cycle arrest and apoptotic signaling may be the cause for the chemosensitizing potential of ferulic acid in P-gp overexpressing cell lines. [ABSTRACT FROM AUTHOR]