Cyanidin suppresses amyloid beta-induced neurotoxicity by inhibiting reactive oxygen speciesmediated DNA damage and apoptosis in PC12 cells

Amyloid beta（Aβ）-induced oxidative stress is a major pathologic hallmark of Alzheimer＇s disease. Cyanidin, a natural flavonoid compound, is neuroprotective against oxidative damage-mediated degeneration. However, its molecular mechanism remains unclear. Here, we investigated the effects of cyanidin pretreatment against Aβ-induced neurotoxicity in PC12 cells, and explored the underlying mechanisms. Cyanidin pretreatment significantly attenuated Aβ-induced cell mortality and morphological changes in PC12 cells. Mechanistically, cyanidin effectively blocked apoptosis induced by Aβ, by restoring the mitochondrial membrane potential via upregulation of Bcl-2 protein expression. Moreover, cyanidin markedly protected PC12 cells from Aβ-induced DNA damage by blocking reactive oxide species and superoxide accumulation. These results provide evidence that cyanidin suppresses Aβ-induced cytotoxicity, by preventing oxidative damage mediated by reactive oxide species, which in turn inhibits mitochondrial apoptosis. Our study demonstrates the therapeutic potential of cyanidin in the prevention of oxidative stress-mediated Aβ neurotoxicity.

Reactive oxygen species, nitric oxide and plant cell death associated with caspase-like protease activity during somatic embryogenesis in Fraxinus mandshurica

Programmed cell death occurs in browning explants of Fraxinus mandshurica during somatic embryogenesis, but the underlying mechanism is unclear. In this study, single cotyledons of zygotic embryos of F. mandshurica were used as explants. Mitochondrial structure and function, caspase-3-like protease activity, hydrogen peroxide metabolism, and nitric oxide accumulation induced by high concentrations of sucrose and plant growth regulators were studied. The results show that plant growth regulators induced somatic embryogenesis and also promoted explant browning. High sucrose concentrations had similar effects. High concentrations of sucrose and plant growth regulators led to the accumulation of hydrogen peroxide and nitric oxide which induced changes in mitochondrial structure and function such as modifications in mitochondrial morphology, increased membrane permeability, decreased membrane potential, and the release of cytochrome c into the cytoplasm. An increase in caspase-3-like protease activity triggered programmed cell death in some browning explant cells. During somatic embryogenesis there were increased activities of superoxide dismutase, peroxidase, and catalase, which are associated with hydrogen peroxide metabolism and jointly maintain reactive oxygen species levels. Intracellular nitric oxide synthase and nitrate reductase activities were not significantly correlated with nitric oxide content. Instead, intracellular nitric oxide may be derived from non-enzymatic reactions. Our results indicate that hydrogen peroxide and nitric oxide may function as signals, playing key roles in somatic embryogenesis and programmed cell death of explant cells of F. mandshurica. The interaction between nitric oxide and reactive oxygen species determines the occurrence of programmed cell death in explant cells;somatic embryogenesis and programmed cell death are positively regulated by hydrogen peroxide. However, the regulation of nitric oxide is complex.

Effect of Mixed Oxide Support for Ni/ZnO in Reactive Adsorption Desulfurization

The effect of mixed oxide support on the performance of Ni/ZnO in the reactive adsorption desulfurization(RADS) reaction was investigated in a fixed bed reactor by using thiophene as the sulfur-containing compound in the model gasoline. A series of oxide supports for Ni/ZnO were synthesized by the co-precipitation method and characterized by XRD, N_2-adsorption, TPR and NH_3-TPD techniques. It was found that the desulfurization capacity of Ni/ZnO was enhanced greatly when active components were supported on the proper mixed oxide. Ni/ZnO supported on oxides exhibited much higher desulfurization efficiency and sulfur adsorption capacity than the unsupported Ni/ZnO and the synthesized Ni/ZnO-SA adsorbent exhibited the highest efficiency for thiophene removal. The higher desulfurization activity and sulfur capacity of Ni/ZnO supported on SiO_2-Al_2O_3 with small particle size, high specific surface area and large pore volume could promote the high dispersion of active metal phase and the transfer of sulfur to ZnO with lower mass transfer resistance. γ-Al_2O_3 species could weaken the interaction of active phases and SiO_2 as well as could increase greatly the amount of weak acids. Therefore, these oxides could impose a great influence on the structure and chemical properties of the catalyst.

