scholarly journals Protective Effect of Blood Cora Polysaccharides on H9c2 Rat Heart Cells Injury Induced by Oxidative Stress by Activating Nrf2/HO-1 Signal Pathway

2021 ◽  
Vol 8 ◽  
Author(s):  
Yong Jiang ◽  
Wei Zhou ◽  
Xin Zhang ◽  
Ying Wang ◽  
Dingyi Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Survival Rate ◽  
Western Blot ◽  
Protective Effect ◽  
Caspase 3 ◽  
Heart Cells ◽  
Cell Survival Rate ◽  
Mda Content ◽  
Cyt C ◽  
Rat Heart Cells

The protective effect of blood cora polysaccharides (BCP) on H9c2 rat heart cells under oxidative stress was explored with the use of a H9c2 cell oxidative stress model. The ability of BCP to scavenge 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), 1,1-diphenyl-2-picrylhydrazyl (DPPH), and hydroxyl radicals and its reducing power were measured in vitro, indicating a more powerful antioxidant effect of BCP compared to a similar concentration of vitamin C. The cellular metabolic activity was tested through the MTT [3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide] assay. Additionally, the relevant oxidation indicator level within the cell supernatant and cells was tested with reagent kits, and mRNA and protein expression levels in the cells were tested through quantitative polymerase chain reaction (qPCR) and western blot. The chemical composition of BCP was determined through high performance liquid chromatography (HPLC). The results show that compared with the normal group, the model group's cell survival rate (28.75 ± 2.56%) decreased, lactate dehydrogenase (LDH) leakage and the malondialdehyde (MDA) content increased, and superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) levels decreased. The results of qPCR and western blot show that compared with the normal group, the model group's Bcl-2 associated X protein (Bax), caspase-3, nuclear factor erythroid-2 related factor 2 (Nrf2), heme oxygenase-1 (HO-1) expression, NAD(P)H:quinoneoxidoreductase 1 (NQO1), and cytochrome c (Cyt C) decreased, and B-cell lymphoma-2 (Bcl-2) expression was increased, with significant statistical differences. Compared with the model group, the cell survival rate for each BCP-treated group increased, the LDH leakage decreased, the SOD, CAT, and GSH levels in the cells increased, the MDA content decreased, the Bax, caspase-3, Nrf2, HO-1, NQO1, and Cyt C expression was weakened, and the Bcl-2 expression was strengthened. BCP inhibited the reduction of mitochondrial membrane potential caused by H2O2 treatment. According to the component analysis, BCP mainly consist of mannitol, ribose, glucosum anhydricum, galactose, and xylose. It was observed that the Nrf2/HO-1 signaling pathway can be activated, regulated, and controlled by functional BCP to protect H9c2 cells injured by oxidative stress.

scholarly journals Protective Effect of Hydroxysafflor Yellow A on Nephropathy by Attenuating Oxidative Stress and Inhibiting Apoptosis in Induced Type 2 Diabetes in Rat

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Maosheng Lee ◽  
Hengxia Zhao ◽  
Xuemei Liu ◽  
Deliang Liu ◽  
Jianping Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Diabetic Nephropathy ◽  
Western Blot ◽  
Protective Effect ◽  
Caspase 3 ◽  
Renal Tissue ◽  
Hydroxysafflor Yellow A

Diabetic nephropathy (DN) is a serious complication of diabetes mellitus, and its prevalence has been increasing all over the world, which is also the leading cause of end-stage renal failure. Hydroxysafflor yellow A (HSYA) is the main active chemical component of Carthamus tinctorius L., and it is commonly used in patients with cardiovascular and cerebrovascular diseases in China. The aim of this study was to investigate the renal protective effects and molecular mechanisms of HSYA on high-fat diet (HFD) and streptozotocin- (STZ-) induced DN in rats. The DN rats were treated with HSYA for eight weeks. We assessed creatinine (CR), urea nitrogen (UN), glomerular volume, podocyte number, renal inflammation, oxidative stress, and cells apoptosis markers after HSYA treatment. The number of apoptotic cells was measured by the TUNEL assay, and apoptosis-related proteins BAX, caspase-3, and BCL-2 in the renal tissue were analyzed by western blot. The treatment with HSYA significantly decreased fasting blood glucose, CR, UN, and blood lipid profile, including triglyceride and total and low-density lipoprotein cholesterol, even though it did not change the rats’ body weights. The western blot results indicated that HSYA reversed the upregulation of BAX and caspase-3 and significantly increased BCL-2 in renal tissue. Moreover, the levels of TNF-α and the inflammatory products, including free fatty acids (FFA) and lactic dehydrogenase (LDH) in the HSYA group, were significantly decreased. For the oxidative stress marker, the superoxide dismutase (SOD) markedly increased in the HSYA treatment group, while the malondialdehyde (MDA) in the serum and kidney tissue evidently decreased. In conclusion, HSYA treatment preserved kidney function in diabetic nephropathy in the HFD- and STZ-induced rats. The potential mechanism of renal protective effect of HSYA might be through inhibiting oxidative stress, reducing inflammatory reaction, and attenuating renal cell apoptosis. Our studies present a promising use for Hydroxysafflor yellow A in the treatment of type 2 diabetes mellitus.

