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Öğe 18β-glycyrrhetinic acid Mitigates bisphenol A-induced liver and renal damage: Inhibition of TNF-α/NF-κB/p38-MAPK, JAK1/STAT1 pathways, oxidative stress and apoptosis(Elsevier Ltd, 2025) Darendelioğlu, Ekrem; Cağlayan, Cüneyt; Küçükler, Sefa; Bayav, İbrahim; Kandemir, Fatih Mehmet; Ayna, Adnan; Sağ, SevdaBisphenol A (BPA) has been commonly used in various consumer products, including water bottles, food containers, and canned food linings. However, there are concerns about its potential toxicity to human health, particularly its impact on the liver and kidneys. The objective of this research was to investigate the potential ameliorative effects of 18β-glycyrrhetinic acid (GA) against BPA-induced hepatotoxicity and nephrotoxicity in rats. The animals were supplemented with BPA (250 mg/kg b.w.) alone or with GA (50 and 100 mg/kg b.w.) for 14 days. GA treatment alleviated the BPA-induced hepato-renal tissue injuries through reducing the serum ALT, AST and ALP levels, and urea and creatinine levels. GA co-treatment also increased activities of SOD, CAT and GPx enzymes and levels of GSH, and suppressed MDA levels in BPA induced tissues. BPA also induced inflammation by increasing the levels of TNF-α, NF-κB, JAK1, STAT1, P38 MAPK and JNK in liver and kidney tissues and GA treatment ameliorated these effects. BPA triggered apoptosis by increasing caspase-3, Bax, and cytochrome c at protein levels and also by decreasing the antiapoptotic Bcl-2 level. However, treatment with GA (50 and 100 mg/kg) decreased apoptosis. Overall, our results have revealed the potential ameliorative mechanisms of GA, as a possible agent for BPA-induced hepatotoxicity and nephrotoxicity.Öğe Abamektin kaynaklı mide toksisitesinde hesperidinin oksidatif stres, inflamasyon ve apoptoz üzerindeki koruyucu etkisi(Ayşe SURUÇ, 2024) Tuncer, Sibel Çiğdem; Gür, Cihan; Şimşek, Hasan; Kandemir, Fatih MehmetAbamektin günümüzde tarım endüstrisinde çok fazla kullanılan bir pestisit türü olup uzun süreli maruziyet sonucunda toksik etkilere sahiptir. Uzun süreli abamektin maruziyeti sonucunda özellikle oksidatif stres ilişkili inflamasyon ve apoptoz artışına neden olmaktadır. Hesperidin, narenciyelerde doğal olarak bulunan antioksidan, antiinflamatuvar ve antiapoptotik etkilere sahip bir flavanoiddir. Bu çalışmada, abamektin kaynaklı mide doku hasarı üzerine doğal bir antioksidan olan hesperidinin kullanımı ve muhtemel etkilerinin araştırılması amaçlanmıştır. GEREÇ VE YÖNTEM: 28 gün boyunca 1 mg/kg dozda abamektin uygulamasından 30 dakika önce grubuna göre 100 ve 200 mg/kg hesperidin uygulaması yapıldı. 29. günde 35 adet hayvan dekapite edilerek mide dokuları alındı ve biyokimyasal yöntemler ile oksidatif stres, inflamasyon ve apoptotik parametrelerin analizi yapıldı. BULGULAR: Abamektin mide dokularında oksidatif stres, inflamasyon ve apoptoz parametrelerin düzeylerini kontrol grubuna göre arttırdı (p<0,001). Hesperidin uygulamasıyla birlikte abamektine bağlı tüm bu artış miktarlarında azalmalar meydana gelmiştir (p<0,001). SONUÇ: Abamektin maruziyetinin neden olduğu mide dokularındaki toksik etkiye karşı hesperidinin potansiyel koruyucu özelliklere sahip olduğu sonucuna varıldı.Öğe Ameliorative effect of morin on diclofenac-induced testicular toxicity in rats: An investigation into different signal pathways(Mashhad University of Medical Sciences, 2025) Şimşek, Hasan; Akaras, Nurhan; Gür, Cihan; Küçükler, Sefa; İleritürk, Mustafa; Kandemir, Fatih MehmetDiclofenac (Diclo) is a therapeutic agent used in the treatment of pain and inflammatory diseases, but it is also toxic to the human body. Morin is a flavonoid found naturally in plants and has many biological and pharmacological activities, including anti-inflammatory, anti-oxidant, and anticancer activities. This study aimed to investigate the efficacy of Morin in Diclo-induced testicular toxicity. Materials and Methods: Morin (50 mg/kg and 100 mg/kg) was administered orally for five days, while Diclo was administered intraperitoneally at 50 mg/kg on days 4 and 5. Biochemical, molecular, and histological methods were used to investigate oxidative stress, inflammation, apoptosis, and endoplasmic reticulum (ER) stress damage indicators in testicular tissue. Results: Morin treatment attenuated Diclo-induced oxidative stress damage by increasing anti-oxidant levels (SOD, CAT, GPx, GSH, Nrf-2, HO-1, and NQO1) and decreasing MDA levels, an indicator of lipid peroxidation. Morin reduced levels of the inflammatory mediators NF-κB protein. Increases in apoptotic Bax and Caspase-3 by Diclo were reduced by Morin, while decreased antiapoptotic Bcl-2 level was increased. Morin reduced Diclo-induced ER stress injury by decreasing ATF-6, PERK, IRE1, GRP-78, and CHOP levels. Also, Diclo decreased COX-2 levels. Conclusion: Overall, Morin may be an effective treatment of choice for testicular tissue damage associated with Diclo toxicity and may reduce the level of damage.