scholarly journals Oxidative stress burden inhibits spermatogenesis in adult male rats: testosterone protective effect

2018 ◽  
Vol 96 (4) ◽  
pp. 372-381 ◽  
Author(s):  
Samy Makary ◽  
Mohamed Abdo ◽  
Ereny Fekry
Keyword(s):  
Oxidative Stress ◽  
Aromatase Inhibitor ◽  
Adult Male ◽  
Male Rats ◽  
Testicular Toxicity ◽  
Oxidative Stress Markers ◽  
Sperm Viability ◽  
Protective Agents ◽  
Stress Markers ◽  
Anti Inflammatory

In this study, we aimed to investigate the protective effects of androgens, using letrozole (LET; an aromatase inhibitor), grape seed extract (GSE; a naturally occurring aromatase inhibitor and antioxidant), and testosterone propionate (Tp), against methotrexate (MTX)-induced testicular toxicity in adult male rats. MTX has been shown to induce oxidative stress and exhibit antiproliferative effects in the testes. Adult male rats received oral saline gavage (control group with no treatment), the potential protective agents (LET, GSE, or Tp) alone, MTX alone, or a combination of one of the potential protective agents and MTX. The testicular levels of oxidative stress markers and cytokines (tumor necrosis factor-α and interleukin-1β) were measured. Spermatogenesis and sperm viability were microscopically evaluated. Administration of LET and GSE 7 days before MTX improved spermatogenesis and sperm viability, as well as reduced the levels of oxidative stress markers and cellular cytokines. Exogenous testosterone exhibited anti-inflammatory and antioxidant activities, similar to GSE and LET. We also showed that enhancing the endogenous androgenic activity by LET and GSE protected spermatogenesis against MTX-induced testicular toxicity via reduction of inflammation and oxidative stress in the testes. Our data suggest that testosterone protected spermatogenesis owing to its antioxidant and anti-inflammatory properties.

scholarly journals Combined Therapy with SS31 and Mitochondria Mitigates Myocardial Ischemia-Reperfusion Injury in Rats

2018 ◽  
Vol 19 (9) ◽  
pp. 2782 ◽  
Author(s):  
Fan-Yen Lee ◽  
Pei-Lin Shao ◽  
Christopher Wallace ◽  
Sarah Chua ◽  
Pei-Hsun Sung ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Ischemia ◽  
Adult Male ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Left Ventricular Ejection ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Myocardial Ischemia Reperfusion ◽  
Sirt3 Expression

Myocardial ischemia-reperfusion (IR) injury contributes to adverse cardiac outcomes after myocardial ischemia, cardiac surgery, or circulatory arrest. In this study, we evaluated the ability of combined SS31-mitochondria (Mito) therapy to protect heart cells from myocardial IR injury. Adult male SD rats (n = 8/each group) were randomized: group 1 (sham-operated control), group 2 (IR, 30-min ischemia/72 h reperfusion), group 3 (IR-SS31 (2 mg intra-peritoneal injection at 30 min/24 h/48 h after IR)), group 4 (IR-mitochondria (2 mg/derived from donor liver/intra-venous administration/30 min after IR procedure)), and group 5 (IR-SS31-mitochondria). In H9C2 cells, SS31 suppressed menadione-induced oxidative-stress markers (NOX-1, NOX-2, oxidized protein) while it increased SIRT1/SIRT3 expression and ATP levels. In adult male rats 72 h after IR, left ventricular ejection fraction (LVEF) was highest in sham-operated control animals and lowest in the IR group. LVEF was also higher in IR rats treated with SS31-Mito than untreated IR rats or those treated with Mito or SS31 alone. Areas of fibrosis/collagen-deposition showed the opposite pattern. Likewise, levels of oxidative-stress markers (NOX-1, NOX-2, oxidized protein), inflammatory markers (MMP-9, CD11, IL-1β, TNF-α), apoptotic markers (mitochondrial-Bax, cleaved-caspase-3, PARP), fibrosis markers (p-Smad3, TGF-β), DNA-damage (γ-H2AX), sarcomere-length, and pressure/volume overload markers (BNP, β-MHC) all showed a pattern opposite that of LVEF. Conversely, anti-apoptotic (BMP-2, Smad1/5) and energy integrity (PGC-1α/mitochondrial cytochrome-C) markers exhibited a pattern identical to that of LVEF. This study demonstrates that the combined SS31-Mito therapy is superior to either therapy alone for protecting myocardium from IR injury and indicates that the responsible mechanisms involved increased SIRT1/SIRT3 expression, which suppresses inflammation and oxidative stress and protects mitochondrial integrity.

