Vinpocetine attenuates fluoxetine-induced liver damage in rats; Role of Nrf2 and PPAR-γ

2021 ◽  
pp. 096032712110515
Author(s):  
Gellan Alaa Mohamed Kamel
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Mrna Expression ◽  
Liver Damage ◽  
B Cell Lymphoma ◽  
Control Group ◽  
Related Factor ◽  
Protective Effects ◽  
Ppar Γ

Background Fluoxetine (FLX) has been widely used as first-line treatment in cases of depression and other neuropsychiatric disorders. Although its safety has been approved, the use of FLX was associated with liver injury and chronic liver disease. Vinpocetine (Vinpo), a nootropic drug, possesses antioxidant and anti-inflammatory effects. Objective This study aimed to evaluate the protective effects of Vinpo on FLX-induced liver damage pointing to the role of peroxisome proliferator-activated receptor-gamma (PPAR-γ) and nuclear factor erythroid 2-related factor 2 (Nrf2). Methods Rats were randomized to four groups: control group, Vinpo group (20 mg/kg/day; orally), FLX group (10 mg/kg/day; orally), and Vinpo + FLX group. Results FLX-induced liver damage was evidenced through elevated liver function biomarkers and induced hepatic histopathological changes. Concurrent Vinpo treatment resulted in a significant decrease in hepatotoxicity biomarkers and histopathological alterations. FLX-induced oxidative stress and inflammation were attenuated by Vinpo. In addition, Vinpo attenuated the hepatic NRF2 and HO-1 levels and up-regulated PPAR-γ expression. Moreover, FLX elevated Bcl-2-associated X protein (Bax) mRNA expression and decreased B-cell lymphoma 2 (Bcl2) mRNA expression were markedly reversed by Vinpo. Conclusion Vinpo possesses ameliorative effects against FLX-induced liver injury in rats. This effect may be due to attenuation of oxidative stress and inflammation, in addition to upregulation of PPAR-γ expression.

scholarly journals Bamboo Stems (Phyllostachys nigra variety henosis) Containing Polyphenol Mixtures Activate Nrf2 and Attenuate Phenylhydrazine-Induced Oxidative Stress and Liver Injury

Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 114 ◽  
Author(s):  
Ji Hye Yang ◽  
Moon-Hee Choi ◽  
Chang-Su Na ◽  
Sam Seok Cho ◽  
Jae Hoon Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Iron Overload ◽  
Liver Damage ◽  
Hepg2 Cells ◽  
Hepatoprotective Effect ◽  
Glutathione Depletion ◽  
Related Factor ◽  
Nrf2 Target Gene ◽  
Phyllostachys Nigra

This study was designed to investigate the hepatoprotective effect of bamboo stems using in vitro and in vivo experimental liver damage models. Ethyl acetate fraction of 80% ethanol extract of Phyllostachys nigra stem (PN3) containing polyphenols had a higher NQO1-ARE reporter gene activity as monitored by the activity of the NF-E2-related factor (Nrf2) antioxidant pathway in cells in comparison to extracts from other species and under other conditions. The Nrf2 was translocated from the cytosol to the nucleus in response to PN3, followed by induction of the Nrf2 target gene expression, including HO-1, GCL, and NQO-1 in HepG2 cells. Phosphorylation of Nrf2 in HepG2 cells was enhanced in PN3, which was mediated by PKCδ, ERK, and p38 MAPK. Consequently, PN3 inhibited arachidonic acid (AA) + iron-induced reactive oxygen species generation and glutathione depletion, and, thus, highlighted their role in cytotoxicity. Treatment with major polyphenols of PN3, including catechin, chlorogenic acid, caffeic acid, and p-coumaric acid, also improved AA + iron-mediated oxidative stress and, thus, improved cell viability. Treatment with phenylhydrazine in mice, i.e., the iron overload liver injury model, increased plasma alanine aminotransferase and aspartate aminotransferase levels and changed histological features in mice—a response that was almost completely blocked by PN3 administration. Moreover, PN3 extract mitigated phenylhydrazine-induced oxidative stress and inflammatory responses. Conclusively, PN3 can exert a hepatoprotective effect against iron overload-induced acute liver damage due to its antioxidant properties.

