WoS İndeksli Yayınlar Koleksiyonu
Permanent URI for this collectionhttps://hdl.handle.net/20.500.14627/6
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Article Citation - Scopus: 1Aqueous Parsley (Petroselinum crispum) Extract Ameliorated Methotrexate-Induced Brain and Small Intestine Damage in Rats(Ankara Univ, 2025) Saçan, Ozlem; Şener, Göksel; Yanardag, Refıye; Tunali-Akbay, Tugba; Sivas, Guzin Goksun; Karaoğlu, Sümeyye Yılmaz; Dursun, Ercan; Akbay, Tugba Tunali; Yilmaz Karaoğlu, Sümeyye; Tufan, Elif; Tunali Akbay, TugbaMethotrexate (MTX) is a widely used antiarthritic and chemotherapeutic agent known to cause damage to various tissues. This study investigated the potential protective effects of parsley extract against MTX-induced brain and intestinal tissue damage. Sprague-Dawley rats were divided into control, control + parsley, MTX, and MTX + parsley. MTX (20 mg/kg, i.p.) was administered to the MTX and MTX + parsley groups. The control + parsley, and MTX + parsley groups were administered 2 g/kg parsley extract by oral gavage for five consecutive days. After the fifth day, brain and small intestinal tissues were taken. Total protein, nitric oxide, lipid peroxidation, glutathione levels, tissue factor, superoxide dismutase, and glutathione S-transferase activities were determined in these tissues. The protein profiles of the tissues were evaluated using SDS polyacrylamide gel electrophoresis. Parsley administration caused a decrease in lipid peroxidation levels in both tissues of the MTX group. On the other hand, glutathione level, glutathione-S-transferase, and superoxide dismutase activities were found to be increased. On the other hand, parsley decreased the nitric oxide level which was increased in the intestinal tissues of the MTX group. There was no significant change in brain nitric oxide level and tissue factor activity between groups. MTX and parsley administration altered protein expression, leading to the appearance or disappearance of specific bands in intestinal and brain tissues. In conclusion, parsley alleviated MTX-induced damage in brain and intestinal tissues by reducing lipid peroxidation and modulating antioxidant defenses.Article Citation - WoS: 3Citation - Scopus: 2Morphological and Biochemical Investigation of the Protective Effects of Panax Ginseng on Methotrexate-Induced Testicular Damage(Istanbul Univ, 2023) Karakaya-Cimen, Fatma Bedia; Macit, Caglar; Sivas, Guzin Goksun; Akbay, Tugba Tunali; Sener, Goksel; Ercan, Feriha; Cımen, Fatma Bedia KarakayaObjective: Methotrexate (MTX) is a chemotherapeutic agent that causes testicular toxicity used in the cure of various types of cancer. The anti-oxidant and anti-cancer effects of Panax ginseng (PxG) have been reported in both experimental and clinical studies. This study aims to examine the healing effect of PxG on testicular damage induced by MTX. Materials and Methods: Sprague Dawley male rats (8-week-olds) were used in the study. A single dose ofMTXdissolved in saline (20 mg/kg) was given to MTX and MTX+PxG groups by intraperitoneal injection. PxG dissolved in saline (100 mg/kg) was given by orogastric gavage once a day for 5 days to the MTX+PxG group. Saline was given to the control and MTX groups orally during the experiments. After decapitation, the testis sampleswere obtained. Seminiferous tubules and basement membranewere evaluated histopathologically. Seminiferous tubule diameter and germinal epithelium thickness were measured. Furthermore, oxidative stress parameters such as malondialdehyde, glutathione, superoxide dismutase, and glutathione-S-transferase were measured. Results: MTX treatment caused seminiferous tubule degeneration with a decrease in Johnsen's score, the seminiferous tubule's diameter, and the germinal epithelium's thickness. Parallel with the histopathological results increased testicular oxidative stress with an increase in malondialdehyde level and a decrease of endogenous anti-oxidant activity with a decrease in glutathione level and glutathione-S-transferase and superoxide dismutase activities. PxG treatment improved these histological and biochemical parameters in MTX-induced testis cytotoxicity. Conclusion: MTX treatment causes testicular damage via the oxidative processes. PxG treatment ameliorates MTX-induced testicular damage by inhibiting oxidative stress.Article Panax Ginseng Extract Ameliorates Methotrexate-Induced Multi-Organ Damage Via the Regulation of Oxidative Stress(Marmara Univ, 2023) Macit, Caglar; Ede-Pazarbasi, Seren; Yilmaz-karaoglu, Suemeyye; Tunali-Akbay, Tugba; Karakaya-Cimen, Fatma Bedia; Ercan, Feriha; Sener, Goksel; Akbay, Tugba Tunalı-Oxidative damage plays an important role in organ toxicities caused by methotrexate (MTX). This study aimed to determine the antioxidant effects of Panax ginseng (PxG) extract against MTX-induced liver, lung, ileum and kidney damage. Twenty-four Sprague Dawley male rats (weight 250-300 g) were used in the study. The animals were randomly separated into three groups: a) Control, b) MTX-treated (MTX) and c) MTX+PxG-treated (MTX+PxG) groups. MTX was administered intraperitoneally at 20 