Bortezomib ile Kalp Hasarı Oluşturulan Ratlarda Berberinin Oksidatif ve Nitrozatif Stres Üzerine Etkisi

Gür, Cihan; Kandemir, Fatih Mehmet; Genç, Aydın

doi:10.46810/tdfd.809220

Cited by 8 publications

(7 citation statements)

References 57 publications

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“…GSH binds the free radicals formed as a result of oxidative metabolism, and as a result, transforms into oxidized form (GSSG), and protects the body from oxidative damage 13 . The overproduction of ROS leads to exceeding the antioxidant capacity and, consequently, to oxidative stress 48 . The fact that oxidative stress is one of the main factors in ABM toxicity is a common conclusion reached by numerous studies.…”

Section: Discussionmentioning

confidence: 99%

Investigation of the effects of hesperidin administration on abamectin‐induced testicular toxicity in rats through oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, autophagy, and JAK2/STAT3 pathways

Gür

Kandemir

2021

Environmental Toxicology

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In this study, the potential effects of hesperidin (HES) on chronic toxicity caused by abamectin (ABM) in the testicular tissue were investigated through oxidative stress, inflammation, endoplasmic reticulum stress (ERS), apoptosis, and autophagy pathways. Male Sprague Dawley rats were used in the study. Animals in the ABM group were orally administered 1 mg/kg ABM every other day for 28 days, while HES used against ABM was given at 100 or 200 mg/kg 30 min after ABM administration for 28 days. Markers of oxidative stress, inflammation, ERS, apoptosis, and autophagy in the testicular tissues removed after the animals are sacrificed were analyzed using biochemical, real‐time polymerase chain reaction (RT‐PCR), or western blot techniques. The results obtained showed that ABM caused oxidative stress, and triggered ERS, inflammation, apoptosis, and autophagy. On the other hand, HES showed antioxidant effect by increasing superoxide dismutase, catalase, glutathione peroxidase enzyme activities, and glutathione levels in testis tissue and attenuated lipid peroxidation. Accordingly, MAPK14 reduced the NF‐κB, IL‐1β, TNF‐α, and IL‐6 expression levels, presenting an anti‐inflammatory effect. In addition, Bax protected against apoptosis and autophagy by reducing the caspase‐3, beclin‐1, LC3A, and LC3B expressions, and increasing Bcl‐2 expression. It was observed that HES also interrupted the JAK2/STAT3 signaling pathway by suppressing IL‐6 expression. Taken into consideration together, HES provided significant protection against the destruction caused by ABM in testicular tissue with antioxidant, anti‐inflammatory, antiapoptotic, and anti‐autophagic effects. Thus, it was revealed that HES has the potential to serve as an alternative treatment option in ABM toxicity.

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Section: Discussionmentioning

confidence: 99%

Investigation of the effects of hesperidin administration on abamectin‐induced testicular toxicity in rats through oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, autophagy, and JAK2/STAT3 pathways

Gür

Kandemir

2021

Environmental Toxicology

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“…Previous studies have reported that arsenic impairs spermatogenesis by inducing oxidative stress, resulting in a decrease in sperm quality and quantity [6]. SOD, CAT and GPx enzymes are at the base of the cellular antioxidant defense line [30,31]. SOD is responsible for scavenging superoxide radicals, and catalase is responsible for the decomposition of H 2 O 2 into water and molecular oxygen [32][33][34].…”

Section: Discussionmentioning

confidence: 99%

Carvacrol reduces abnormal and dead sperm counts by attenuating sodium arsenite‐induced oxidative stress, inflammation, apoptosis, and autophagy in the testicular tissues of rats