scholarly journals Anti-Inflammatory Effects of Vardenafil Against Cholestatic Liver Damage in Mice: a Mechanistic Study

2018 ◽  
Vol 47 (2) ◽  
pp. 523-534 ◽  
Author(s):  
Dina S. El-Agamy ◽  
Hamdi H. Almaramhy ◽  
Nishat Ahmed ◽  
Bsmah Bojan ◽  
Waad D. Alrohily ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Mrna Expression ◽  
Inflammatory Cytokines ◽  
Liver Damage ◽  
Nlrp3 Inflammasome ◽  
Target Genes ◽  
Hepatic Tissue ◽  
Nuclear Factor ◽  
Phosphodiesterase 5

Background/Aims: Phosphodiesterase-5 inhibitors have beneficial effects in multiple liver diseases possibly through the reduction of oxidative stress and inflammatory response. However, these effects have not yet been examined in cholestatic liver dysfunction. Hence, this study aimed to explore the ability of vardenafil, a known phosphodiesterase-5 inhibitor, to repress lithocholic acid (LCA)-induced cholestatic liver injury and investigate the possible molecular pathways. Methods: Male Swiss albino mice were treated with LCA (0.125 mg/g) twice daily for 7 days to induce cholestatic liver damage. Vardenafil was administered 3 days before and throughout the administration of LCA. Serum markers of hepatotoxicity and hepatic nitro-oxidative stress along with antioxidant parameters were measured, and the histopathology of liver tissues was assessed. The expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its target genes was examined using PCR. The activation of nuclear factor kappa-B (NF-κB) and the levels of inflammatory cytokines were determined. NLRP3 inflammasome and its components were studied by PCR and western blot. Results: LCA induced marked cholestatic liver damage as demonstrated by increased serum transaminases, alkaline phosphatase (ALP), lactate dehydrogenase (LDH), bilirubin, and bile acids. Examination of liver specimens confirmed the biochemical results. Nitro-oxidative stress parameters were significantly elevated along with reduced antioxidant capacity in hepatic tissue following LCA administration. LCA suppressed Nrf2 and its target genes and decreased the mRNA expression and binding capacity of Nrf2 as well as the mRNA expression of GCLm, GCLc, Nqo1, and HO-1. Additionally, LCA enhanced the activation of NF-κB, which was accompanied by elevations of inflammatory cytokines. Importantly, LCA induced the activation of NLRP3 inflammasome. LCA increased the expression of NLRP3, ASC, caspase-1, and IL-1β genes and proteins in hepatic tissue. The activities of IL-1β and caspase-1 were increased in the LCA group. Interestingly, vardenafil ameliorated LCA-induced hepatic injury and alleviated all biochemical, histopathological, and inflammatory parameters. Conclusions: These data elucidated the effects of Nrf2 inhibition and NLRP3 inflammasome activation in LCA-induced liver injury. The hepatoprotective activity of vardenafil in LCA-induced cholestatic damage may result from the drug’s ability to activate Nrf2 signaling and prevent the activation of NLRP3, which could suppress the inflammatory responses in hepatic tissue. Thus, vardenafil can be considered a novel anti-inflammatory remedy for cholestatic liver damage.

scholarly journals SS-31 Protects Liver from Ischemia-Reperfusion Injury via Modulating Macrophage Polarization

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Longcheng Shang ◽  
Haozhen Ren ◽  
Shuai Wang ◽  
Hanyi Liu ◽  
Anyin Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Reperfusion Injury ◽  
Liver Damage ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Macrophage Polarization ◽  
Protective Effects ◽  
Inflammation Response ◽  
Stat3 Signaling