scholarly journals Protective Effect of L-carnitine on the Oxidative Stress Injury of Human Ovarian Granulosa Cells

2021 ◽  
Author(s):  
Xuening Li ◽  
Xiaodong Wu ◽  
Yuemin Zhang ◽  
Tianyi Ma ◽  
Pingping Sun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Cell Viability ◽  
Granulosa Cells ◽  
Blank Group ◽  
Stress Injury ◽  
Ovarian Granulosa Cells ◽  
Nuclear Pyknosis ◽  
Mda Content

Abstract The protective effect of L-carnitine (LC) on the oxidative stress (OS) injury and the effect of L-carnitine on follicular stimulating hormone receptor (FSHR) of ovarian granulosa cells (GCs) were investigated. OS was induced by treatment with H2O2. We cultured KGN cells in four groups: the blank group, OS group and two L-carnitine pretreatment group (low, high). In the OS group, cell nuclear pyknosis was observed, mitochondria swelled irregularly and their cristae were fractured. Meanwhile, the cell viability, superoxide dismutase (SOD) and glutathione (GSH) contents, mitochondrial membrane potential (ΔΨm) and the level of FSHR expression were significantly decreased in the OS group. However, malonaldehyde (MDA) content, reactive oxygen species (ROS) level and apoptosis rate were significantly increased. Compared with the OS group, the morphology of cells and mitochondria in the L-carnitine pretreatment group were improved, the cell viability and the expression of FSHR was significantly increased, and the OS level was decreased. These results indicated that L-carnitine can protect the cells from OS damage induced by H2O2, enhance the antioxidant and anti-apoptotic ability of GCs, and alleviate the decrease of FSHR expression on GCs caused by OS. Therefore, L-carnitine may help prevent the ovarian aging and improve the quality of follicles.

Mitigation of IL-1β, IL-6, TNF-α, and markers of apoptosis by ursolic acid against cisplatin-induced oxidative stress and nephrotoxicity in rats

2021 ◽  
Vol 40 (12_suppl) ◽  
pp. S397-S405
Author(s):  
Pankaj Tripathi ◽  
Saeed Alshahrani
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Uric Acid ◽  
Inflammatory Cytokines ◽  
Caspase 3 ◽  
Caspase 9 ◽  
Histological Damage ◽  
Tnf Α ◽  
Mda Content ◽  
Pro Inflammatory Cytokines

Background: Ursolic acid (UA) is a natural pentacyclic triterpenoid that is known for its benefits under several pathological conditions. Cisplatin (CP) is among the most preferred chemotherapeutic agents; however, its nephrotoxicity limits its clinical utility. Purpose: This study was aimed to determine the role of UA in the reduction of CP-induced nephrotoxicity and mitigation of pro-inflammatory cytokines and apoptosis in a rat model. Methodology: Male Wistar rats were randomized into vehicle control, CP (7.5 mg/kg), UA 10 mg/kg, and CP with UA 5 and 10 mg/kg groups. Kidney and blood samples were collected for assessment of renal function, measurement of pro-inflammatory cytokines, apoptosis markers, antioxidant activity, and tissue histology. Results: CP significantly increased the levels of serum Cr, BUN, and uric acid; it also induced histological damage reflecting the pathophysiology observed during nephrotoxicity. CP has also shown its pro-oxidant activity in kidney tissue because CP decreased the levels of GSH, SOD, and CAT; it increased the lipid peroxidation as measured by MDA content. In addition, CP significantly upregulated the activity of pro-inflammatory cytokines and expression of apoptotic markers, that is, there were increased levels of IL-1β, IL-6, TNF-α, caspase-3, and caspase-9. Two weeks of continuous treatment of UA showed significant recovery against CP-induced nephrotoxicity; UA decreased the levels of Cr, BUN, and uric acid and ameliorated histological damage. UA also downregulated the activities of IL-1β, IL-6, and TNF-α as well as expression of caspase-3 and caspase-9. Furthermore, CP-induced oxidative stress that was antagonized by UA—the levels of GSH, SOD, and CAT were significantly increased while MDA content was decreased. Conclusions: UA has a protective effect against CP-induced nephrotoxicity, which may be due to its antioxidant activity and mitigation of ILβ-1, ILβ-6, TNF-α, and markers of apoptosis.