mg/kg, as a single dose to MTX and MTX+PxG groups. PxG was administered orally at 100 mg/kg to the MTX+PxG group for five days. Saline was given to the control and MTX groups for 5 days. At the end of the experiment, liver, lung, ileum, and kidney samples were obtained. Malondialdehyde (MDA) and glutathione (GSH) levels, superoxide dismutase (SOD), glutathione-S-transferase (GST) and tissue factor (TF) activities were determined in all tissues. In addition, histological examinations were done through light microscopy. GraphPad Prism 5v. was used for statistics, and p<0.05 were considered significant. Administration of MTX caused severe injury in tissues. Findings showed that MDA level, SOD, and GST activities were significantly normalized in the MTX+PxG group compared to the control group. A significant reduction in GSH level observed in the MTX group was reversed with PxG administration In addition, TF activity and total protein levels were found to be impaired in the MTX group, but TF activity was significantly improved in liver and lung tissues and total protein level was significantly reversed in lung and ileum in MTX+PxG group. The results of histological examinations showed that MTX-induced damage was ameliorated with the PxG administration. In conclusion, this study shows that Panax ginseng, thanks to its antioxidant properties, reversed MTX-induced tissue damage and therefore may be beneficial against side effects in patients undergoing chemotherapy.Article Citation - WoS: 1Citation - Scopus: 2The Effect of Whey Proteins on the Brain and Small Intestine Nitric Oxide Levels: Protein Profiles in Methotrexate-Induced Oxidative Stress(Istanbul Univ, 2022) Yilmaz, Sumeyye; Tufan, Elif; Sivas, Guzin Goksun; Gokmen, Begum Gurel; Dursun, Ercan; Ozbeyli, Dilek; Tunali-Akbay, Tugba; Şener, Göksel; Karaoğlu, Sümeyye YılmazObjectives: The aim of this study was to determine the effects of whey proteins on methotrexate (MTX)-induced brain and small intestine damage. Materials and Methods: 30 Sprague Dawley rats (200-300 g) were divided into four groups: Control, control + whey, MTX, and MTX+whey. MTX was administered at 20 mg/kg (single dose) intraperitoneally to the MTX group rats, and 2 mg/kg of whey protein were administered by oral gavage for 10 days to the whey groups. Lipid peroxidation, glutathione, and nitric oxide (NO) levels, as well as glutathione-Stransferase and superoxide dismutase activities were measured in the brain and small intestine. SDS-polyacrylamide gel electrophoresis of the brain and intestine tissues were also carried out. Results: While MTX treatment caused oxidative damage in the brain and small intestine, whey protein administration ameliorated MTXinduced oxidative stress. MTX administration did not change the brain's NO level, while an increase in intestinal NO level was detected. Conclusion: MTX induced oxidative stress in the brain and small intestine changed the protein metabolism in these tissues regardless of reduced food intake. Consecutive 10-day administration of whey proteins has shown its therapeutic effect on MTX-induced brain and small intestine oxidative damage.Article Citation - WoS: 1The Protective Effects Of<i> Momordica</I><i> Charantia</I> Fruit Extract in Methotrexate Induced Liver Damage in Rats(Galenos Publ House, 2022) Ozbeyli, Dilek; Sen, Ali; Cevik, Ozge; Erdogan, Omer; Kaya, Ozlem Tugce Cilingir; Ede, Seren; Sener, Goksel; Ede-pazarbasi, Seren; Cilingir-kaya, Ozlem TugceBACKGROUND/AIMS: Methotrexate (MTX), a cytotoxic therapeutic agent, is used for the cure of malignancies and rheumatologic disorders. However, the significant side effects of MTX limits its use. In this study, we aim to assess the hepatoprotective properties of Momordica charantia (MC) against MTX-induced liver damaged in rats.MATERIALS AND METHODS: Following one dose of MTX (20 mg/kg), the rats were given either distilled water or MC extract (300 mg/kg, po) for 5 days. After the dissection of the rats, the liver was removed to analyse tumour necrosis factor -a (TNF-a), interleukin-113 (IL-113), transforming growth factor 13 (TGF-13) and 8-hydroxy-2'-deoxy-guanosine (8-OhdG) levels and superoxide dismutase (SOD), catalase (CAT), and caspase-3 activities. The tissues were also examined histopathologically.RESULTS: The hepatic TNF-a, IL-113, TGF-13, 8-OhdG levels, and Caspase-3 activity in the MTX group were found to be significantly increased compared to the control group. However, MC extract was able to significantly decrease TNF-a, TGF-13, 8-OhdG levels, and Caspase-3 activity. Also, both the SOD and CAT activity of the MTX group decreased compared to the control group. Although only the SOD levels elevated significantly with MC treatment, the SOD and CAT activities of the MC treated group were similar to the control group. Supporting these biochemical parameters, MTX-induced histologic alterations in the liver were also ameliorated via MC treatment.CONCLUSION: Our results demonstrated that MC has a protective role against MTX-induced hepatic tissue injury by reducing apoptosis, oxidative damage, and the expression of pro-inflammatory cytokines.