The ameliorative effect of thymol against hydrocortisone-induced hepatic oxidative stress injury in adult male rats

2015 ◽  
Vol 93 (4) ◽  
pp. 282-289 ◽  
Author(s):  
Hanaa R. Aboelwafa ◽  
Hany N. Yousef
Keyword(s):  
Oxidative Stress ◽  
Adult Male ◽  
Serum Levels ◽  
Male Rats ◽  
Necrosis Factor Alpha ◽  
Stress Injury ◽  
Ultrastructural Alterations ◽  
Oxidative Stress Injury ◽  
Tnf Α ◽  
Ameliorative Effect

The aim of the present study was to investigate whether hydrocortisone induces oxidative stress in hepatocytes and to evaluate the possible ameliorative effect of thymol against such hepatic injury. Twenty-four adult male rats were divided into control, thymol, hydrocortisone, and hydrocortisone+thymol groups. The 4 groups were treated daily for 15 days. Hydrocortisone significantly induced oxidative stress in the liver tissues, marked by increased serum levels of alanine transaminase (ALT), aspartate transaminase (AST), total oxidative capacity (TOC), and tumor necrosis factor-alpha (TNF-α) accompanied by marked decline of serum levels of total protein, albumin, and total antioxidant capacity (TAC). Also, marked elevation in the levels of the thiobarbituric acid reactive substances (TBARS) and TNF-α, beside significant decrease in the level of glutathione (GSH) in hepatic tissues were recorded. These biochemical alterations were accompanied by histopathological changes marked by destruction of the normal hepatic architecture, in addition to ultrastructural alterations represented by degenerative features covering almost all the cytoplasmic organelles of the hepatocytes. Supplementation of hydrocortisone-treated rats with thymol reversed most of the biochemical, histological, and ultrastructural alterations. The results of our study confirm that thymol has strong ameliorative effect against hydrocortisone-induced oxidative stress injury in hepatic tissues.

scholarly journals Bone marrow mesenchymal stem cells stimulated by tumor necrosis factor-α can promote the repair of fatty liver cell oxidative stress injury and fatty liver ischemia-reperfusion injury

2021 ◽  
Author(s):  
Yuying Tan ◽  
Jiali Qiu ◽  
Weiqi Zhang ◽  
Yan Xie ◽  
Chiyi Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Fatty Liver ◽  
Liver Cell ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Tnf Α

Mesenchymal stem cells (MSCs) have great prospects for the treatment of ischemia-reperfusion injury (IRI) after liver transplantation. At this stage, the main factor limiting MSCs in the treatment of fatty liver IRI of the donor liver is the residence time of stem cells at the site of inflammatory injury. This study investigated whether bone marrow mesenchymal stem cells (BMSCs) stimulated by tumor necrosis factor-α (TNF-α) can promote the repair of fatty liver cell oxidative stress injury and fatty liver IRI in rats. The results indicated the BMSCs treatment group stimulated by TNF-α had lower indexes and significantly improved oxidative stress damage in vitro through Transwell chamber co-culture experiment, compared with the control group. In vivo, compared with the PBS group and the BMSCs group, the indexes of the BMSCs treatment group stimulated by TNF-α were reduced, and the degree of tissue damage was significantly reduced. BMSCs can repair fatty liver cell oxidative stress injury and fatty liver IRI, however, BMSCs stimulated by TNF-α can promote the repair of tissues and cells.

Comparisons of the Effects of Anesthesia and Stress on Release of Tumor Necrosis Factor-α, Leptin, and Nitric Oxide in Adult Male Rats

2001 ◽  
Vol 226 (4) ◽  
pp. 296-300 ◽  
Author(s):  
Claudio A. Mastronardi ◽  
Wen H. Yu ◽  
Samuel M. McCann
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Adult Male ◽  
Tumor Necrosis ◽  
Fold Increase ◽  
Male Rats ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Bacterial lipopolysaccharide (LPS) stimulates massive release of tumor necrosis factor-alpha (TNF-α) together with nitric oxide (NO) and a lessor release of leptin. We hypothesized that other types of stress such as that of surgery might also release these cytokines and NO. Adult male rats were anesthetized with ketamine/acepromazine/xylazine anesthesia (90 + 2 + 6 mg/ml, respectively) and an external jugular catheter was inserted for removal of blood samples (0.6 ml) at various times postoperatively. Plasma TNF-α was almost undetectable in decapitated rats and was near zero immediately following the placement of the jugular catheter (time zero [to]). As the rats awakened from anesthesia, there was a rise in TNF-α at 30 min that peaked at 2 hr with a 400-fold increase and then precipitously declined 40-fold to a level still greater than zero at 3 hr. At 6 hr on the following morning, TNF-α values were near zero, but following connection of tubing and withdrawal of the initial blood sample, there was a 100-fold increase 1 hr later, followed by a decline over the next 3 hr. In contrast, plasma [NO3/NO2] from decapitated rats was 117 μM. Values at t0 were decreased and plummeted 4-fold within 30 min, then rose slightly in the ensuing 3 hr. At 6 hr on the next day [NO3/NO2] values were lower than at t0 and declined gradually during the next 4 hr. Leptin gradually declined from pre-operative concentrations, reaching a minimum at 3 hr and its concentration was unaffected by the bleeding stress of the second day. We conclude that release of TNF-α, [NO3/NO2], and leptin are neurally controlled since plasma levels of all three declined as a result of anesthesia. TNF-α secretion was remarkably stress responsive, whereas NO release appeared to be suppressed by the combined operative and bleeding stress, and leptin was stress unresponsive.