β-Amyrin, a pentacyclic triterpene, exhibits anti-fibrotic, anti-inflammatory, and anti-apoptotic effects on dimethyl nitrosamine–induced hepatic fibrosis in male rats

2016 ◽  
Vol 36 (2) ◽  
pp. 113-122 ◽  
Author(s):  
A Thirupathi ◽  
PC Silveira ◽  
RT Nesi ◽  
RA Pinho
Keyword(s):  
Oxidative Stress ◽  
Hepatic Fibrosis ◽  
Caspase 3 ◽  
Inflammatory Marker ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Male Rats ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Tnf Α ◽  
Anti Inflammatory

Hepatic fibrosis is a leading cause of morbidity and mortality worldwide. Attenuation of fibrogenic process can significantly lower the mortality rate. However, pharmaceutical intervention at fibrogenesis stage remains a major task in medicine. So there is a need for a natural compound to treat hepatic fibrosis. This study was outlined to investigate the anti-fibrotic effect of β-amyrin in dimethylnitrosamine (DMN)-induced hepatic fibrosis male rats. Serum liver function markers (aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase), oxidative stress markers (malondialdehyde, superoxide dismutase, catalase, glutathione peroxidase, glutathione reduced content and vitamin C), tissue inflammatory marker (tumor necrosis factor α (TNF-α)), apoptosis marker (caspase 3) and fibrolytic marker (tissue inhibitor of metalloproteinase 1 (TIMP-1)) were evaluated before and after β-amyrin treatment in DMN-induced rat. β-Amyrin treatment attenuated the altered levels of the serum enzyme markers produced by DMN and caused a subsequent recovery toward normalization. Oxidative stress markers and TNF-α levels were reduced significantly ( p < 0.001) as well as proteins’ (caspase-3 and TIMP-1) expression was reduced in β-amyrin –treated DMN rats. By virtue of β-amyrin properties of inhibiting oxidative stress, apoptosis, inflammation, and fibrogenesis, it might act as an ideal anti-inflammatory and anti-fibrogenic agent to halt the progression of liver fibrosis to chronicity.

scholarly journals Protective Role of Probiotic Supplements in Hepatic Steatosis: A Rat Model Study

2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Aein Azarang ◽  
Omid Farshad ◽  
Mohammad Mehdi Ommati ◽  
Akram Jamshidzadeh ◽  
Reza Heidari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Steatosis ◽  
Bacillus Coagulans ◽  
Male Rats ◽  
Health Priorities ◽  
Oxidative Stress Markers ◽  
Oxidative Stress Biomarkers ◽  
Nonalcoholic Fatty Liver ◽  
Stress Markers ◽  
And Oxidative Stress

Background. Treating nonalcoholic fatty liver disease (NAFLD) is considered one of the public health priorities in the past decade. So far, probiotics have represented promising results in controlling the signs and symptoms of NAFLD. However, attempts to find the ideal probiotic strain are still ongoing. The present study is designed to find the best strain amongst suitable probiotic strains according to their ability to ameliorate histopathological and oxidative stress biomarkers in hepatic steatosis-induced rats. Methods. Initially, four probiotics species, including Lactobacillus (L.) acidophilus, L. casei, L. reuteri, and Bacillus coagulans, were cultured and prepared as a lyophilized powder for animals. The experiment lasted for fifty days. Initially, hepatic steatosis was induced by excessive ingestion of D-fructose in rats for eight weeks, followed by eight weeks of administering probiotics and D-fructose concurrently. Forty-two six-week-old male rats were alienated to different groups and were supplemented with different probiotics ( 1 ∗ 10 9   CFU in 500 mL drinking water). After eight weeks, blood and liver samples were taken for further evaluation, and plasma and oxidative stress markers corresponding to liver injuries were examined. Results. Administration of probiotics over eight weeks reversed hepatic and blood triglyceride concentration and blood glucose levels. Also, probiotics significantly suppressed markers of oxidative stress in the liver tissue. Conclusions. Although some of the single probiotic formulations were able to mitigate oxidative stress markers, mixtures of probiotics significantly ameliorated more symptoms in the NAFLD animals. This enhanced effect might be due to probiotics’ cumulative potential to maintain oxidative stress and deliver improved lipid profiles, liver function markers, and inflammatory markers.