Ischemia-reperfusion injury (IRI) is a common complication in liver surgeries. It is a focus to discover effective treatments to reduce ischemia-reperfusion injury. Previous studies show that oxidative stress and inflammation response contribute to the liver damage during IRI. SS-31 is an innovated mitochondrial-targeted antioxidant peptide shown to scavenge reactive oxygen species and decrease oxidative stress, but the protective effects of SS-31 against hepatic IRI are not well understood. The aim of our study is to investigate whether SS-31 could protect the liver from damages induced by IRI and understand the protective mechanism. The results showed that SS-31 treatment can significantly attenuate liver injury during IRI, proved by HE staining, serum ALT/AST, and TUNEL staining which can assess the degree of liver damage. Meanwhile, we find that oxidative stress and inflammation were significantly suppressed after SS-31 administration. Furthermore, the mechanism revealed that SS-31 can directly decrease ROS production and regulate STAT1/STAT3 signaling in macrophages, thus inhibiting macrophage M1 polarization. The proinflammation cytokines are then significantly reduced, which suppress inflammation response in the liver. Taken together, our study discovered that SS-31 can regulate macrophage polarization through ROS scavenging and STAT1/STAT3 signaling to ameliorate liver injury; the protective effects against hepatic IRI suggest that SS-31 may be an appropriate treatment for liver IRI in the clinic.

scholarly journals THE PROTECTIVE EFFECTS OF ECHINOPS HETEROPHYLLUS AQUEOUS EXTRACT AGAINST METHOTREXATE-INDUCED HEPATOTOXICITY IN RABBITS

2019 ◽  
Vol 12 (1) ◽  
pp. 384 ◽  
Author(s):  
Heba Abdulmohsin ◽  
Ahmed Abu Raghif ◽  
Mohammed Jabbar Manna
Keyword(s):  
Oxidative Stress ◽  
Liver Damage ◽  
Crude Extract ◽  
Negative Control ◽  
Control Group ◽  
Protective Effects ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Study Results ◽  
Flavonoid Fraction

Objective: The aim of this study was to investigate antioxidant and hepatoprotective properties of Iraqi Echinops heterophyllus aqueous crude extract and its flavonoid fraction against methotrexate (MTX)-induced hepatotoxicity in rabbits.Methods: MTX-induced hepatotoxicity by administration of 20 mg/kg MTX intraperitoneally for 3 successive days was used as animal model, and animals were arrayed in four groups with eight animals in each group: Group 1 was the healthy control, Group 2 - the negative control receiving MTX only, Group 3 received MTX+crude extract of E. heterophyllus, and Group 4 administered MTX+flavonoid fraction of E. heterophyllus. The study duration was 10 days; at day 11, animals were sacrificed, and the blood samples were obtained for the measurement of serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, total bilirubin, total protein, and albumin as well as ELISA assay of the oxidative stress markers such as glutathione (GSH) and malondialdehyde (MDA). The liver was dissected and processed for histopathological investigation and scoring. Statistical analysis was performed to investigate the significance of each result.Results: The study results revealed severe liver damage due to MTX administration in the negative control (induced-non treated) group in comparison with healthy group, also there was significant hepatoprotective effect after administration of the crude extract of E. heterophyllus, and flavonoid fraction from E. heterophyllus shown after biochemical liver function tests and anti-oxidant properties demonstrated by the measurement of oxidative stress markers MDA and GSH. The crude extract of E. heterophyllus shown superior hepatoprotective and antioxidant effect. Histopathological scoring showed a remarkable decrease in the scores of the treatment groups in comparison with the high score in the MTX only treated group.Conclusions: MTX administered in a dose of 20 mg/kg for 3 successive days causes marked liver injury, while treatment with the crude extract and flavonoid fraction of E. heterophyllus significantly ameliorates MTX-induced liver damage, although the crude extract of E. heterophyllus seems to have the most hepatoprotective properties.

scholarly journals Hepatoprotective effects of chamazulene against alcohol-induced liver damage by alleviation of oxidative stress in rat models

2020 ◽  
Vol 15 (1) ◽  
pp. 251-258
Author(s):  
Xu Wang ◽  
Ke Dong ◽  
Yujing Ma ◽  
Qizhi Jin ◽  
Shujun Yin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Serum Alkaline Phosphatase ◽  
Positive Control ◽  
Ethanol Administration ◽  
Control Group ◽  
Protective Effects ◽  
Alcoholic Liver Injury ◽  
Rat Models ◽  
Hepatoprotective Effects