scholarly journals Overexpression of miR-506-3p Aggravates DBP-Induced Testicular Oxidative Stress in Rats by Downregulating ANXA5 via Nrf2/HO-1 Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Min Tang ◽  
Lei Zhang ◽  
Zheng Zhu ◽  
Ran Li ◽  
Shangqian Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Male Rats ◽  
Adolescent Male ◽  
Seminiferous Tubules ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Testicular Injury

Background. Di-N-butylphthalate (DBP) is a kind of unique endocrine toxicity linked to hormonal disruptions that affects the male reproductive system and has given rise to more and more attention. However, the mechanism of DBP-induced testicular injury remains unclear. Here, the objective of this study was to investigate the potential molecular mechanism of miR-506-3p in DBP-induced rat testicular oxidative stress injury via ANXA5 (Annexin A5)/Nrf2/HO-1 signaling pathway. Methods. In vivo, a total of 40 adolescent male rats were treated from 2 weeks with 800 mg/kg/day of DBP in 1 mL/kg corn oil administered daily by oral gavage. Among them, some rats were also injected subcutaneously with 2 nmol agomir-506-3p and/or 10 nmol recombinant rat ANXA5. The pathomorphological changes of testicular tissue were assessed by histological examination, and the antioxidant factors were evaluated. Subsequently, ANXA5, Nrf2, and its dependent antioxidant enzymes, such as HO-1, NQO1, and GST, were detected by Western blotting or immunohistochemical staining. In vitro, TM3 cells (Leydig cells) were used to detect the cell activity by CCK-8 and the transfection in the DBP-treated group. Results. Differentially expressed miRNAs between the DBP-treated and normal rats were analyzed, and qRT-PCR showed miR-506-3p was highly expressed in testicular tissues of the DBP-treated rats. DBP-treated rats presented severe inflammatory infiltration, increased abnormal germ cells, and missed cell layers frequently existed in seminiferous tubules, resulted in oxidative stress and decreased testicular function. Meanwhile, upregulation of miR-506-3p aggravated the above changes. In addition, miR-506-3p directly bound to ANXA5, and overexpression of miR-506-3p could reduce the ANXA5 expression and also decrease the protein levels of Nrf2/HO-1 signaling pathway. Additionally, we found that recombinant rat ANXA5 reversed the DBP-treated testicular oxidative stress promoting injury of miR-506-3p in rats. In vivo results were reproduced in in vitro experiments. Conclusions. This study provided evidence that miR-506-3p could aggravate the DBP-treated testicular oxidative stress injury in vivo and in vitro by inhibiting ANXA5 expression and downregulating Nrf2/HO-1 signaling pathway, which might provide novel understanding in DBP-induced testicular injury therapy.

scholarly journals Effect of total flavonoids of Cuscuta chinensis Lam. (Convolvulaceae) on oxidative stress injury in mouse testis and epididymis, and on serum levels of reproductive hormones in oligoasthenospermia mice model

2021 ◽  
Vol 18 (6) ◽  
pp. 1253-1258
Author(s):  
Hongliang Cui ◽  
Panpan Dong ◽  
Bin Chen
Keyword(s):  
Oxidative Stress ◽  
Sperm Quality ◽  
Serum Levels ◽  
Reproductive Hormones ◽  
Control Group ◽  
Total Flavonoids ◽  
Mice Model ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Cuscuta Chinensis

