Cisplatin-induced oxidative stress stimulates renal Fas ligand shedding

We extracted the primary pulmonary fibroblasts of the normal and bleomycin-induced pulmonary fibrosis mice and investigated the functioning mechanism of citrus alkaline extract (CAE) in the induction of pulmonary fibroblast apoptosis. The expression intensity of vimentin of the pulmonary fibroblasts in the model mice was higher than that in the normal mice. Meanwhile, the positive expression rate and expression intensity of alpha smooth muscle actin (α-SMA) of the pulmonary fibroblasts in the model mice were higher than those in the normal mice. Results of MTT showed that pulmonary fibroblast activity of the normal and model mice has been significantly inhibited by CAE in a concentration-dependent manner. The results of flow cytometer analysis showed that the proportion of pulmonary fibroblast apoptosis in the model mice has been profoundly increased by CAE treatment in a dosage-dependent manner. Besides we found that the expression of Cleaved-Caspase 3, Cleaved-Caspase 8, Cleaved-poly-ADP-ribose polymerase (Cleaved-PARP), and Fas and Fas Ligand (FasL) was markedly increased after CAE treatment. A further study showed that the expression of Cyclooxygenase-2 (COX-2) and prostaglandin E receptor 2 (EP2) was dependant on the concentration of CAE, indicating that CAE-regulated receptor apoptosis of Fas was probably related to COX-2. The results of fluorescence detection of oxidative stress showed that the level of oxidative stress was significantly increased after CAE treatment. Furthermore, the results of Western Blot showed that the phosphorylation level of p38 (p-p38) was markedly increased, suggesting that CAE probably has regulated COX-2 through increased p-p38 following oxidative stress. Our results therefore suggest that CAE can effectively induce pulmonary fibroblast apoptosis of the normal and model mice, and its functioning mechanism is probably related to the p38/COX-2/Fas signaling pathway regulated by oxidative stress.

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Lactobacillus plantarum And Inulin: Therapeutic Agents to Enhance Cardiac Ob Receptor Expression and Suppress Cardiac Apoptosis in Type 2 Diabetic Rats

Journal of Diabetes Research ◽

10.1155/2020/4745389 ◽

2020 ◽

Vol 2020 ◽

pp. 1-14 ◽

Cited By ~ 1

Author(s):

Safa Sefidgari-Abrasi ◽

Pouran Karimi ◽

Leila Roshangar ◽

Mohammad Morshedi ◽

Khadijeh Bavafa-Valenlia ◽

...

Keyword(s):

Oxidative Stress ◽

Type 2 Diabetes ◽

Lactobacillus Plantarum ◽

Fas Ligand ◽

Probiotic Strain ◽

Receptor Expression ◽

Necrosis Factor Alpha ◽

Apoptotic Markers ◽

Cardiac Apoptosis

Background. T2DM may cause increased levels of oxidative stress and cardiac apoptosis through elevated blood glucose. The present study investigated the effects of Lactobacillus plantarum (L. plantarum) as a probiotic strain and inulin as a prebiotic supplement on cardiac oxidative stress and apoptotic markers in type 2 diabetes mellitus (T2DM) rats. Methods. A high-fat diet and a low dose of streptozotocin were used to induce type 2 diabetes. The rats were divided into six groups which were supplemented with L. plantarum, inulin, or their combination for 8 weeks. Results. The results showed improved activity of cardiac antioxidant parameters including total antioxidant capacity (TAC), superoxide dismutase (SOD), and glutathione peroxidase (GPx) (P<0.001, P<0.01, and P<0.01, respectively) and decreased level of cardiac malondialdehyde (MDA) concentration (P<0.05). These changes were accompanied with increased protein expression of cardiac obesity receptor (Ob-R) (P=0.05) and reduced apoptotic markers such as tumor necrosis factor-alpha (TNF-α), Fas ligand (FasL), and caspase proteins (P<0.001, P=0.003, and P<0.01, respectively) in T2DM rats after concurrent L. plantarum and inulin supplementation. Moreover, a remarkable correlation of cardiac Ob-R and oxidative stress parameters with cardiac apoptotic markers was observed (P<0.01). Conclusion. The concurrent use of L. plantarum and inulin seems to be beneficial, as they can lead to decreased heart complications of T2DM via reducing cardiac apoptotic markers.

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Progesterone (P4) attenuates oxidative stress induced and FAS ligand mediated apoptosis of human granulosa/luteal (hGL) cells by different mechanisms

Fertility and Sterility ◽

10.1016/j.fertnstert.2017.07.1142 ◽

2017 ◽

Vol 108 (3) ◽

pp. e318

Author(s):

E. Anspach Will ◽

X. Liu ◽

J. Peluso

Keyword(s):

Oxidative Stress ◽

Fas Ligand

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NRF2 Protection against Liver Injury Produced by Various Hepatotoxicants

Oxidative Medicine and Cellular Longevity ◽

10.1155/2013/305861 ◽

2013 ◽

Vol 2013 ◽

pp. 1-8 ◽

Cited By ~ 64

Author(s):

Jie Liu ◽

Kai Connie Wu ◽

Yuan-Fu Lu ◽

Edugie Ekuase ◽

Curtis D. Klaassen

Keyword(s):