Impact of microplastics and nanoplastics on liver health:Current understanding and future research directions

With continuous population and economic growth in the 21st century,plastic pollution is a major global issue.However,the health concern of microplastics/nanoplastics(MPs/NPs)decomposed from plastic wastes has drawn public attention only in the recent decade.This article summarizes recent works dedicated to understanding the impact of MPs/NPs on the liver-the largest digestive organ,which is one of the primary routes that MPs/NPs enter human bodies.The interrelated mechanisms including oxidative stress,hepatocyte energy re-distribution,cell death and autophagy,as well as immune responses and inflammation,were also featured.In addition,the disturbance of microbiome and gut-liver axis,and the association with clinical diseases such as metabolic dysfunction-associated fatty liver disease,steatohepatitis,liver fibrosis,and cirrhosis were briefly discussed.Finally,we discussed potential directions in regard to this trending topic,highlighted current challenges in research,and proposed possible solutions.

Evaluation of the Oxidation Reactivity and Behavior of Exhaust Soot Particles from Diesel Engines with Different Emission Levels

The aim of this study was to investigate the oxidation reactivity and behavior of exhaust particulate matter(PM)from diesel engines.PM samples from two diesel engines(1K,CY4102)with different emission levels were collected by a thermophoretic system and a quartz filter.The oxidation reactivity,oxidation behaviors,and physicochemical properties of the PM samples were analyzed using thermogravimetric analysis(TGA),high-resolution transmission electron microscopy(HRTEM),Fourier-transform infrared spectrometry(FTIR),and Raman spectroscopy.The results showed that there was a great difference in the oxidation reactivity of soot particles emitted by the two different diesel engines.A qualitative analysis of the factors influencing oxidation reactivity showed that the nanostructure,degree of graphitization,and relative concentration of aliphatic C—H functional groups were the most important factors,whereas no significant correlation was found between the primary particle size and activation energy of the diesel soot.Based on the oxidation behavior analysis,the diesel soot particles exhibited both internal and surface oxidation modes during the oxidation process.Surface oxidation was dominant during the initial stage,and as oxidation progressed,the mode gradually changed to internal oxidation.Internal oxidation mode of soot particles from the 1K engine was significantly higher than that of CY4102.

Experimental and Theoretical Study of Hydrogen Atom Abstraction from C2H6 and C4H10 by Zirconium Oxide Clusters Anions

The reactions of anionic zirconium oxide clusters ZrxOy- with C2H6 and C4H10 are investi-gated by a time of flight mass spectrometer coupled with a laser vaporization cluster source.Hydrogen containing products Zr2O5H- and Zr3O7H- are observed after the reaction. Den-sity functional theory calculations indicate that the hydrogen abstraction is favorable in the reaction of Zr2O5- with C2H6, which supports that the observed Zr2O5H- and Zr3O7H- are due to hydrogen atom abstraction from the alkane molecules. This work shows a newpossible pathway in the reaction of zirconium oxide cluster anions with alkane molecules.

Induction of endoplasmic reticulum-derived oxidative stress by an occult infection related S surface antigen variant

AIM: To investigate the mechanism of endoplasmic reticulum(ER) stress induction by an occult infection related hepatitis B virus S surface antigen(HBsAg)variant.METHODS: We used an HBsAg variant with lower secretion capacity, which was a KD variant from a Korean subject who was occultly infected with the genotype C. We compared the expression profiles of ER stress-related proteins between HuH-7 cells transfected with HBsAg plasmids of a wild-type and a KD variant using Western blot.RESULTS: Confocal microscopy indicated that the KD variant had higher levels of co-localization with ER than the wild-type HBsAg. The KD variant upregulated ER stress-related proteins and induced reactive oxygen species(ROS) compared to the wildtype via an increase in calcium. The KD variant also down-regulated anti-oxidant proteins(HO-1, catalase and SOD) compared to the wild-type, which indicates positive amplification loops of the ER-ROS axis. The KD variant also induced apoptotic cell death via the upregulation of caspase proteins(caspase 6, 9 and 12).Furthermore, the KD variant induced a higher level of nitric oxide than wild-type HBsAg via the up-regulation of the iNOS protein.CONCLUSION: Our data indicate that occult infection related HBsAg variants can lead to ER-derived oxidative stress and liver cell death in HuH-7 cells.