Purpose: To investigate the effect of total flavonoids of Cuscuta chinensis (TFCC) on oxidative stress injury in testis and epididymis, and serum levels of reproductive hormones in an oligoasthenospermia (OAS) mice model. Methods: Thirty male Wistar mice were randomly assigned to three groups of 10 mice each: control group, OAS group and TFCC group. With the exception of control group, OAS was orally induced in the mice with ornidazole. The TFCC group received TFCC. Reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) were determined. Serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone were also measured. Results: The levels of ROS and MDA in the testis and epididymis significantly increased in OAS group, when compared to control mice (p < 0.05). However, TFCC administration significantly reduced their levels in these tissues (p < 0.05). In contrast, SOD activity significantly decreased in the testis and epididymis of mice in OAS group, relative to control group, but increased significantly after TFCC exposure (p < 0.05). Serum FSH and LH were markedly elevated in OAS group, but treatment with TFCC significantly reduced the levels of these hormones (p < 0.05). Conclusion: These results suggest that TFCC effectively improves sperm quality and reduces oxidative damage in testis and epididymis of mice with oligoasthenospermia via a mechanism involving the regulation of serum levels of reproductive hormones. Thus, TFCC may be useful in the treatment of oligoasthenospermia.

scholarly journals Antioxidant Herbs Supplementation Inhibits Endometriosis Extension in Mice

2019 ◽  
Vol 5 (2) ◽  
pp. 53-61
Author(s):  
Yuli Trisetiyono ◽  
Widjiati Widjiati ◽  
Syarief Thaufik Hidayat ◽  
Noor Pramono
Keyword(s):  
Oxidative Stress ◽  
Green Tea ◽  
Cucumis Melo ◽  
Serum Levels ◽  
Green Tea Extract ◽  
Control Group ◽  
Vegf Expression ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Tea Extract

Background: Increased oxidative stress causes inflammation and increases angiogenesis. It presumed to promote the proliferation of endometriosis tissue. Kebar grass (Biophytum petersianum) and other herbs such as green tea and Cucumis melo, which contain high antioxidants, are expected to decrease oxidative stress, inflammation, angiogenesis, and reduced endometriosis implants.Objective: To investigate the effects of Kebar grass, green tea, and Cucumis melo to malondialdehyde serum, tumor necrosis factor alpha, and vascular endothelial growth factor expression, and the area of the endometriotic implants.Methods: Twenty-eight mice were divided into four groups, i.e., the first group of endometriosis mice was given Kebar grass extract; the second group was assigned green tea extract, the third group was given the combination of Cucumis melo extract–gliadin, and the last containing the untreated endometriosis mice as the control. Each treatment was given for 14 days. The data of MDA serum level, the area of the endometriotic implants, TNF-α, and VEGF expression were collected and analyzed.Results: The MDA serum levels of the groups treated with Kebar grass extract, green tea extract, and Cucumis melo extract – gliadin were significantly lower (p=0.001) than the control group. TNF-α expression of the groups provided with each treatment also lower than the control groups (p=0.002). However, only the administration of the Cucumis melo extract–gliadin resulted in lower VEGF expression compare with the control (p=0.017). Finally, the area of the endometriotic implants of the mice models administered with each treatment was smaller than the control group (p=0.003).Conclusion: Kebar grass as well as green tea and Cucumis melo–gliadin inhibits endometriotic implants extension by decreasing MDA serum and TNF-α expression.

scholarly journals Effects of Various Densities of 50 Hz Electromagnetic Field on Serum IL-9, IL-10, and TNF-α Levels

2020 ◽  
Vol 11 (1) ◽  
pp. 24-32
Author(s):  
Hanie Mahaki ◽  
Naghi Jabarivasal ◽  
Khosro Sardarian ◽  
Alireza Zamani
Keyword(s):  
Immune System ◽  
Magnetic Flux ◽  
Inflammatory Cytokines ◽  
Low Frequency ◽  
Serum Levels ◽  
Male Rats ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Background: Extremely low-frequency electromagnetic fields (ELF-EMFs) are abundantly produced in modern societies. In recent years, interest in the possible effects of ELF-EMFs on the immune system has progressively increased. Objective: To examine the effects of ELF-EMFs with magnetic flux densities of 1, 100, 500, and 2000 µT on the serum levels of interleukin (IL)-9, IL-10, and tumor necrosis factor-alpha (TNF-α). Methods: 80 adult male rats were exposed to ELF-EMFs at a frequency of 50 Hz for 2 h/day for 60 days. The serum cytokines were measured at two phases of pre- and post-stimulation of the immune system by human serum albumin (HSA). Results: Serum levels of IL-9 and TNF-α, as pro-inflammatory cytokines, were decreased due to 50 Hz EMFs exposure compared with the controls in the pre- and post-stimulation phases. On the contrary, exposures to 1 and 100 µT 50 Hz EMFs increased the levels of antiinflammatory cytokine, and IL-10 only in the pre-stimulation phase. In the post-stimulation phase, the mean level of serum IL-10 was not changed in the experimental groups. Conclusion: The magnetic flux densities of 1 and 100 µT 50 Hz EMFs had more immunological effects than EMFs with higher densities. Exposure to 50 Hz EMFs may activate anti-inflammatory effects in rats, by down-modulation of pro-inflammatory cytokines (IL-9 and TNF-α) and induction of the anti-inflammatory cytokine (IL-10).