scholarly journals Celecoxib Decrease Seizures Susceptibility in a Rat Model of Inflammation by Inhibiting HMGB1 Translocation

2021 ◽  
Vol 14 (4) ◽  
pp. 380
Author(s):  
Hadeel Alsaegh ◽  
Hala Eweis ◽  
Fatemah Kamal ◽  
Aziza Alrafiah
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Control Group ◽  
Protective Effects ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Inflammatory Models ◽  
Anti Inflammatory ◽  
Lung And Kidney ◽  
Pro Inflammatory Cytokines

The risk of developing epilepsy is strongly linked to peripheral inflammatory disorders in humans. High-mobility group box protein 1 (HMGB1) has the most focus for being a suspect in this scenario. The current study aimed to detect the celecoxib effect, an anti-inflammatory drug, on decreasing seizure susceptibility and organ damage in lipopolysaccharides (LPS)/pilocarpine (PILO) pretreated Wistar rats. Rats were divided into 6 groups (8 each): group 1 (control), group 2 (PILO), group 3 (PILO+LPS), group 4 (PILO+LPS+(VPA) Valproic acid), group 5 (PILO+LPS+Celecoxib), and group 6 (PILO+LPS+VPA+Celecoxib). LPS was used to induce sepsis and PILO to induce seizures. Oxidative stress markers, pro-inflammatory cytokines, and HMGB1 levels in serum and brain homogenate were evaluated. Histopathological studies were conducted on the hippocampus, liver, lung, and kidney. Treatment with celecoxib either alone or in combination with VPA significantly reduced Racine score and delays latency to generalized tonic-clonic seizures onset with a significant decrease in hippocampal levels of pro-inflammatory cytokines, oxidative stress markers, and increase in reduced glutathione. In addition, celecoxib treatment either alone or in combination with VPA suppressed HMGB1translocation into peripheral circulation more than treatment with VPA alone. Furthermore, hippocampus, liver, lung, and kidney histopathological changes were improved in contrast to other epileptic groups. Celecoxib either alone or combined with VPA has antiepileptic and multiorgan protective effects on acute seizures and inflammatory models induced by PILO with LPS. It decreased histopathological findings, oxidative, and inflammatory effects induced by VPA and LPS. This might be due to its anti-oxidative, anti-inflammatory and anti-HMGB1 mediated effects.

scholarly journals Antifibrotic Activity of Phaleria macrocarpa Extract in Rat Liver-fibrosis Model: Focus on Oxidative Stress Markers, TGF-β1 and MMP-13

2020 ◽  
Vol 8 (A) ◽  
pp. 555-562
Author(s):  
Bantari W. K. Wardhani ◽  
Nanik Sundari ◽  
Raymond R. Tjandrawinata ◽  
Ahmad Aulia Jusuf ◽  
Vivian Soetikno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Liver Fibrosis ◽  
Liver Function ◽  
Cell Activation ◽  
Stellate Cell ◽  
Male Rats ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Phaleria Macrocarpa

AIM: This study was aimed to determine the antifibrotic activity of Phaleria macrocarpa (PM) extract in liver fibrosis (LF) and its possible mechanism in the rat model. METHODS: Sprague Dawley male rats were injected with 2 mL/kg BW of carbon tetrachloride intraperitoneally twice a week for 2 weeks, followed by 1 mL/kg BW for 6 weeks. Afterward, the treatments began from the 3rd week: Silymarin 100 mg/kg BW/day, standardized PM extract (Proliverenol) 75 or 150 mg/kg BW/day orally. Rats were sacrificed in the 8th week. Blood and liver were collected to analyze liver function, liver damage and fibrosis marker, oxidative stress markers, pro-fibrogenic cytokine, and antifibrotic marker. RESULTS: Our study showed that the treatment of silymarin and PM resulted in the normalized activity of liver function, followed by the amelioration of oxidative stress, demonstrated by the decreased malondialdehyde levels and an increased ratio of glutathione and glutathione disulfide. All markers examined showed that PM extract has antioxidant activity due to decreased hepatic stellate cell activation. We also found a decrease in tumor growth factors-β1 and protein expressions of matrix metalloproteinases-13 in all treatment groups compared to the carbon tetrachloride group. There were tendencies of the decreased fibrotic area following improvements of biochemical parameters. CONCLUSION: PM extracts ameliorate carbon tetrachloride-induced LF. The proposed mechanism is by overcoming oxidative stress and regulating pro-fibrogenic cytokine and antifibrotic markers.

