Search

The aim of this study was to investigate the protective effects of Nano-Se against nickel (Ni)-induced hepatotoxicity and the potential mechanism. Hence, we constructed in vivo and in vitro models of Ni-induced hepatotoxicity. Sprague-Dawley (SD) rats were exposed to nickel sulfate (NiSO4 , 5.0 mg/kg, i.p.) with or without Nano-Se (0.5, 1, and 2 mg/kg, oral gavage) co-administration for 14 days, and HepG2 cells were exposed to NiSO4 (1500 μM) with or without Nano-Se (20 μM) for 24 h. Nano-Se obviously prevented Ni-induced hepatotoxicity indicated by ameliorating pathological change and decreasing Ni accumulation in rat livers. Ni induced a significant increase in hepatic activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GSH-Px), and malondialdehyde (MDA) level, decreased the glutathione (GSH) content while compared to those in the control group. Nano-Se administration improved the hepatic antioxidant capacity through increase hepatic GSH contents and GSH-Px activity, decrease the activities of SOD, CAT, and MDA level. Nano-Se improved the cell viability, decreased active oxygen (ROS) generation and ameliorated morphological changes of nuclear structures in Ni-treated HepG2 cells. In addition, Nano-Se inhibited the Ni-induced increases of cytochrome c, caspase-9, cleaved caspase-3, increased PI3K and AKT phosphorylation both in vivo and in vitro. Besides, the PI3K inhibitor Y294002 could inhibit the protective effects of Nano-Se on apoptosis. Thus, Nano-Se significantly activates PI3K/AKT signaling to ameliorate apoptosis in Ni-induced hepatotoxicity.

During the pathogenesis and progression of diabetes, lipotoxicity is a major threat to the function and survival of pancreatic β-cells. To battle against the lipotoxicity induced cellular damages, the present study investigated the beneficial effects of acacetin, a natural antioxidant, on free fatty acid (FFA) stressed RINm5F cells and the potential mechanism involved.RINm5F cells with or without 1 h pretreatment of acacetin were treated with 0.35 mM sodium palmitate for 24 h. Cell viability, intracellular reactive oxygen species (ROS) level, antioxidant capacity, cellular apoptosis, and endoplasmic reticulum (ER) stress biomarker expression were investigated.Our experiments demonstrated that acacetin treatment significantly scavenged the intracellular ROS, upregulated the endogenous antioxidant enzymes, and diminished the sub-GAcacetin may antagonize lipotoxicity in pancreatic cells by attenuating the oxidative stress and ER stress.

Overproduction of reactive species, notably reactive oxygen (ROS) and nitrogen (RNS) species, along with the failure of balancing effects of endogenous antioxidant defenses result in destruction of cellular structures, lipids, proteins, and genetic material, which lead to oxidative stress. Oxidative stress-induced neuronal apoptosis plays a pivotal role in pathogenesis of neurodegeneration. Antioxidants represent one of the medical choice strategies for protecting against this unbalanced oxidation-antioxidation status. Recently, natural compounds with neuroprotective potential that can scavenge free radicals and protect cells from oxidative damage have received extensive attention.In this review, we summarized the detailed research progress on the medicinal plants-derived natural compounds with potential anti-oxidation effects and their molecular mechanisms on modulating the neurotoxin (6-OHDA, HThe natural compounds that efficacious in modulating reactive species production and mitochondrial function include flavonoids, glucosides, alkaloids, polyphenols, lignans, coumarins, terpenoids, quinones and others. They decreased the neurotoxin-induced oxidative damage and apoptosis by (1) decreasing ROS/RNS generation, lipid peroxidation, caspase-3 and caspase-9 activities, LDH release, the ratio of Bax/Bcl-2, CaThe present work reviews the role of oxidative stress in neurodegeneration, highlighting the potential anti-oxidation effects of natural compounds as a promising approach to develop innovative neuroprotective strategy.

