Apigenin inhibits oxidative stress‐induced macromolecular damage in N‐nitrosodiethylamine (NDEA)‐induced hepatocellular carcinogenesis in Wistar albino rats

Abstract

Apigenin (4',5,7-trihydroxyflavone), a flavone subclass of flavonoid widely distributed in many herbs, fruits, and vegetables is a substantial component of the human diet and has been shown to possess a variety of biological activities including tumor growth inhibition and chemoprevention. Recent studies in several biological systems have shown that apigenin induces tumor growth inhibition, cell cycle arrest, and apoptosis. Free radical-induced degradation of polyunsaturated fatty acid results in electrophilic products and causes severe oxidative stress. Oxidative stress induced by free radicals, nonoxidizing species, electrophiles, and associated DNA damages have been frequently coupled with carcinogenesis. In the present study, the protective role of apigenin was examined against the oxidative stress caused by N-nitrosodiethylamine (NDEA) and phenobarbital (PB) in Wistar albino rats. Oxidative stress was measured in terms of lipid peroxidation (LPO) and protein carbonyl formation. Oxidative stress-induced DNA damage was measured by single cell gel electrophoresis (comet assay). Apigenin exhibited its antioxidant defense against NDEA-induced oxidative stress. We have observed minimal levels of LPO and DNA damage in apigenin-treated hepatoma bearing animals. Based on the results, we suggest that apigenin may be developed as a promising chemotherapeutic agent against the development of chemical carcinogenesis.

Apigenin Attenuates 2-Deoxy-D-ribose-Induced Oxidative Cell Damage in HIT-T15 Pancreatic .BETA.-Cells

“…Several recent studies have shown that apigenin has antiapoptotic and antioxidative properties in a variety of in vitro and in vivo systems. [26][27][28] To the best of our knowledge, this is the first report that apigenin attenuates dRib-induced oxidative cell damage in pancreatic β-cells, which may promote cell recovery under oxidative stress conditions.…”

“…Apigenin has been shown to have antiapoptotic and antioxidative properties in a variety of in vitro and in vivo systems. [26][27][28] With respect to the regulation of diabetes, apigenin is known to inhibit high glucose levels and tumor necrosis factor-α (TNF-α)-induced adhesion molecule levels in human endothelial cells. 29) It has also been noted that apigenin has the potential to regulate diabetes as well as disease-induced thyroid dysfunction and lipid peroxidation.…”

Apigenin and cancer chemoprevention: Progress, potential and promise (Review)

“…The results indicate that both flavonoids exhibited cell growth inhibitory effects which were due to cell cycle arrest and down-regulation of the expression of CDK4 with induction of p53 and p21, respectively. In addition, Jeyabal et al (115) have shown the in vivo protective effects of apigenin on N-nitrosodiethylamine-induced and phenobarbitol promoted hepatocarcinogenesis in Wistar albino rats. Apigenin treatment at 25 mg/kg body weight for two weeks to these rats provided protection against the oxidative stress and DNA damage caused by the carcinogen.…”

Apigenin Causes Biochemical Modulation, Glut4 and Cd38 Alterations to Improve Diabetes and to Protect Damages of Some Vital Organs in Experimental Diabetes

“…Free radical scavenging property of apigenin depends on the number of OH groups present at 4, 5 and 7th positions of its C-ring structure (Sharma et al, 2012). The antioxidant property of apigenin has been reported due to double bond between the C 2 and C 3 carbon atoms of the C-ring and presence of oxo group in 4th position of C-ring (Jeyabal et al, 2005) (Fig. 7).…”