Öğe Ameliorative effects of sinapic acid against vancomycin-induced testicular oxidative damage, apoptosis, inflammation, testicular histopathologic disorders and decreased epididymal sperm quality(Elsevier, 2024) Akarsu, Serkan Ali; İleritürk, Mustafa; Küçükler, Sefa; Akaras, Nurhan; Gür, Cihan; Kandemir, Fatih MehmetIn this study, it was aimed to determine the effect of sinapic acid (SNP), a polyphenol with antioxidant, anti-inflammatory and antibacterial properties, on testicular damage caused by vancomycin (VCM), a widely used antibiotic against gram positive bacteria. A total of 35 male Sprague Dawley rats were used in the study, divided into five groups: control, VCM, SNP, VCM + SNP 10, and VCM + SNP 20. Following a week of oral administration, the rats were euthanized under sevoflurane anesthesia. While the VCM group had a significant increase in MDA levels, the SNP administration inhibited the increase in MDA levels. VCM led to a significant decrease in GSH levels, SOD, CAT, and GPx activity in the testicular tissue of rats, while SNP administration increased these antioxidant levels. SNP administration decreased the mRNA expression levels of VCM induced Nrf-2, HO-1, and NQO1 in testicular tissue while increasing the levels of MAPK14, MAPK15, JNK, P53, Apaf-1, Caspase-3, Caspase-6, Caspase-9, and Beclin-1 mRNA transcript levels. The VCM group showed a significant increase in Bax and NF-?B levels in testicular tissue, while Bcl-2 levels decreased. VCM significantly decreased sperm motility and increased the percentage of damaged sperm in rats. Histopathological results revealed that VCM caused disruption of basement membranes and disorganization of seminiferous tubules, but SNP administration preserved testicular histology. As a result, VCM increased oxidative stress, apoptosis, and autophagy in the testicular tissue of rats, altered testicular histopathology, and decreased sperm quality, while SNP decreased these effects.Öğe Anti-oxidant, Anti-inflammatory, and Anti-apoptotic Effects of Rutin in Spleen Toxicity Induced by Sodium Valproate in Rats(Bingöl Üniversitesi Fen Bilimleri Enstitüsü, 2023) Akaras, Nurhan; Kandemir, Fatih Mehmet; Şimşek, Hasan; Gür, Cihan; Aygörmez, SerpilLong-term exposure to sodium valproate, an anti-epileptic drug, causes toxic effects in tissues, especially by increasing oxidative stress and inflammation. Rutin is a flavanoid with anti- oxidant, anti-inflammatory and anti-apoptotic effects found naturally in many plants. In this study, we aimed to investigate the effects of rutin, a natural anti-oxidant, on sodium valproate- induced spleen tissue damage. 35 male rats were divided into 5 groups as control, sodium valproate, rutin, sodium valproate+Rutin 50 and sodium valproate+Rutin 100 groups. For 14 days, 500 mg/kg dose of sodium valproate and 50 or 100 mg/kg of rutin were administered by oral gavage. On day 15, spleen tissues were removed and biochemical methods, oxidative stress, inflammation and apoptotic parameters were analyzed and histologic analysis was performed. The levels of sodium valproate-induced oxidative stress, inflammation and apoptosis parameters increased in spleen tissues compared to the control group (p<0.05). With routine administration, all of these sodium valproate-induced increases were decreased (p<0.05). It was concluded that rutin has potential protective properties against the toxic effect caused by sodium valproate exposure in spleen tissues.Öğe Beneficial effects of Chrysin on Cadmium-induced nephrotoxicity in rats: Modulating the levels of Nrf2/HO-1, RAGE/NLRP3, and Caspase-3/Bax/Bcl-2 signaling pathways(Elsevier B.V., 2023) Şimşek, Hasan; Akaras, Nurhan; Gür, Cihan; Küçükler, Sefa; Kandemir, Fatih MehmetCadmium (Cd) is a toxic heavy metal that targets the kidney directly in the body. Chrysin (CHR) is a natural flavonoid with many properties such as antioxidant, anti-inflammatory and anti-apoptotic. The current study discloses new evidence as regards of the curative effects of CHR on Cd-induced nephrotoxicity by regulating oxidative stress, apoptosis, autophagy, and inflammation. Cd was administered orally at a dose of 25 mg/kg body weight alone or in combination with orally administered CHR (25 and 50 mg/kg body weight) for 7 days. Biochemical, molecular, and histological methods were used to investigate