Radiation-induced damage to the mitochondrial macromolecules and electron transfer chain (ETC), causing the generation of primary and secondary reactive oxygen (ROS) species. The continuous ROS production after radiation will trigger cell oxidative stress and ROS-mediated nucleus apoptosis and autophagy signaling pathways. Scavenging radiation-induced ROS effectively can help mitochondria to maintain their physiological function and relief cells from oxidative stress. Nicotinamide is a critical endogenous antioxidant helping to neutralize ROS in vivo. In this study, we designed and synthetized a novel mitochondrial-targeted dihydronicotinamide (Mito-N) with the help of mitochondrial membrane potential to enter the mitochondria and scavenge ROS. According to experiment results, Mito-N significantly increased cell viability by 30.75% by neutralizing the accumulated ROS and resisting DNA strands breaks after irradiation. Furthermore, the mice survival rate also improved with the treatment of Mito-N, by effectively ameliorating the hematopoietic system infliction under lethal dose irradiation.

The pathogenesis of diabetes is associated with dysfunction of pancreatic β-cells. To ameliorate the β-cell dysfunction, it has propelled great interest to search pharmacological agents from natural plants. This study explored the protective effect of apigetrin, a flavonoid present in natural plants, against streptozotocin (STZ)-induced cell damages in RINm5F cells and the potential mechanisms. Apigetrin was found to inhibit the elevation of intracellular reactive oxygen species levels, restore the impairment of antioxidant enzymes, and recover the disruption of redox homeostasis in the STZ-treated pancreatic β-cells. Moreover, treatment of apigetrin significantly suppressed the STZ-induced apoptosis in the analysis of apoptotic sub-G1 population and the protein expressions of cleaved poly(ADP-ribose) polymerase and caspase-3. Furthermore, apigetrin attenuated STZ-induced endoplasmic reticulum (ER) stress, indicated by the reduction of ER stress biomarkers, including overloading of mitochondrial calcium, increase in glucose-regulated protein 78, phosphorylation of protein kinase RNA-like ER kinase and its downstream eukaryotic initiation factor 2α, cleavage of activating transcription factor 6 and caspase-12, up-regulation of CCAAT/enhancer binding protein homologous protein, and induction of spliced X-box binding protein 1. Additionally, pretreatment with 4-phenylbutyric acid, a classic ER stress inhibitor, augmented these beneficial effects of apigetrin. In conclusion, these results demonstrated that apigetrin could improve the STZ-induced pancreatic β-cell damages via mitigation of oxidative stress and ER stress and supported the application of apigetrin to developing the novel therapeutics of diabetes.

Alginate oligosaccharide (AOS) was reported to possess antioxidant and free radical scavenging activities, but the specific effects and mechanisms remain unclear. We investigated the effects of AOS on H2O2-induced oxidative stress and apoptosis in human umbilical vein endothelial cells (HUVECs) and the associated mechanisms. HUVECs were treated with 100-800 µM hydrogen peroxide (H2O2) for various periods (12, 24, and 36 h) to establish an in vitro oxidative stress and apoptosis HUVEC model. AOS protects HUVEC cells against oxidative stress-induced apoptosis by decreasing the expression levels of caspase 3 and Bax, and increasing Bcl-2 expression. Microarray assay, real-time PCR and western blot results revealed that AOS was able to effectively suppress H2O2-induced apoptosis via regulated integrin-α/FAK/PI3K pathway by influencing the expression of integrin-α, FAK, PI3K, PTEN, P21, and CDK2. In conclusion, our study suggests that AOS can protect endothelial cells against oxidative stress injury caused by H2O2, providing novel alternative strategies to prevent atherosclerosis in the future.

Pancreatic beta cells are very sensitive to oxidative stress, which is one of the major causes of cell damages in diabetes. Growing interest has focused on the development of effective therapeutics to protect pancreatic cells from oxidative stress and searching for potentially protective antioxidants for treating diabetes. Apigenin, a plant-derived flavonoid, was investigated to determine whether it could protect rat insulinoma cell lines (RINm5F pancreatic beta cells) against streptozotocin (STZ)-induced oxidative damages and the mechanisms implicated. Our results showed that STZ treatment could induce oxidative stress and consequent cytotoxic effects in RINm5F cells. Pretreatment with apigenin effectively decreased the intracellular reactive oxygen species (ROS) production, attenuated cellular DNA damage, diminished lipid peroxidation, relieved protein carbonylation, and restored the cell apoptosis of pancreatic beta cells stressed by STZ. Our further experiments demonstrated that the beneficial effects of apigenin were related to ameliorate the loss of antioxidant enzymes of the STZ-treated cells in the level of gene transcription, protein expression, and enzyme activity. That suggested apigenin was not only a free radical scavenger but also a regulator to antioxidant defenses of pancreatic cells. Taken all together, our findings suggested that apigenin could attenuate the STZ-induced oxidative damages in pancreatic beta cells and might serve as a novel agent for the treatment of diabetes.