scholarly journals Silymarin mitigates diclofenac-induced liver toxicity through inhibition of inflammation and oxidative stress in male rats

2019 ◽  
Vol 8 (3) ◽  
pp. 231-237 ◽  
Author(s):  
Pantea Ramezannezhad ◽  
Ali Nouri ◽  
Esfandiar Heidarian
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Total Bilirubin ◽  
Liver Toxicity ◽  
Treated Group ◽  
Male Rats ◽  
Control Group ◽  
Tnf Α ◽  
Ameliorative Effect ◽  
And Oxidative Stress

Introduction: Diclofenac (DIC) is one of the compounds derived from acetic acid which isknown for its anti-inflammatory and analgesic attributes. Silymarin is a flavonoid compoundwhich is derivate from Silybum marianum seeds. This research was done to assess the protectiverole of silymarin against liver toxicity induced by DIC in male rats.Methods: Randomly, 40 male Wistar rats were assigned into five groups as follows: Group 1:control group, Group 2: DIC-only treated (50 mg/kg, i.p), Group 3: silymarin-only treated (200mg/kg, p.o); Groups 4 and 5: DIC (50 mg/kg, i.p) plus silymarin (100 mg/kg and 200 mg/kg, p.o,respectively) treated. Various biochemical, molecular, and histological parameters were evaluatedin serum and tissue.Results: In the DIC-only treated group, the levels of liver glutathione peroxidase (GPx), superoxidedismutase (SOD), intracellular glutathione (GSH) and catalase (CAT) significantly diminished andthe levels of total bilirubin, alkaline phosphatase (ALP), nitrite, alanine aminotransferase (ALT),malondialdehyde (MDA), serum tumor necrosis factor-α (TNF-α), aspartate aminotransferase(AST), and TNF-α gene expression were remarkably elevated relative to control animals. In otherhands, treatment with silymarin caused a noticeable elevation in GPx, SOD, GSH, CAT and aremarkable reduction in levels of total bilirubin, ALP, nitrite content, ALT, MDA, serum TNF-α,AST and TNF-α gene expression relative to DIC-only treated group. Histopathological injurieswere also improved by silymarin administration.Conclusion: The results confirm that silymarin has an ameliorative effect on liver toxicity inducedby DIC and oxidative stress in male rats.

scholarly journals Translocator Protein Modulation by 4′-Chlorodiazepam and NO Synthase Inhibition Affect Cardiac Oxidative Stress, Cardiometabolic and Inflammatory Markers in Isoprenaline-Induced Rat Myocardial Infarction

2021 ◽  
Vol 22 (6) ◽  
pp. 2867
Author(s):  
Ana Ilic ◽  
Dusan Todorovic ◽  
Slavica Mutavdzin ◽  
Novica Boricic ◽  
Biljana Bozic Nedeljkovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Myocardial Injury ◽  
Cardiac Tissue ◽  
Troponin T ◽  
Serum Levels ◽  
Translocator Protein ◽  
Male Rats ◽  
Necrosis Factor Alpha ◽  
Factor Alpha

The possible cardioprotective effects of translocator protein (TSPO) modulation with its ligand 4′-Chlorodiazepam (4′-ClDzp) in isoprenaline (ISO)-induced rat myocardial infarction (MI) were evaluated, alone or in the presence of L-NAME. Wistar albino male rats (b.w. 200–250 g, age 6–8 weeks) were divided into 4 groups (10 per group, total number N = 40), and certain substances were applied: 1. ISO 85 mg/kg b.w. (twice), 2. ISO 85 mg/kg b.w. (twice) + L-NAME 50 mg/kg b.w., 3. ISO 85 mg/kg b.w. (twice) + 4′-ClDzp 0.5 mg/kg b.w., 4. ISO 85 mg/kg b.w. (twice) + 4′-ClDzp 0.5 mg/kg b.w. + L-NAME 50 mg/kg b.w. Blood and cardiac tissue were sampled for myocardial injury and other biochemical markers, cardiac oxidative stress, and for histopathological evaluation. The reduction of serum levels of high-sensitive cardiac troponin T hs cTnT and tumor necrosis factor alpha (TNF-α), then significantly decreased levels of serum homocysteine Hcy, urea, and creatinine, and decreased levels of myocardial injury enzymes activities superoxide dismutase (SOD) and glutathione peroxidase (GPx) as well as lower grades of cardiac ischemic changes were demonstrated in ISO-induced MI treated with 4′-ClDzp. It has been detected that co-treatment with 4′-ClDzp + L-NAME changed the number of registered parameters in comparison to 4′-ClDzp group, indicating that NO (nitric oxide) should be important in the effects of 4′-ClDzp.

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