AbstractLiver injury and disease caused by alcohol is a common complication to human health worldwide. Chamazulene is a natural proazulene with antioxidant and anti-inflammatory properties. This study aims to investigate the hepatoprotective effects of chamazulene against ethanol-induced liver injury in rat models. Adult Wistar rats were orally treated with 50% v/v ethanol (8–12 mL/kg body weight [b.w.]) for 6 weeks to induce alcoholic liver injury. Chamazulene was administered orally to rats 1 h prior to ethanol administration at the doses of 25 and 50 mg/kg b.w. for 6 weeks. Silymarin, a commercial drug for hepatoprotection, was orally administered (50 mg/kg b.w.) for the positive control group. Chamazulene significantly reduced (p < 0.05) the levels of serum alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, and malondialdehyde, whereas the levels of antioxidant enzymes (glutathione peroxidase, catalase, and superoxide dismutase) and reduced glutathione were significantly restored (p < 0.05) in contrast to the ethanol model group. The levels of pro-inflammatory cytokines (tumour necrosis factor-α and interleukin-6) were suppressed by chamazulene (p < 0.05) with relevance to ethanol-induced liver injury. Histopathological alterations were convincing in the chamazulene-treated groups, which showed protective effects against alcoholic liver injury. Chamazulene has a significant hepatoprotective effect against ethanol-induced liver injury through alleviation of oxidative stress and prevention of inflammation.

scholarly journals Epigallocatechin-3-gallate protects against hepatic ischaemia–reperfusion injury by reducing oxidative stress and apoptotic cell death

2016 ◽  
Vol 44 (6) ◽  
pp. 1248-1262 ◽  
Author(s):  
Eunyoung Tak ◽  
Gil-Chun Park ◽  
Seok-Hwan Kim ◽  
Dae Young Jun ◽  
Jooyoung Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Reperfusion Injury ◽  
Apoptotic Cell ◽  
B Cell Lymphoma ◽  
Protective Effects ◽  
Ischaemia Reperfusion Injury ◽  
Treatment Groups ◽  
Markers Of Inflammation ◽  
Ischaemia Reperfusion

Objective To investigate the protective effects of epigallocatechin-3-gallate (EGCG), a major polyphenol source in green tea, against hepatic ischaemia–reperfusion injury in mice. Methods The partial hepatic ischaemia–reperfusion injury model was created by employing the hanging-weight method in C57BL/6 male mice. EGCG (50 mg/kg) was administered via an intraperitoneal injection 45 min before performing the reperfusion. A number of markers of inflammation, oxidative stress, apoptosis and liver injury were measured after the ischaemia–reperfusion injury had been induced. Results The treatment groups were: sham-operated (Sham, n = 10), hepatic ischaemia–reperfusion injury (IR, n = 10), and EGCG with ischaemia–reperfusion injury (EGCG-treated IR, n = 10). Hepatic ischaemia–reperfusion injury increased the levels of biochemical and histological markers of liver injury, increased the levels of malondialdehyde, reduced the glutathione/oxidized glutathione ratio, increased the levels of oxidative stress and lipid peroxidation markers, decreased B-cell lymphoma 2 levels, and increased the levels of Bax, cytochrome c, cleaved caspase-3, and cleaved caspase-9. Pretreatment with EGCG ameliorated all of these changes. Conclusion The antioxidant and antiapoptotic effects of EGCG protected against hepatic ischaemia–reperfusion injury in mice.

Effects of ANG II type 1 and 2 receptors on oxidative stress, renal NADPH oxidase, and SOD expression

2003 ◽  
Vol 285 (1) ◽  
pp. R117-R124 ◽  
Author(s):  
Tina Chabrashvili ◽  
Chagriya Kitiyakara ◽  
Jonathan Blau ◽  
Alex Karber ◽  
Shakil Aslam ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Mrna Expression ◽  
Candesartan Cilexetil ◽  
Superoxide Dismutases ◽  
Protective Effects ◽  
Ang Ii