Ultraviolet B (UVB) radiation on human skin induces pathophysiological processes such as oxidative stress and inflammation. In previous reports, the antioxidant effects of triphlorethol-A were shown to protect cells against hydrogen peroxide-induced cell damage and gamma ray-induced oxidative stress. In this study, the role of triphlorethol-A in protecting human keratinocytes (HaCaT) against UVB-induced cell damage was investigated. Triphlorethol-A-treated cells were irradiated with UVB (150 mJ/cm2). Triphlorethol-A decreased UVB-induced intracellular ROS and restored the activities of antioxidant enzymes decreased by UVB radiation. Triphlorethol-A decreased UVB damage to cellular components, such as lipid membrane and DNA, restored cell viability and reduced UVB-induced apoptosis by inhibiting the mitochondria-mediated caspase pathway. Triphlorethol-A also reduced the UVB-induced loss of ΔΨm and the active forms of caspase 9 and caspase 3. The anti-apoptotic effect of triphlorethol-A was found to involve the inhibition of c-Jun NH2-terminal kinase, which was induced by UVB exposure. And triphlorethol-A showed an absorptive capacity at range of UVB. These results suggest that triphlorethol-A protects human keratinocytes against UVB by enhancing the activities of the antioxidant system, inhibiting cellular damage and absorbing the UVB.

This study investigated the cytoprotective effect of baicalein (5,6,7-trihydroxyflavone) against oxidative stress-induced mitochondrial dysfunction. Electron spin resonance (ESR) spectrometry revealed that baicalein showed significant scavenging effects on superoxide radicals and hydroxyl radicals. When H 2 O 2 treatment induces an increase in mitochondrial reactive oxygen species (ROS), baicalein treatment decreased high level of ROS. Baicalein significantly reduced alteration of Bcl-2 family proteins, the release of cytochrome c from mitochondria into the cytosol via inhibition of mitogen-activated protein kinase kinase-4 (MKK4/SEK1) and c-Jun NH 2 -terminal kinase (JNK) cascades induced by H 2 O 2 treatment. Manganese superoxide dismutase (MnSOD) is an important antioxidant enzyme in mitochondria against oxidative stress. Baicalein restored both MnSOD protein expression and activity, which were abolished by H 2 O 2 treatment. The transcription factor NF-E2-related factor 2 (Nrf2) is a critical regulator of MnSOD, achieved by binding to the antioxidant response element (ARE). Baicalein restored nuclear Nrf2 protein expression and its ARE binding activity, which were abolished by H 2 O 2 treatment. These studies demonstrate that baicalein attenuates mitochondrial oxidative stress by activating Nrf2-mediated MnSOD induction.

The toxicity of formaldehyde (HCHO) has been attributed to its ability to form adducts with DNA and proteins. Triphlorethol-A, derived from Ecklonia cava, was reported to exert a cytoprotective effect against oxidative stress damage via an antioxidant mechanism. The aim of this study was to examine the mechanisms underlying the triphlorethol-A ability to protect Chinese hamster lung fibroblast (V79-4) cells against HCHO-induced damage. Triphlorethol-A significantly decreased the HCHO-induced intracellular reactive oxygen species (ROS) production. Triphlorethol-A prevented increased cell damage induced by HCHO via inhibition of mitochondria-mediated caspase-dependent apoptosis pathway. Triphlorethol-A diminished HCHO-induced mitochondrial dysfunction, including loss of mitochondrial membrane action potential (Δψ) and adenosine triphosphate (ATP) depletion. Furthermore, the anti-apoptotic effect of triphlorethol-A was exerted through inhibition of c-Jun NH(2)-terminal kinase (JNK), which was enhanced by HCHO. Our data indicate that triphlorethol-A exerts a cytoprotective effect in V79-4 cells against HCHO-induced oxidative stress by inhibiting the mitochondria-mediated caspase-dependent apoptotic pathway.