Gür

Akarsu

Akaras

et al. 2023

Environmental Toxicology

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Background: The present study investigated the protective effects of carvacrol (CAR) against testicular toxicity induced by sodium arsenite (SA).Methods and Results: Rats were given SA and/or CAR for 14 days. Semen analyzes showed that CAR increased sperm motility and decreased the percentage of anarmol and dead sperm. It was determined that the oxidative stress induced by SA decreased with the increase of Nrf-2 and HO-1 expressions, SOD, CAT, GPx and GSH levels, and MDA levels decreased after CAR treatment. It was observed that autophagy and in ammation triggered by SA in testicular tissue were alleviated by suppressing the expressions of LC3A, LC3B, MAPK-14, NF-kB, TNF-a, IL-1b, iNOS and COX-2 biomarkers in rats given CAR. CAR treatment protected against apoptosis by suppressing Bax and Caspase-3 expressions and triggering Bcl-2 expression in testicles.Conclusions: As a result, it was seen that CAR could provide protection against SA-induced damage in testicular tissues of rats.

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“…GSH ise oksidatif metabolizma sonucu meydana gelen serbest radikalleri bağlayarak okside forma (GSSG) dönüşmekte ve vücudu oksidatif hasardan korumaktadır (Gur et al, 2021b). Öte yandan çeşitli toksik ajanlar antioksidan enzimlerin aktivitelerinde azalmaya neden olmaktadır (Adeyemi and Olayaki, 2018;Gür et al;Gur et al, 2021a;Kandemir et al, 2017). Ayrıca artan ROT'lar GSH'ı GSSG formuna dönüştürerek GSH depolarının tükenmesine sebep olmaktadır (Aja et al, 2020;Radwan et al, 2018).…”

Section: Discussionunclassified

Ratlarda diklofenak ile indüklenen kardiyotoksisite üzerine krisinin etkilerinin oksidatif stres, endoplazmik retikulum stresi ve apoptoz belirteçleri ile değerlendirilmesi

Gür¹,

Kandemir²,

Kandemir³

2022

Kocatepe Veterinary Journal

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Diclofenac (DF) is among non-steroidal anti-inflammatory drugs and in high doses it has toxic effects on various tissues, including the heart. Chrysin (CRS) has many beneficial effects such as antioxidant and anti-apoptotic. In the present study, the effects of CRS on DF-induced cardiotoxicity were investigated. For this purpose, after DF and/or CRS treatments were applied to Sprague Dawley rats, the markers of oxidative stress, endoplasmic reticulum stress and apoptosis in heart tissues and serum CK-MB levels were analyzed. The data obtained displayed that oxidative stress induced by DF was alleviated by triggering the expression of SOD, CAT and GPx enzymes and increasing GSH levels after CRS administration, and a decrease in MDA levels occurred. It was also determined that the expressions of ATF-6, PERK, IRE1 and GRP78, which are ER stress markers and induced by DF, were downregulated after CRS treatment. Additionally, CRS suppressed Bax and Caspase-3 expressions and increased Bcl-2 expression in connection with ER stress. Another finding of this study demonstrated that CK-MB levels, which are an important indicator of heart damage, decreased after CRS administration. As a result, CRS provided a significant protection against cardiotoxicity caused by DF.

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Bortezomib ile Kalp Hasarı Oluşturulan Ratlarda Berberinin Oksidatif ve Nitrozatif Stres Üzerine Etkisi

Cited by 8 publications

References 57 publications

Investigation of the effects of hesperidin administration on abamectin‐induced testicular toxicity in rats through oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, autophagy, and JAK2/STAT3 pathways

Investigation of the effects of hesperidin administration on abamectin‐induced testicular toxicity in rats through oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, autophagy, and JAK2/STAT3 pathways

Carvacrol reduces abnormal and dead sperm counts by attenuating sodium arsenite‐induced oxidative stress, inflammation, apoptosis, and autophagy in the testicular tissues of rats

Ratlarda diklofenak ile indüklenen kardiyotoksisite üzerine krisinin etkilerinin oksidatif stres, endoplazmik retikulum stresi ve apoptoz belirteçleri ile değerlendirilmesi

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