scholarly journals THE EFFICACY OF 200 ΜG/KGBW/IP HEAT SHOCK PROTEIN-70 IN REDUCTION OF CYT C, BAX, AND CASPASE 3 EXPRESSION, AND MORTALITY IN MICE MODEL WITH MULTIPLE ORGAN DYSFUNCTION SYNDROME

2018 ◽  
Vol 11 (11) ◽  
pp. 482
Author(s):  
Igl Sukamto ◽  
Suroto Suroto ◽  
Ambar Mudigdo ◽  
Bambang Purwanto
Keyword(s):  
Survival Rate ◽  
Organ Dysfunction ◽  
Multiple Organ Dysfunction Syndrome ◽  
Heat Shock Protein 70 ◽  
Caspase 3 ◽  
Multiple Organ ◽  
Multiple Organ Dysfunction ◽  
Mice Model ◽  
Lung Epithelial ◽  
Cyt C

Objective: Heat shock protein 70 (HSP70) decreases Cyt expression c, Bax, and Caspase 3 in apoptosis multiple organ dysfunction syndrome (MODS), thus inhibiting death. This study aimed to analyze the efficacy of HSP70 200 μg/KgBB/ip to decrease Cyt c, Bax, and Caspase 3 expression, to reduce mortality, and to increase survival rate, in the MOD alveolar lung epithelial of 78-h sepsis model.Methods: This was a post-test only quasi-experiment conducted at Inter-University Central Laboratory of Gadjah Mada University, Yogyakarta, and the Anatomy Pathology Laboratory, Faculty of Medicine, Universitas Sebelas Maret, Surakarta. The study used a type of Balb/c mice, male, aged of 6–8 weeks, body weight of 25–33 g. Sepsis induction used LIG SIGMA L2880-10MG Lot #025M4040V from Escherichia coli 055:B5 purified by phenol extraction. Medication to reduce mortality used HSP70 Lot #L16020515 and then continued with 400× immunohistochemistry (IHC) examination. A sample of 30 mice were divided into three groups: (1) Control group without 78 h treatment, (2) lipopolysaccharide (LPS) group with a dose of 0.25 mg/kgBW/ip 78 h, and (3) HSP70 group with a dose of 200 μg/kgBB/ip after LPS injection 0.25 mg/kgBW/ip 78 h. The outcome variables included expression of Cyt, Bax, Caspase 3, and mortality in mice model with multiple organ dysfunction syndrome. The data were analyzed by Kruskal–Wallis and continued by Mann–Whitney U-test. Results: Administration of HSP70 200 mg/KgBW/ip after LPS 0.25 mg/kgBW/ip significantly decreased Cyt c expression (p=0.014), Bax (p=0.004), and Caspase 3 (p=0.015) in 78 h pulmonary alveolar cells, reduced mortality rate, and increased the number of survivors. Expressions of Cyt c, Bax, and Caspase 3 of IHC 400× magnification had a near-normal image change.Conclusion: There is a decrease of Cyt c, Bax, and Caspase 3 expression in the MOD alveolar lung epithelial cells of the 78-h sepsis model mice, a decrease of mortality rate, and an increase of survival rate, and the image of IHC is almost normal.

scholarly journals Klotho protects chondrocyte viability via FOXO1/3 in osteoarthritis

2021 ◽  
Vol 20 (9) ◽  
pp. 1961-1968
Author(s):  
Wei Wei ◽  
Liefeng Ji ◽  
Wanli Duan ◽  
Jiang Zhu
Keyword(s):  
Oxidative Stress ◽  
Survival Rate ◽  
Protective Effect ◽  
Collagen I ◽  
Inflammatory Factors ◽  
Ros Production ◽  
Chondrocyte Viability ◽  
Tnf Α ◽  
Collagen Ii