Aim of the study Fruits of Lycium chinense Miller (Solanaceae), distributed in northeast Asia, have gained attraction for their hepatoprotective role in traditional oriental medicine. The excessive production of reactive oxygen species (ROS) is hazardous for living organisms and damage major cellular constituents such as DNA, lipid, and protein. The cytoprotective effect of Lycium chinense fruits ( Lycium extract) was assessed against H 2 O 2 -induced Chang liver cell damage. Materials and methods The effect of Lycium extract against H 2 O 2 -induced cell death was determined by the MTT assay. Radical scavenging activity was determined through the assessments of 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals, intracellular ROS, hydroxyl radicals, and superoxide. The inductions of antioxidant enzymes were determined via their protein expressions and activities. DNA damage was measured using comet assay and expression of phospho-histone H2A.X. Lipid peroxidation was measured using 8-isoprostane level and fluorescent probe. Protein modification was measured using protein carbonyl moiety. Results and conclusion Lycium extract scavenged the DPPH free radicals, intracellular ROS, hydroxyl radicals, and superoxide. Lycium extract recovered activities of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) decreased by H 2 O 2 . Lycium extract decreased DNA damage, lipid peroxidation and protein carbonyl values increased by H 2 O 2 exposure. In addition, Lycium extract increased the cell viability of Chang liver cells exposed to H 2 O 2 via inhibition of apoptosis. These results show that Lycium extract protected Chang liver cells against oxidative stressed cell damage by H 2 O 2 via scavenging ROS and enhancing antioxidant enzyme activity.

The present study investigated the cytoprotective properties of glycitein, a metabolite formed by the transformation of glycitin by intestinal microflora, against oxidative stress. Glycitein was found to scavenge intracellular reactive oxygen species (ROS), and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and thereby preventing lipid peroxidation and DNA damage. Glycitein inhibited apoptosis of Chinese hamster lung fibroblast (V79-4) cells exposed to hydrogen peroxide (H(2)O(2)) via radical scavenging activity. Glycitein abrogated the activation of c-Jun N-terminal kinase (JNK) induced by H(2)O(2) treatment and inhibited DNA binding activity of activator protein-1 (AP-1), a downstream transcription factor of JNK. Taken together, these findings suggest that glycitein protected H(2)O(2) induced cell death in V79-4 cells by inhibiting ROS generation and JNK activation.

Baicalein (5,6,7-trihydroxyflavone) is a phenolic flavonoid compound derived mainly from the root of Scutellaria baicalensis Georgi, a medicinal plant traditionally used in oriental medicine. In our previous study, baicalein attenuated mitochondrial oxidative stress by scavenging reactive oxygen species (ROS) and by induction of nuclear factor erythroid 2-related factor 2 transcription factor-mediated manganese superoxide dismutase. In the present study, the protective effects of baicalein against oxidative stress-induced damage, especially cellular components including DNA, lipid, and protein, were studied. The results of this study showed that baicalein scavenged intracellular ROS. Baicalein inhibited the H2O2-induced DNA damage that was demonstrated by decreased phospho-H2A.X expression and DNA tail formation. In addition, it prevented the lipid peroxidation shown by the fluorescence intensity of diphenyl-1-pyrenylphosphine and the formation of thiobarbituric acid reactive substances. Moreover, baicalein inhibited protein oxidation demonstrated by protein carbonyl formation. Furthermore, baicalein protected cells via the inhibition of apoptosis induced by H2O2. The findings of this study suggest that baicalein provides protection for cellular components against oxidative damage via scavenging ROS and inhibiting apoptosis.