Treatment with dimethyl fumarate ameliorates liver ischemia/reperfusion injury

To investigate the hypothesis that treatment with dimethyl fumarate (DMF) may ameliorate liver ischemia/reperfusion injury (I/RI). METHODSRats were divided into 3 groups: sham, control (CTL), and DMF. DMF (25 mg/kg, twice/d) was orally administered for 2 d before the procedure. The CTL and DMF rats were subjected to ischemia for 1 h and reperfusion for 2 h. The serum alanine aminotransferase (ALT) and malondialdehyde (MDA) levels, adenosine triphosphate (ATP), NO × metabolites, anti-oxidant enzyme expression level, anti-inflammatory effect, and anti-apoptotic effect were determined. RESULTSHistological tissue damage was significantly reduced in the DMF group (Suzuki scores: sham: 0 ± 0; CTL: 9.3 ± 0.5; DMF: 2.5 ± 1.2; sham vs CTL, P < 0.0001; CTL vs DMF, P < 0.0001). This effect was associated with significantly lower serum ALT (DMF 5026 ± 2305 U/L vs CTL 10592 ± 1152 U/L, P = 0.04) and MDA (DMF 18.2 ± 1.4 μmol/L vs CTL 26.0 ± 1.0 μmol/L, P = 0.0009). DMF effectively improved the ATP content (DMF 20.3 ± 0.4 nmol/mg vs CTL 18.3 ± 0.6 nmol/mg, P = 0.02), myeloperoxidase activity (DMF 7.8 ± 0.4 mU/mL vs CTL 6.0 ± 0.5 mU/mL, P = 0.01) and level of endothelial nitric oxide synthase expression (DMF 0.38 ± 0.05-fold vs 0.17 ± 0.06-fold, P = 0.02). The higher expression levels of anti-oxidant enzymes (catalase and glutamate-cysteine ligase modifier subunit and lower levels of key inflammatory mediators (nuclear factor-kappa B and cyclooxygenase-2 were confirmed in the DMF group. CONCLUSIONDMF improved the liver function and the anti-oxidant and inflammation status following I/RI. Treatment with DMF could be a promising strategy in patients with liver I/RI.

Hyperbaric oxygen preconditioning improves postoperative cognitive dysfunction by reducing oxidant stress and inflammation

Postoperative cognitive dysfunction is a crucial public health issue that has been increasingly studied in efforts to reduce symptoms or prevent its occurrence. However, effective advances remain lacking. Hyperbaric oxygen preconditioning has proved to protect vital organs, such as the heart, liver, and brain. Recently, it has been introduced and widely studied in the prevention of postoperative cognitive dysfunction, with promising results. However, the neuroprotective mechanisms underlying this phenomenon remain controversial. This review summarizes and highlights the definition and application of hyperbaric oxygen preconditioning, the perniciousness and pathogenetic mechanism underlying postoperative cognitive dysfunction, and the effects that hyperbaric oxygen preconditioning has on postoperative cognitive dysfunction. Finally, we conclude that hyperbaric oxygen preconditioning is an effective and feasible method to prevent, alleviate, and improve postoperative cognitive dysfunction, and that its mechanism of action is very complex, involving the stimulation of endogenous antioxidant and anti-inflammation defense systems.

Comparison in copper accumulation and physiological responses of Gracilaria lemaneiformis and G. lichenoides (Rhodophyceae)

Heavy metal pollution has become a worldwide problem in aquaculture. We studied copper （Cu^2＋） accumulation and physiological responses of two red algae Gracilaria lemaneiformis and Gracilaria lichenoides from China under Cu^2＋ exposure of 0-500 μg/L in concentration. Compared with G. lemaneiformis, G. lichenoides was more capable in accumulating Cu^2＋, specifically, more Cu〉 on extracellular side （cell wall） than on intracellular side （cytoplasm） and in cell organelles （especially chloroplast, cell nucleus, mitochondria, and ribosome）. In addition, G. lichenoides contained more insoluble polysaccharide in cell wall, which might promote the extracellular Cu^2＋-binding as an efficient barrier against metal toxicity. Conversely, G. lemaneiformis was more vulnerable than G. lichenoides to Cu^2＋ toxin for decreases in growth, pigment （chlorophyll a, chlorophyll b, phycobiliprotein, and B-carotene） content, and photosynthetic activity. Moreover, more serious oxidative damages in G. lemaneiformis than in G. lichenoides, in accumulation of reactive oxidative species and malondialdehyde, and in electrolyte leakage, because of lower antioxidant enzyme （superoxide dismutase and glutathione reductase） activities. Therefore, G. lichenoides was less susceptible to Cu〉 stress than G. lemaneiformis.