Purpose: To investigate the effect of Klotho and FOXO1/3 on the CH viability in OA.Methods: The survival rate of CHs, Klotho and FOXO1/3 protein expression, and ROS production were measured in the OA cartilages of different degenerative phases. H2O2 was also used to injure CHs, and the cell viability, Klotho and FOXO1/3 expressions, as well as ROS levels were investigated to clarify the effect of exogenic Klotho on the injured CHs. Additionally, in order to verify the role of FOXO1/3 in Klotho-treated CHs, SOD2, GPX1, inflammatory factors, collagen I/II, SOX9, and Runx-2 levels were analyzed by silencing FOXO1 and FOXO3 expression via siRNA transfection.Results: Klotho and FOXO1/3 expressions significantly decreased, and ROS production increased in severely human OA cartilage (p <0.05). Besides, H2O2 affected CHs viability with the suppression of Klotho and FOXO1/3 expression but ROS production was elevated. Exogenic Klotho application partly reversed the injury caused by H2O2. Furthermore, Klotho treatment of the injured CHs contributed to SOD2 and GPX1 expressions, and suppressed IL-1β, IL-6, TNF-α and MMP-13 production, resulting in  the upregulation of collagen II and SOX9 as well as downregulation of collagen I and Runx-2. However, the protective effect of Klotho was weakened by FOXO1 and FOXO3 gene silencing.Conclusion: Klotho protects CHs viability by suppressing oxidative stress and inflammation, which is associated with the mediation of FOXO1 and FOXO3. These findings provide new insights into the treatment of OA.

Protective effect of chloroform extract of Stereospermum chelonoides bark against amyloid beta42 induced cell death in SH-SY5Y cells and against inflammation in Swiss albino mice

2018 ◽  
Vol 29 (6) ◽  
pp. 621-630
Author(s):  
Md. Imamul Islam ◽  
Meena Afroze Shanta ◽  
Milon Mondal ◽  
Nazia Hoque ◽  
Senjuti Majumder ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Protective Effect ◽  
Antioxidant Capacity ◽  
Caspase 3 ◽  
Radical Scavenging ◽  
Chloroform Extract ◽  
Dependent Manner ◽  
Dose Dependent

Abstract Background This study was designed to evaluate the free radical scavenging property of chloroform extract of the bark of Stereospermum chelonoides (SCBC) and to investigate its potential in Alzheimer’s disease and inflammation, two oxidative stress related disorders. Methods Preliminary phytochemical analysis and in vitro antioxidant potential of SCBC were evaluated using 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging assay, ferric reducing antioxidant power (FRAP) assay, cupric reducing antioxidant capacity (CUPRAC) and total antioxidant capacity determination assay. Total phenol and total flavonoid contents were also determined. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) based cytotoxicity and cyto-protective assays were performed on human neuroblastoma SH-SY5Y cells. Thioflavin-T assay and caspase activation measurement assay were carried out to elucidate the mechanism of cytoprotection of SCBC observed here. In vivo anti-inflammatory potential was measured using croton oil and xylene induced ear edema tests. Results Phytochemical screening of SCBC revealed the presence of various phytoconstituents. Dose-dependent in vitro antioxidant activity was observed. The extract was enriched in flavonoids and polyphenolic compounds too. SCBC was found to inhibit amyloid-β peptide 1-42 (Aβ42) induced cell death in a dose-dependent manner. Encouraged by the cyto-protective effect, its effects on Aβ42 fibrillogenesis and caspase-3 activated apoptosis were observed. SCBC significantly slowed down the Aβ42 fibrillogenesis and caspase-3 activation in a concentration-dependent manner indicating its probable mechanism of rendering cyto-protection. SCBC has been able to reduce inflammation significantly in croton oil induced ear edema in both doses. Conclusions Thus, this study could form the basis for further study for the potential use of SCBC in oxidative stress associated cell death and inflammation.

scholarly journals Molecular Mechanism of Vitamin K2 Protection against Amyloid-β-Induced Cytotoxicity

Biomolecules ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 423
Author(s):  
Shu-Hsiang Huang ◽  
Sheng-Ting Fang ◽  
Yi-Cheng Chen
Keyword(s):  
Western Blot ◽  
Protective Effect ◽  
Caspase 3 ◽  
Cell Model ◽  
Serum Vitamin ◽  
Amyloid Β ◽  
Protective Role ◽  
Vitamin K2 ◽  
Neural Cells ◽  
Apoptosis Inhibitor