Recently, we demonstrated that butin (7,3',4'-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H(2)O(2))-induced apoptosis by: (1) scavenging reactive oxygen species (ROS), activating antioxidant enzymes such superoxide dismutase and catalase; (2) decreasing oxidative stress-induced 8-hydroxy-2'-deoxyguanosine levels via activation of oxoguanine glycosylase 1, and (3), reducing oxidative stress-induced mitochondrial dysfunction. The objective of this study was to determine the cytoprotective effects of butin on oxidative stress-induced mitochondria-dependent apoptosis, and possible mechanisms involved. Butin significantly reduced H(2)O(2)-induced loss of mitochondrial membrane potential as determined by confocal image analysis and flow cytometry, alterations in Bcl-2 family proteins such as decrease in Bcl-2 expression and increase in Bax and phospho Bcl-2 expression, release of cytochrome c from mitochondria into the cytosol and activation of caspases 9 and 3. Furthermore, the anti-apoptotic effect of butin was exerted via inhibition of mitogen-activated protein kinase kinase-4, c-Jun NH(2)-terminal kinase (JNK) and activator protein-1 cascades induced by H(2)O(2) treatment. Finally, butin exhibited protective effects against H(2)O(2)-induced apoptosis, as demonstrated by decreased apoptotic bodies, sub-G(1) hypodiploid cells and DNA fragmentation. Taken together, the protective effects of butin against H(2)O(2)-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathway.

This study determined whether nickel sulfate (Ni)-induced reproductive damage occurs via apoptosis and oxidative stress and to examine the expression of Bax and c-kit and their effects on Ni exposure. The study also explored the protective effects of grape seed proanthocyanidin extract (GSPE) against Ni toxicity in the testes. Wistar rats were treated with normal saline, Ni alone (1.25, 2.5, and 5 mg/kg/day), and Ni (2.5 mg/kg/day) plus GSPE (50 and 100 mg/kg/day). After 30 days, Ni significantly decreased sperm motility and the percentage of S-phase cells and enhanced testicular apoptosis in the 2.5 and 5 mg groups. The levels of malondialdehyde (MDA), hydrogen peroxide (H₂O₂), and nitric oxide (NO) significantly increased. The decreased activity of glutathione peroxidase and catalase in the Ni groups showed that Ni could increase oxidative stress, especially at 2.5 and 5 mg. Western blot analysis showed that the expression of Bax protein and c-kit increased in 2.5 and 5 mg Ni groups compared with controls. Conversely, these changes were partially attenuated in rats simultaneously administered GSPE, especially in the 100 mg group. These results demonstrate the following: (1) Ni exhibits reproductive toxicity in rats by decreasing sperm at concentrations of 2.5 and 5 mg; (2) intratesticular apoptosis, oxidative stress, and c-kit overexpression play pivotal roles in reproductive damage induced by Ni; and (3) GSPE enhances sperm motility by down-regulating c-kit expression and offsetting the apoptosis and oxidative stress induced by Ni by directly decreasing MDA and NO, scavenging H₂O₂, and down-regulating Bax expression.

The radioprotective effect of geraniin, a tannin compound isolated from Nymphaea tetragona Georgi var. (Nymphaeaceae), against γ-radiation-induced damage was investigated in Chinese hamster lung fibroblast (V79-4) cells. Geraniin recovered cell viability detected by MTT test and colony formation assay, which was compromised by γ-radiation, and reduced the γ-radiation-induced apoptosis by the inhibition of loss of the mitochondrial membrane potential. Geraniin protected cellular components (lipid membrane, cellular protein, and DNA) damaged by γ-radiation, which was detected by lipid peroxidation, protein carbonyl formation, and comet assay. Geraniin significantly reduced the level of intracellular reactive oxygen species generated by γ-radiation, which was detected using spectrofluorometer, flow cytometer, and confocal microscope after 2',7'-dichlorodihydrofluorescein diacetate staining. Geraniin normalized the superoxide dismutase and catalase activities, which were decreased by γ-radiation. These results suggest that geraniin protects cells against radiation-induced oxidative stress via enhancing of antioxidant enzyme activities and attenuating of cellular damage.