scholarly journals Effect of the Antihypertensive Drug Enalapril on Oxidative Stress Markers and Antioxidant Enzymes in Kidney of Spontaneously Hypertensive Rat

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
G. Chandran ◽  
K. N. S. Sirajudeen ◽  
Nik Syamimi Nik Yusoff ◽  
M. Swamy ◽  
Mutum S. Samarendra
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Antihypertensive Drug ◽  
Spontaneously Hypertensive Rat ◽  
Male Rats ◽  
Oxidative Stress Markers ◽  
Spontaneously Hypertensive ◽  
Stress Markers ◽  
Hypertensive Rat ◽  
Enalapril Treatment

Oxidative stress has been suggested to play a role in hypertension and hypertension induced organ damage. This study examined the effect of enalapril, an antihypertensive drug, on oxidative stress markers and antioxidant enzymes in kidney of spontaneously hypertensive rat (SHR) and Nω-nitro-L-arginine methyl ester (L-NAME) administered SHR. Male rats were divided into four groups (SHR, SHR+enalapril, SHR+L-NAME, and SHR+enalapril+L-NAME). Enalapril (30 mg kg−1day−1) was administered from week 4 to week 28 and L-NAME (25 mg kg−1day−1) was administered from week 16 to week 28 in drinking water. Systolic blood pressure (SBP) was measured during the experimental period. At the end of experimental periods, rats were sacrificed; urine, blood, and kidneys were collected for the assessment of creatinine clearance, total protein, total antioxidant status (TAS), thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), and catalase (CAT), as well as histopathological examination. Enalapril treatment significantly enhanced the renal TAS level (P<0.001) and SOD activity (P<0.001), reduced the TBARS levels (P<0.001), and also prevented the renal dysfunction and histopathological changes. The results indicate that, besides its hypotensive and renoprotective effects, enalapril treatment also diminishes oxidative stress in the kidneys of both the SHR and SHR+L-NAME groups.

scholarly journals Effects of aqueous extract of polyherbal formulation against hyperthyroidism induced by L-thyroxin in a rat model

2018 ◽  
Vol 5 (12) ◽  
pp. 2876-2887 ◽  
Author(s):  
Sahar B. Ahmed ◽  
Asmaa M. Moghazy ◽  
Omar A. Ahmed-Farid ◽  
Hassan A. Esebery
Keyword(s):  
Oxidative Stress ◽  
Thyroid Hormone ◽  
Low Dose ◽  
Colorimetric Method ◽  
The Body ◽  
Male Rats ◽  
High Dose ◽  
Phytochemical Analysis ◽  
Oxidative Stress Markers ◽  
Stress Markers

Background: Hyperthyroidism is a disorder that occurs when the thyroid gland secretes more thyroid hormone than the body needs. Thyroid hormone is essential for the normal growth and development of normal organs. Polyherb (POH) formulation has proven to be useful in number of diseases and has been used in folk medicine as an anti-hyperthyroidism, anti-oxidant, and appetitestimulating agent. The aim of the study was to evaluate the curative effect of POH against L-thyroxin (LT4)-induced hyperthyroidism in male rats. Methods: Seven groups (10 rats each) were used for this purpose. Determination of phytochemical analysis, oxidative stress markers, brain appetite marker and cell energy marker were determined via high-performance liquid chromatography (HPLC) techniques. Thyroid hormones were detected via ELISA, and liver functions were determined by colorimetric method. Results: The data showed that LT4 altered thyroid function via decreasing serum Thyroid-stimulating hormone (TSH), serum total protein, albumin and globulin, while increasing Triiodothyronine (T3), Thyroxine (T4), and Aspartate aminotransferase (AST). Moreover, oxidative stress markers in liver tissues were increased, via up-regulation of nitric oxide (NO), oxidized glutathione (GSSG), malondialdehyde (MDA), and 8-hydroxy-2'-deoxyguanosine (8OHdG). Meanwhile, glutathione (GSH) and ATP were alleviated; in contrast, metabolites of ADP and AMP were elevated. Neuronal appetite marker in brain tissue was decreased via low serotonin levels. On the other hand, rat groups treated with POH and Carbimazole (CBZ) showed markedly amelioration of hyperthyroidism in rats at low dose only but did not show complete amelioration at high dose of POH. The data were confirmed through histopathological examination of the thyroid. Conclusion: The data obtained demonstrated that POH, at low dose, can be very effective for completely treating hyperthyroidism in rats, and was safer than Carbimazole (CBZ) and ameliorated most signaling pathways and in different tissues.

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