Oxidative Stress ◽

Liver Injury ◽

Fas Ligand ◽

Inflammatory Responses ◽

Lithocholic Acid ◽

Antioxidant Genes ◽

Stress Genes ◽

Nrf2 Activation ◽

Genes Encoding

To investigate the role of Nrf2 as a master defense against the hepatotoxicity produced by various chemicals, Nrf2-null, wild-type, Keap1-knock down (Keap1-Kd) and Keap1-hepatocyte knockout (Keap1-HKO) mice were used as a “graded Nrf2 activation” model. Mice were treated with 14 hepatotoxicants at appropriate doses, and blood and liver samples were collected thereafter (6 h to 7 days depending on the hepatotoxicant). Graded activation of Nrf2 offered a Nrf2-dependent protection against the hepatotoxicity produced by carbon tetrachloride, acetaminophen, microcystin, phalloidin, furosemide, cadmium, and lithocholic acid, as evidenced by serum alanine aminotransferase (ALT) activities and by histopathology. Nrf2 activation also offered moderate protection against liver injury produced by ethanol, arsenic, bromobenzene, and allyl alcohol but had no effects on the hepatotoxicity produced by D-galactosamine/endotoxin and the Fas ligand antibody Jo-2. Graded Nrf2 activation reduced the expression of inflammatory genes (MIP-2, mKC, IL-1β, IL-6, and TNFα), oxidative stress genes (Ho-1, Egr1), ER stress genes (Gadd45 and Gadd153), and genes encoding cell death (Noxa, Bax, Bad, and caspase3). Thus, this study demonstrates that Nrf2 prevents the liver from many, but not all, hepatotoxicants. The Nrf2-mediated protection is accompanied by induction of antioxidant genes, suppression of inflammatory responses, and attenuation of oxidative stress.

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Evaluation of serum and follicular fluid levels of soluble Fas, soluble Fas ligand and oxidative stress parameters of patients undergoing IVF

Fertility and Sterility ◽

10.1016/j.fertnstert.2013.07.206 ◽

2013 ◽

Vol 100 (3) ◽

pp. S507-S508 ◽

Cited By ~ 1

Author(s):

A. Pekel ◽

A. Gonenc ◽

N. Ozturk Turhan ◽

H. Kafali ◽

S. Gurcan

Keyword(s):

Oxidative Stress ◽

Follicular Fluid ◽

Fas Ligand ◽

Oxidative Stress Parameters ◽

Soluble Fas ◽

Soluble Fas Ligand ◽

Fluid Levels ◽

And Oxidative Stress ◽

Stress Parameters

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Oxidative stress and hypoxia/reoxygenation trigger CD95 (APO-1/Fas) ligand expression in microglial cells

FEBS Letters ◽

10.1016/s0014-5793(98)00562-6 ◽

1998 ◽

Vol 429 (1) ◽

pp. 67-72 ◽

Cited By ~ 94

Author(s):

Markus Vogt ◽

Manuel K.A Bauer ◽

Davide Ferrari ◽

Klaus Schulze-Osthoff

Keyword(s):

Oxidative Stress ◽

Fas Ligand ◽

Microglial Cells ◽

Ligand Expression ◽

Hypoxia Reoxygenation

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The role of Fas ligand protein in the oxidative stress induced by azoxymethane on crypt colon of rats

Acta Cirurgica Brasileira ◽

10.1590/s0102-86502010000600008 ◽

2010 ◽

Vol 25 (6) ◽

pp. 501-506 ◽

Cited By ~ 3

Author(s):

Luiz Antonio Maksoud Bussuan ◽

Djalma José Fagundes ◽

Guido Marks ◽

Priscila Maksoud Bussuan ◽

Roberto Teruya

Keyword(s):

Oxidative Stress ◽

Fas Ligand ◽

Saline Solution ◽

Subcutaneous Administration ◽

Proximal Colon ◽

Fasl Expression ◽

Colon Crypt ◽

Significant Difference ◽

Student Test

PURPOSE: To study the protein Fas ligand (FasL) on the expression of apoptosis, using a model of oxidative stress induced by azoxymethane (AOM), in the crypt of colon in rats. METHODS: Wistar rats (n=14) were assigned into two groups: control (n=7) and AOM (n=7). A single subcutaneous administration of AOM (5mg/kg) or saline solution was performed at the beginning of third week and after three hours samples of proximal colon were collected. The expression of FasL was quantified (Software ImageLab) in percentage of areas in the top, base and all crypt. Results were expressed as mean ± sd (Shapiro-Wilks test and t Student test) (p < 0.05). RESULTS: In the animals of CG there was no significant difference between the FasL expression of the top (10.75±3.33) and basal (11.14±3.53) colon crypt (p=0.34293740). In the animals of AOM there was no significant difference between the FasL expression of the top (8.86±4.19) and basal (8.99±4.08) colon crypt (p=0.78486003). In the animals of CG (10.95±3.43) and AOM (8.92±4.13) there was a significant difference of the FasL expression (p=0.026466821). A significantly decrease on the FasL expression was observed in the animals of CG (10.75±3.33) and AOM (8.86±4.19) in the top crypt (p=0.00003755*). A significant decrease was also observed in the animals of CG (11.14±3.53) and AOM (8.99±4.08) in the basal colon crypt (p=0.00000381**). CONCLUSION: Azoxymethane induce the oxidative stress and the significantly decrease of FasL expression, although there is no significant difference between basal and top of colon crypt linked to consumption-activation of Fas ligand.

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