We elucidated the cytoprotective effects of hyperoside (quercetin-3- O -galactoside) against hydrogen peroxide (H 2 O 2 )-induced cell damage. We found that hyperoside scavenged the intracellular reactive oxygen species (ROS) detected by fluorescence spectrometry, flow cytometry, and confocal microscopy. In addition, we found that hyperoside scavenged the hydroxyl radicals generated by the Fenton reaction (FeSO 4 + H 2 O 2 ) in a cell-free system, which was detected by electron spin resonance (ESR) spectrometry. Hyperoside was found to inhibit H 2 O 2 -induced apoptosis in Chinese hamster lung fibroblast (V79-4) cells, as shown by decreased apoptotic nuclear fragmentation, decreased sub-G 1 cell population, and decreased DNA fragmentation. In addition, hyperoside pretreatment inhibited the H 2 O 2 -induced activation of caspase-3 measured in terms of levels of cleaved caspase-3. Hyperoside prevented H 2 O 2 -induced lipid peroxidation as well as protein carbonyl. In addition, hyperoside prevented the H 2 O 2 -induced cellular DNA damage, which was established by comet tail, and phospho histone H2A.X expression. Furthermore, hyperoside increased the catalase and glutathione peroxidase activities. Conversely, the catalase inhibitor abolished the cytoprotective effect of hyperoside from H 2 O 2 -induced cell damage. In conclusion, hyperoside was shown to possess cytoprotective properties against oxidative stress by scavenging intracellular ROS and enhancing antioxidant enzyme activity.

The antioxidant property of butin was investigated for cytoprotective effect against H(2)O(2)-induced cell damage. This compound showed intracellular reactive oxygen species (ROS) scavenging, 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging, inhibition of lipid peroxidation, and DNA damage. This radical scavenging activity of butin protected cell damage exposed to H(2)O(2). Also, butin reduced the apoptotic cells induced by H(2)O(2), as demonstrated by the decreased DNA fragmentation, apoptotic body formation, and caspase 3 activity. In addition, butin restored the activity and protein expression of cellular antioxidant enzymes, superoxide dismutase (SOD), and catalase (CAT) in H(2)O(2)-treated cells. Taken together, these findings suggest that butin protected cells against H(2)O(2)-induced cell damage via antioxidant property.

We have elucidated the cytoprotective effect of annphenone (2,4-dihyroxy-6-methoxy-acetophenone 4- O -β- d -glucopyranoside) against oxidative stress-induced apoptosis. Annphenone scavenged intracellular reactive oxygen species (ROS) and increased antioxidant enzyme activities. It thereby prevented lipid peroxidation and DNA damage, which was demonstrated by the inhibition of the formation of thiobarbituric acid reactive substance (TBARS), inhibition of the comet tail and decreased phospho-H2A.X expression. Annphenone protected Chinese hamster lung fibroblast (V79-4) cells from cell death via the inhibition of apoptosis induced by hydrogen peroxide (H 2 O 2 ), as shown by decreased apoptotic nuclear fragmentation, decreased sub-G 1 cell population and inhibited mitochondrial membrane potential (Δ ψ ) loss. Taken together, these findings suggest that annphenone exhibits antioxidant properties by inhibiting ROS generation and thus protecting cells from H 2 O 2 -induced cell damage.

The protective properties of irisolidone (a metabolite of kakkalide by intestinal bacteria) against hydrogen peroxide (H(2)O(2)) induced cell damage were investigated. Irisolidone was found to scavenge 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and the intracellular reactive oxygen species (ROS), thereby preventing lipid peroxidation and DNA damage. Irisolidone inhibited apoptosis in Chinese hamster lung fibroblast (V79-4) cells induced by H(2)O(2) via radical scavenging activity. This was achieved by the activation of the extracellular signal regulated kinase (ERK) and DNA binding activity of activator protein-1 (AP-1) (a downstream transcription factor of ERK) by irisolidone.

The antioxidant properties of rhapontigenin and rhaponticin isolated from Rheum undulatum were investigated. Rhapontigenin was found to scavenge intracellular reactive oxygen species (ROS), the 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and hydrogen peroxide (H2O2). The radical scavenging effect of rhapontigenin was more effective than rhaponticin. Rhapontigenin protected against H2O2-induced membrane lipid peroxidation and cellular DNA damage, which are the main targets of oxidative stress-induced cellular damage. The radical scavenging activity of rhapontigenin protected Chinese hamster lung fibroblast (V79-4) cells exposed to H2O2 by inhibiting apoptosis. Rhapontigenin inhibited cell damage induced by serum starvation and was also found to increase the activity of catalase and its protein expression. Further, rhapontigenin increased phosphorylation of extracellular signal-regulated kinase (ERK) and inhibited the activity of activator protein 1 (AP-1), a redox-sensitive transcription factor. In summary, these results suggest that rhapontigenin protects V79-4 cells against oxidative damage by enhancing the cellular antioxidant activity and modulating cellular signal pathways.