The pathological role of vitamin K2 in Alzheimer’s disease (AD) involves a definite link between impaired cognitive functions and decreased serum vitamin K levels. Vitamin K2 supplementation may have a protective effect on AD. However, the mechanism underlying vitamin K2 protection has not been elucidated. With the amyloid-β (Aβ) cascade hypothesis, we constructed a clone containing the C-terminal fragment of amyloid precursor protein (β-CTF/APP), transfected in astroglioma C6 cells and used this cell model (β-CTF/C6) to study the protective effect of vitamin K2 against Aβ cytotoxicity. Both cellular and biochemical assays, including cell viability and reactive oxygen species (ROS), assays assay, and Western blot and caspase activity analyses, were used to characterize and unveil the protective role and mechanism of vitamin K2 protecting against Aβ-induced cytotoxicity. Vitamin K2 treatment dose-dependently decreased the death of neural cells. The protective effect of vitamin K2 could be abolished by adding warfarin, a vitamin K2 antagonist. The addition of vitamin K2 reduced the ROS formation and inhibited the caspase-3 mediated apoptosis induced by Aβ peptides, indicating that the mechanism underlying the vitamin K2 protection is likely against Aβ-mediated apoptosis. Inhibitor assay and Western blot analyses revealed that the possible mechanism of vitamin K2 protection against Aβ-mediated apoptosis might be via regulating phosphatidylinositol 3-kinase (PI3K) associated-signaling pathway and inhibiting caspase-3-mediated apoptosis. Our study demonstrates that vitamin K2 can protect neural cells against Aβ toxicity.

scholarly journals Desoxyrhapontigenin attenuates neuronal apoptosis in an isoflurane-induced neuronal injury model by modulating the TLR-4/cyclin B1/Sirt-1 pathway

AMB Express ◽  
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Feng Liang ◽  
Xin Fu ◽  
Yunpengfei Li ◽  
Fanglei Han
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Protein Expression ◽  
Protective Effect ◽  
Neuronal Apoptosis ◽  
Caspase 3 ◽  
Neuronal Injury ◽  
Cyclin B1 ◽  
The Brain ◽  
And Oxidative Stress

Abstract This study investigated the protective effect of desoxyrhapontigenin (DOP) against isoflurane (ISF)-induced neuronal injury in rats. Neuronal injury was induced in pups by exposing them to 0.75% ISF on postnatal day 7 with 30% oxygen for 6 h. The pups were treated with DOP 10 mg/kg, i.p., for 21 days after ISF exposure. The protective effect of DOP was estimated by assessing cognitive function using the neurological score and the Morris water maze. Neuronal apoptosis was assessed in the hippocampus using the TUNEL assay, and protein expression of caspase-3, Bax, and Bcl-2 was measured by Western blotting. The levels of cytokines and oxidative stress parameters were assessed by ELISA. Western blotting and RT-PCR were performed to measure the expression of NF-kB, TLR-4, Sirt-1, and cyclin B1 protein in the brain. The cognitive function and neurological function scores were improved in the DOP group compared with the ISF group. Moreover, DOP treatment reduced the number of TUNEL-positive cells and the expression of caspase-3, Bax, and Bcl-2 protein in the brains of rats with neuronal injury. The levels of mediators of inflammation and oxidative stress were reduced in the brain tissue of the DOP group. Treatment with DOP attenuated the protein expression of TLR-4, NF-kB, cyclin B1, and Sirt-1 in the brain tissue of rats with neuronal injury. In conclusion, DOP ameliorates neuronal apoptosis and improves cognitive function in rats with ISF-induced neuronal injury. Moreover, DOP treatment can prevent neuronal injury by regulating the TLR-4/cyclin B1/Sirt-1 pathway.

scholarly journals Neuroprotective effects of proanthocyanidins of grape seed extracts against oxidative stress and apoptosis induced by 6-hydroxydopamine in PC12 cells