Oxidative stress accompanies angiotensin (ANG) II infusion, but the role of ANG type 1 vs. type 2 receptors (AT1-R and AT2-R, respectively) is unknown. We infused ANG II subcutaneously in rats for 1 wk. Excretion of 8-isoprostaglandin F2α (8-Iso) and malonyldialdehyde (MDA) were related to renal cortical mRNA abundance for subunits of NADPH oxidase and superoxide dismutases (SODs) using real-time PCR. Subsets of ANG II-infused rats were given the AT1-R antagonist candesartan cilexetil (Cand) or the AT2-R antagonist PD-123,319 (PD). Compared to vehicle (Veh), ANG II increased 8-Iso excretion by 41% (Veh, 5.4 ± 0.8 vs. ANG II, 7.6 ± 0.5 pg/24 h; P < 0.05). This was prevented by Cand (5.6 ± 0.5 pg/24 h; P < 0.05) and increased by PD (15.8 ± 2.0 pg/24 h; P < 0.005). There were similar changes in MDA excretion. Compared to Veh, ANG II significantly ( P < 0.005) increased the renal cortical mRNA expression of p22 phox (twofold), Nox-1 (2.6-fold), and Mn-SOD (1.5-fold) and decreased expression of Nox-4 (2.1-fold) and extracellular (EC)-SOD (2.1-fold). Cand prevented all of these changes except for the increase in Mn-SOD. PD accentuated changes in p22 phox and Nox-1 and increased p67 phox. We conclude that ANG II infusion stimulates oxidative stress via AT1-R, which increases the renal cortical mRNA expression of p22 phox and Nox-1 and reduces abundance of Nox-4 and EC-SOD. This is offset by strong protective effects of AT2-R, which are accompanied by decreased expression of p22 phox, Nox-1, and p67 phox.

scholarly journals Inhibition of TRIM32 Attenuates the Apoptosis, Oxidative Stress and Inflammatory Injury of Podocytes Induced by High Glucose by Affecting the Akt/GSK-3β/Nrf2 Pathway

2021 ◽  
Author(s):  
Zhao Chen ◽  
Lifang Tian ◽  
Li Wang ◽  
Xiaotao Ma ◽  
Fuqian Lei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Inflammatory Response ◽  
High Glucose ◽  
Glycogen Synthase ◽  
Related Factor ◽  
Protective Effects ◽  
Gsk 3Β ◽  
Induced Apoptosis

Abstract Hyperglycemia-induced oxidative stress of podocytes exerts a major role in the pathological process of diabetic nephropathy. Tripartite motif-containing protein 32 (TRIM32) has been reported as a key protein in the modulation of cellular apoptosis and oxidative stress under various pathological processes. However, whether TRIM32 participates in the regulation of high glucose (HG)-induced injury in podocytes has not been investigated. The aims of this work were to assess the possible role of TRIM32 in mediating HG-induced apoptosis, oxidative stress and inflammatory response in podocytes in vitro. Herein, our results showed a marked increase in TRIM32 expression in HG-exposed podocytes. Loss-of-function experiments showed that the knockdown of TRIM32 improved the viability of HG-stimulated podocytes, and suppressed HG-induced apoptosis, oxidative stress and inflammatory response in podocytes. Further investigation revealed that the inhibition of TRIM32 enhanced the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling associated with modulation of the Akt/glycogen synthase kinase-3β (GSK-3β) axis in podocytes following HG exposure. However, the suppression of Akt abrogated the TRIM32-knockdown-mediated activation of Nrf2 in HG-exposed podocytes. In addition, the knockdown of Nrf2 markedly abolished the TRIM32-inhibition-induced protective effects in HG-exposed podocytes. In summary, the results of this work show that the inhibition of TRIM32 protects podocytes from HG-induced injury by potentiating Nrf2 signaling via the modulation of Akt/GSK-3β signaling. This study indicates a potential role of TRIM32 in mediating podocyte injury during the progression of diabetic nephropathy.

scholarly journals Resveratrol Relieved Acute Liver Damage in Ducks (Anas platyrhynchos) Induced by AFB1 via Modulation of Apoptosis and Nrf2 Signaling Pathways