Morphology,Nanostructure,and Oxidation Reactivity of Particulate Matter Emitted by Diesel Blending with Various Aromatics

This study aims to analyze the influence of the polycyclic aromatic hydrocarbon(PAH)content in diesel on the physical and chemical properties of diesel soot particles.Four diesel fuels with different PAH content were tested on a 11.6 L direct-injection diesel engine.The raw particulate matter(PM)before the after-treatment devices was collected using the thermophoresis sampling system and the filter sampling system.A transmission electron microscope and Raman spectrometer are used to analyze the physical properties of the soot particles,including morphology,primary particle size distribution,and graphitization degree.A Fourier transform infrared spectrometer and thermogravimetric analyzer are used to characterize the surface chemical composition and oxidation reactivity of soot particles,respectively.The results show that as the PAH content in the fuel decreases,the size of the primary soot particles decreases from 29.58 to 26.70 nm.The graphitization degree of soot particles first increases and then decreases,and the relative content of the aliphatic hydrocarbon functional groups of soot particles first decreases and then increases.The T_(10),T_(50),and T_(90) of soot from high-PAH fuel are 505.3,589.3,and 623.5℃,while those from low-PAH fuel are 480.1,557.5,and 599.2℃,respectively.This indicates that exhaust PM generated by the low-PAH fuel has poor oxidation reactivity.However,as the PAH content in fuel is further decreased,the excessively high cetane number may cause uneven mixing and incomplete combustion,leading to enhanced oxidation reactivity.

Characteristics of alumina particles in dispersion-strengthened copper alloys

Two types of alumina dispersion-strengthened copper（ADSC） alloys were fabricated by a novel in-situ reactive synthesis（IRS） and a traditional internal oxidation（IO） process. The features of alumina dispersoids in these ADSC alloys were investigated by X-ray diffraction, scanning electron microscopy, and high-resolution transmission electron microscopy. It is found that nano-sized γ-Al2O3 particles of approximately 10 nm in diameter are homogeneously distributed in the IRS-ADSC composites. Meanwhile, larger-sized, mixed crystal structure alumina with rod-shaped morphology is embedded in the IO-ADSC alloy. The IRS-ADSC composites can obtain better mechanical and physical properties than the IO-ADSC composites; the tensile strength of the IRS-ADSC alloy can reach 570 MPa at room temperature, its electrical conductivity is 85% IACS, and the Rockwell hardness can reach 86 HRB.

Toxicity of superparamagnetic iron oxide nanoparticles: Research strategies and implications for nanomedicine

Superparamagnetic iron oxide nanoparticles （SPIONs） are one of the most versatile and safe nanoparticles in a wide variety of biomedical applications. In the past decades, considerable efforts have been made to investigate the potential adverse biological effects and safety issues associated with SPIONs, which is essential for the development of next-generation SPIONs and for continued progress in translational research. In this mini review, we summarize recent developments in toxicity studies on SPIONs, focusing on the relationship between the physicochemical properties of SPIONs and their induced toxic biological responses for a better toxicological understanding of SPIONs.

Two-dimensional modeling of the self-limiting oxidation in silicon and tungsten nanowires

Self-limiting oxidation of nanowires has been previously described as a reaction- or diffusion-controlled process. In this letter, the concept of finite reactive region is introduced into a diffusion-controlled model, based upon which a two-dimensional cylindrical kinetics model is developed for the oxidation of silicon nanowires and is extended for tungsten. In the model, diffusivity is affected by the expansive oxidation reaction induced stress. The dependency of the oxidation upon curvature and temperature is modeled. Good agreement between the model predictions and available experimental data is obtained. The de- veloped model serves to quantify the oxidation in two-dimensional nanostructures and is expected to facilitate their fabrication via thermal oxidation techniques.