Conjecturas ◽  
2021 ◽  
Vol 21 (2) ◽  
pp. 68-86
Author(s):  
Patricia de Araújo Rodrigues ◽  
Selene Maia de Morais ◽  
Juliana Fernandes Pereira ◽  
Albert Layo Costa de Assis ◽  
Amanda Aragão Alves ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Western Blot ◽  
Caspase 3 ◽  
Grape Seed ◽  
Vitis Vinifera L ◽  
Neuroprotective Effects ◽  
Caspase 7 ◽  
6 Hydroxydopamine ◽  
Grape Seed Extracts ◽  
Seed Extracts

A doença de Parkinson (DP) é um distúrbio neurológico caracterizado pela destruição neuronal dopaminérgica. Devido à óbvia existência de ácidos graxos poliinsaturados (PUFA) principalmente em sementes de uva, Vitis Vinifera L era mais comumente usado em doenças cardiovasculares. O objetivo deste estudo foi investigar o papel das proantocianidinas do extrato de semente de uva exibindo efeitos neurocitoprotetores contra a citotoxicidade induzida por 6-hidroxidopamina (6-OHDA) em células PC12, prevenindo a depleção do conteúdo de GSH e reduzindo os níveis de nitrito e malondialdeído. As células foram pré-tratadas com proantocianidinas (100 µg / ml) e subsequentemente expostas a 6-OHDA a 50% da concentração letal. Nossos resultados demonstraram que a resposta ao PA em células PC12 aumentou significativamente a viabilidade celular, diminuiu a citotoxicidade. A atividade de apoptose induzida por OHDA foi determinada por citometria de fluxo usando anexina v e caspase-3 clivada e expressão de caspase-7 foram analisadas por western blot. Além disso, medimos marcadores de estresse oxidativo, como; Níveis de MDA, GSH e nitrito em células PC12. As proantocianidinas preveniram a citotoxicidade induzida por 6-OHDA, preveniram a depleção do conteúdo de GSH e reduziram os níveis de nitrito e malondialdeído. Além disso, as proantocianidinas atenuaram a redução induzida por 6-OHDA das proteínas caspase-3 e caspase-7 clivadas. Esses resultados sugerem que as proantocianidinas protegem as células PC12 contra a neurotoxicidade induzida pela 6-OHDA por meio da atividade antioxidante e apoptótica.

scholarly journals Resveratrol Alleviates Pyraclostrobin Induced Lipid Peroxidation, Oxidative Stress, and DNA Damage in Rats

2021 ◽  
Author(s):  
FAHRIYE ZEMHERI NAVRUZ ◽  
Sinan INCE ◽  
Damla ARSLAN-ACAROZ ◽  
Ulaş ACAROZ ◽  
Hasan Hüseyin DEMIREL ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Protective Effect ◽  
Caspase 3 ◽  
Male Rats ◽  
Histopathological Changes ◽  
Caspase 9 ◽  
Oral Gavage ◽  
Protective Properties ◽  
Expression Levels

Abstract Pyraclostrobin (Pyra) is a fungicide in the strobilurin class and has proven to be very toxic to aquatic species. Resveratrol (Res) is a phytoalexin that exhibits multiple bioactivities as antioxidative, anti-inflammatory, cardiovascular protective, and anti-aging in animals and is found in plant species such as mulberry, peanut, and grape. This study aimed to determine the protective effect of Res against Pyra-induced oxidative stress in rats. For this purpose, a total of 48 male rats divided into 6 groups − 8 in each group - were exposed to 30 mg/kg Pyra by oral gavage once a day for 4 weeks and to 3 different concentrations of Res (5, 10 and 20 mg/kg) together with Pyra. It was observed that, in groups administered with Pyra, malondialdehyde (MDA) levels increased whereas glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) levels decreased. It was observed that, in the group administered with Pyra, expression levels of CYP2E1 gene, which is associated with increased cancer risk, pro-apoptotic BAX gene, apoptotic caspase-3, caspase-8 and caspase-9 genes, NFκB gene, which is a pro-inflammatory transcription factor, and p53 gene, which plays a regulatory role in the cell, increased whereas expression level of anti-apoptotic bcl-2 gene decreased. It was determined that Res administrations improved Pyra-induced oxidative damage, histopathological changes and expression levels of various genes. According to the ssDNA analysis obtained from the DNA isolated from the blood; when DNA damage and histopathological damage in tissues were examined, it was observed that the highest damage was in the group administered with Pyra and the damage decreased depending on the increase in dose of Res. Consequently, it was observed that Res, known for its antioxidant protective properties, exhibited a protective effect against oxidative stress caused by Pyra.

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