Animals ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 3516
Author(s):  
Fangju Liu ◽  
Yingjie Wang ◽  
Xin Zhou ◽  
Mengru Liu ◽  
Sanjun Jin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Damage ◽  
Biological Activities ◽  
Control Group ◽  
Related Factor ◽  
Acute Liver Damage ◽  
Basic Diet ◽  
Significant Difference ◽  
Specific Pathogen ◽  
Male Specific

The presence of aflatoxin B1 (AFB1) in feed is a serious threat to livestock and poultry health and to human food safety. Resveratrol (Res) is a polyphenolic compound with antioxidant, anti-apoptotic and other biological activities; however, it is not clear whether it can improve AFB1 induced hepatotoxicity. Therefore, this study was conducted to investigate the effects of dietary Res on liver injury induced by AFB1 and its mechanisms. A total of 270 one-day-old male specific pathogen free (SPF) ducks, with no significant difference in weight, were randomly assigned to three groups: the control group, the AFB1 group and the AFB1 + Res group, which were fed a basic diet, a basic diet and a basic diet containing 500 mg/kg Res, respectively. On the 70th day, the ducks in theAFB1 group and the AFB1+ 500 mg/kg Res group were given 60 μg/kg AFB1 via gavage. When comparing the AFB1 group and the AFB1 + Res group and also with the control group, AFB1 significantly increased liver damage, cytochrome P450 (CYP450) and AFB1-DNA adduct content, increased oxidative stress levels and induced liver apoptosis, which was improved by Res supplementation. In sum, the addition of Res to feed can increase the activity of the II-phase enzyme, activate the nuclear factor E2-related factor 2 (Nrf2) signal pathway, and protect ducks’ livers from the toxicity, oxidative stress and inflammatory reaction induced by AFB1.

scholarly journals Ameliorative effects of crocin on paraquat-induced oxidative stress in testis of adult mice: An experimental study

2019 ◽  
Author(s):  
Fahime Sadat Kamali ◽  
Rasoul Shahrooz ◽  
Golamreza Najafi ◽  
Mazdak Razi
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Properties ◽  
B Cell Lymphoma ◽  
Testicular Tissue ◽  
Control Group ◽  
Protective Effects ◽  
Adult Mice ◽  
Oxidative Damages ◽  
Sham Control Group ◽  
Annual Weeds

Background: Paraquat (PQ), as a pyridine compound, is widely used worldwide to control annual weeds. The oxidative stress caused by PQ can cause deleterious changes in the testicular tissue. Objective: An investigation on the protective effects of Crocin (CCN) against PQinduced oxidative damages and apoptotic indices in testicular tissue. Materials and Methods: Twenty-eight adult male albino mice (20-25 gr) were divided into four groups (n = 7/each). The control group received 0.1 ml/day of normal saline by intraperitoneal injection (IP); sham-control group received PQ 5 mg/kg/day, IP, and the experimental groups received PQ (CCN+PQ) and CCN-sole (200 mg/kg/day, IP), respectively, for 35 continuous days. At the end of the treatment period, the testes were dissected out and used for biochemical, molecular, and histological analyses. The expressions of tumor suppressor p53, B-cell lymphoma 2 (bcl-2), and caspase-3 were considered as hallmark factors of mitochondria-dependent apoptosis. Moreover, the testicular superoxide dismutase (SOD) and malondialdehyde (MDA) were evaluated as key biomarkers for oxidative stress. Results: The PQ significantly (p < 0.02, p < 0.01) diminished the spermatogenesis indices and SOD, increased MDA levels, and enhanced the apoptosis-related gene expression. However, the co-administration of CCN and PQ significantly (p < 0.01, p < 0.01, p < 0.02) ameliorated the spermatogenesis ratio, upregulated the SOD level as well as bcl-2 expression, and reduced the MDA content and apoptosis vs the PQ-sole group. Conclusion: This study showed that the antioxidant properties of CCN enable to ameliorate the PQ-induced destructive effects by upregulating the testicular structure, antioxidant and apoptotic status. Key words: Histology, Testis, Paraquat, Crocin, Mice.

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