Reactive Oxygen Species and Oxidative Stress in the Pathogenesis of MAFLD

The pathogenesis of metabolic-associated fatty liver disease(MAFLD)is complex and thought to be dependent on multiple parallel hits on a background of genetic susceptibility.The evidence suggests that MAFLD progression is a dynamic two-way process relating to repetitive bouts of metabolic stress and inflammation interspersed with endogenous anti-inflammatory reparative responses.In MAFLD,excessive hepatic lipid accumulation causes the production of lipotoxins that induce mitochondrial dysfunction,endoplasmic reticular stress,and over production of reactive oxygen species(ROS).Models of MAFLD show marked disruption of mitochondrial function and reduced oxidative capacitance with impact on cellular processes including mitophagy,oxidative phosphorylation,and mitochondrial biogenesis.In excess,ROS modify insulin and innate immune signaling and alter the expression and activity of essential enzymes involved in lipid homeostasis.ROS can also cause direct damage to intracellular structures causing hepatocyte injury and death.In select cases,the use of anti-oxidants and ROS scavengers have been shown to diminish the proapoptopic effects of fatty acids.Given this link,endogenous anti-oxidant pathways have been a target of interest,with Nrf2 activation showing a reduction in oxidative stress and inflammation in models of MAFLD.Thyroid hormone receptorβ(THRβ)agonists and nuclear peroxisome proliferationactivated receptor(PPAR)family have also gained interest in reducing hepatic lipotoxicity and restoring hepatic function in models of MAFLD.Unfortunately,the true interplay between the clinical and molecular components of MAFLD progression remain only partly understood.Most recently,multiomics-based strategies are being adopted for hypothesis-free analysis of the molecular changes in MAFLD.Transcriptome profiling maps the unique genotype-phenotype associations in MAFLD and with various single-cell tran scriptome-based projects underway,there is hope of novel physiological insights to MAFLD progression and uncover therapeutic targets.

Vascular endothelial growth factor up-regulates the expression of intracellular adhesion molecule-1 in retinal endothelial cells via reactive oxygen species, but not nitric oxide

Background The vascular endothelial growth factor （VEGF） is involved in the initiation of retinal vascular leakage and nonperfusion in diabetes. The intracellular adhesion molecule-1 （ICAM-1） is the key mediator of the effect of VEGFs on retinal leukostasis. Although the VEGF is expressed in an early-stage diabetic retina, whether it directly up-regulates ICAM-1 in retinal endothelial cells （ECs） is unknown. In this study, we provided a new mechanism to explain that VEGF does up-regulate the expression of ICAM-1 in retinal ECs. Methods Bovine retinal ECs （BRECs） were isolated and cultured. Immunohistochemical staining was performed to identify BRECs. The cultured cells were divided into corresponding groups. Then, VEGF （100 ng/ml） and other inhibitors were used to treat the cells. Cell lysate and the cultured supernatant were collected, and then, the protein level of ICAM-1 and phosphorylation of the endothelial nitric oxide synthase （eNOS） were detected using Western blotting. Griess reaction was used to detect nitric oxide （NO）. Results Western blotting showed that the VEGF up-regulated the expression of ICAM-1 protein and increased phosphorylation of the eNOS in retinal ECs. Neither the block of NO nor protein kinase C （PKC） altered the expression of ICAM-1 or the phosphorylation of eNOS. The result of the Western blotting also showed that inhibition of phosphatidylinositol 3-kinase （PI3K） or reactive oxygen species （ROS） significantly reduced the expression of ICAM-1. Inhibition of PI3K also reduced phosphorylation of eNOS. Griess reaction showed that VEGF significantly increased during NO production. When eNOS was blocked by L-NAME or PI3K was blocked by LY294002, the basal level of NO production and the increment of NO caused by VEGF could be significantly decreased. Conclusion ROS-NO coupling in the retinal endothelium may be a new mechanism that could help to explain why VEGF induces ICAM-1 expression and the resulting leukostasis in diabetic retinopathy.

Comparing dark-and photo-Fenton-like degradation of emerging pollutant over photo-switchable Bi2WO6/CuFe2O4: Investigation on dominant reactive oxidation species

The extensive use of tetracycline hydrochloride(TCH)poses a threat to human health and the aquatic environment.Here,magnetic p-n Bi2WO6/CuFe2O4 catalyst was fabricated to efficiently remove TCH.The obtained Bi2WO6/CuFe2O4 exhibited 92.1%TCH degradation efficiency and 50.7%and 35.1%mineralization performance for TCH and raw secondary effluent from a wastewater treatment plant in a photo-Fenton-like system,respectively.The remarkable performance was attributed to the fact that photogenerated electrons accelerated the Fe(III)/Fe(II)and Cu(II)/Cu(I)conversion for the Fenton-like reaction between Fe(II)/Cu(I)and H2O2,thereby generating abundant·OH for pollutant oxidation.Various environmental factors including H2O2 concentration,initial pH,catalyst dosage,TCH concentration and inorganic ions were explored.The reactive oxidation species(ROS)quenching results and electron spin resonance(ESR)spectra confirmed that·O2-and·OH were responsible for the dark and photo-Fenton-like systems,respectively.The degradation mechanisms and pathways of TCH were proposed,and the toxicity of products was evaluated.This work contributes a highly efficient and environmentally friendly catalyst and provides a clear mechanistic explanation for the removal of antibiotic pollutants in environmental remediation.

Reactive oxidative species enhance amyloid toxicity in APP/PS1 mouse neurons

Objective To investigate whether intracellular amyloid β （iAβ） induces toxicity in wild type （WT） and APP/PS1 mice, a mouse model of Alzheimer＇s disease. Methods Different forms of Aβ aggregates were microinjected into cultured WT or APP/PS1 mouse hippocampal neurons. TUNEL staining was performed to examine neuronal cell death. Reactive oxidative species （ROS） were measured by MitoSOXTM Red mitochondrial superoxide indicator. Results Crude, monomer and protofibrilAβ induced more toxicity inAPP/PS1 neurons than in WT neurons. ROS are involved in mediating the vulnerability of APP/PS1 neurons to iAβ toxicity. Conclusion Oxidative stress may mediate cell death induced by iAβ in neurons.

Evaluation of the antibacterial mechanism and biofilm removal effect of eugenol on Vibrio vulnificus and its application in fresh oysters

Eugenol is a natural active substance with high antibacterial activity,but its antibacterial activity against Vibrio vulnificus has not been extensively studied.The purpose of this study was to investigate the antibacterial and biofilm-clearing abilities and potential mechanisms of eugenol against V.vulnificus,and to provide knowledge for the use of eugenol to prevent oyster contamination.It was found that eugenol had an encouraging antibacterial effect on V.vulnificus with a minimum inhibitory concentration(MIC)of 0.2 mg/mL.The accumulation of reactive oxygen species(ROS)and the increase of malondialdehyde(MDA)content suggest that oxidative stress is involved in the bactericidal mechanism.Moreover,cell membrane hyperpolarization,changes in cell membrane integrity and morphology suggest that eugenol can reduce the permeability and integrity of cell membranes in V.vulnificus.In addition,eugenol produced a significant biofilm clearance effect on V.vulnificus,as evidenced by the reduced amount of biofilm and the reduction of polysaccharides and viable cells in the biofilm.Finally,eugenol was able to effectively inhibit the activity of V.vulnificus in artificially contaminated oyster at 4°C and 25°C.But sensory analysis showed that 0.10%eugenol was most acceptable to trained panelists.All of these highlight the great promise of eugenol as a natural bacteriostatic agent for the food industry.

Extracts of passion fruit peel and seed of Passiflora edulis(Passifloraceae) attenuate oxidative stress in diabetic rats

This study was aimed at evaluating the anti-diabetic potential of passion fruit Passiflora edulis(EPE) extracts in diabetic rats, following Streptozotocin(STZ) induced oxidative stress. Thirty adult Wistar rats were divided into five groups, with six rats in each group. The control rats were injected intraperitoneally with citrate buffer(pH 4.5). The remaining groups of rats were administered single dose of 45 mg·kg-1 of STZ by intraperitoneal route to induce diabetes. The diabetic animals were treated with 250 and 500 mg·kg-1 of EPE and glibenclamide 0.6 mg·kg-1 for fifteen days by oral route. Blood glucose, end organ oxidative stress marker, and anti-oxidants were assayed. Further, histopathological investigation of pancreas was studied at the end of the experimentation. The results revealed that subacute administration of EPE significantly(P < 0.001) controlled the blood glucose level in the diabetic rats. In addition, EPE extract protected the end organs by restoring the anti-oxidants enzyme, significantly increasing super oxide dismutase level(SOD) and decreasing catalase(CAT) and TBARS level in visceral organs. In conclusion, that EPE extracts showed anti-diabetic and anti-oxidant potential against streptozotocin-induced diabetes.