inflammation, apoptosis, autophagy, and oxidant pathways in renal tissue. Renal function tests were also evaluated. Cd caused an increase in serum toxicity markers, lipid peroxidation and a decrease in the activities of antioxidant enzymes. Nrf-2 triggered inflammatory responses by suppressing HO-1 and NQO1 mRNA transcripts and increasing NF-?B, TNF-?, IL-1? and iNOS mRNA transcripts. Cd caused inflammasome by increasing RAGE and NLRP3 mRNA transcripts. In addition, Cd application caused apoptosis by increasing Bax, Apaf-1 and Caspase-3 mRNA transcripts and decreasing Bcl-2 mRNA transcript level. It caused autophagy by increasing the activity of Beclin-1 level. CHR treatment had the opposite effect on all these values and reduced the damage caused by all these signal pathways. Overall, the data of this study indicate that renal damage associated with Cd toxicity could be ameliorated by CHR administration.Öğe Beneficial effects of quercetin on vincristine-induced liver injury in rats: Modulating the levels of Nrf2/HO-1, NF-kB/STAT3, and SIRT1/PGC-1?(Wiley, 2023) Çomaklı, Selim; Özdemir, Selçuk; Küçükler, Sefa; Kandemir, Fatih MehmetOur experimental objective was to investigate the hepatotoxic effect of vincristine (VCR) administration in rats and determined whether combined therapy with Quercetin (Quer) ensured protection. Five groups with seven rats each were used for this purpose, and experimental groups were formulated as follows: Control group; Quer group; VCR group; VCR plus Quer 25 group; VCR plus Quer 50 group. The results showed that VCR significantly increased the activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) enzymes. Besides, VCR caused considerable increases in the malondialdehyde (MDA) contents, along with significant decreases in reduced glutathione levels, superoxide dismutase, catalase, and glutathione peroxidase enzyme activities in the rat livers. Quer treatment in VCR toxicity markedly decreased the activity of ALT, AST, ALP enzymes, and MDA contents and enhanced the activities of antioxidant enzymes. The results also showed that VCR significantly increased the levels of NF-kB, STAT3, and the expression of caspase 3, Bax, and MAP LC3 and decreased the expression of Bcl2 and levels of Nrf2, HO-1, SIRT1, and PGC-1?. Compared to the VCR group, Quer treatment exhibited significantly lower levels of NF-kB, STAT3, and the expression of caspase 3, Bax, and MAP LC3, and higher levels of Nrf2, HO-1, SIRT1, and PGC-1?. In conclusion, our study demonstrated that Quer could alleviate the harmful effects of VCR via activation of NRf2/HO-1 and SIRT1/PGC-1? pathways, and via attenuation of oxidative stress, apoptosis, autophagy, and NF-kB/STAT3 pathways.Öğe Carvacrol Coadministration Ameliorates Lambda-Cyhalothrin-Induced Peripheral Neuropathy in Rats: Behavioral and Molecular Evidence(Wiley, 2025) Kandemir, Özge; İleriturk, Mustafa; Gür, Cihan; Akaras, Nurhan; Şimşek, Hasan; Yılmaz, Selçuk; Kandemir, Fatih MehmetThis study aimed to investigate the possible neuroprotective effects of Carvacrol (CRV) against Lambda-cyhalothrin (CYH)-induced peripheral neuropathy. Thirty-five rats were divided into five groups: Control, CRV, CYH, CYH+CRV25, and CYH+CRV50. CRV 25 or 50 mg/kg and CYH 6.23 mg/kg were administered orally for 21 days. The effects of these treatments were evaluated by hot plate and rotarod tests, followed by molecular, biochemical, histopathological, and immunohistochemical analyses of sciatic nerve tissues. CYH administration significantly impaired both sensory and motor functions. CRV doses (25 mg/kg and 50 mg/kg) administered with CYH significantly improved these impairments (p < 0.001). Additionally, CYH increased MDA levels and decreased antioxidants, while CRV treatment reversed these effects. CRV also suppressed inflammation (p < 0.01), apoptosis (p < 0.001), and endoplasmic reticulum stress (p < 0.001), with the 50 mg/kg dose being more effective. Morphological and immunohistochemical analyses showed that CRV treatment partially repaired CYH-induced nerve damage, with both doses reducing 8-OHdG and beclin-1 immunoreactions. The data revealed that CYH induced inflammation, oxidative stress, ER stress, and apoptosis in sciatic tissue, while CRV exhibited antioxidant, anti-inflammatory, and antiapoptotic effects, reducing the damage and suggesting its potential as a supportive treatment for CYH-induced sciatic damage.Öğe Carvacrol protects against ?-Cyhalothrin-induced hepatotoxicity and nephrotoxicity by modulating oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress, and autophagy(John Wiley and Sons Inc, 2023) İleritürk, Mustafa; Kandemir, Fatih Mehmet?-Cyhalothrin, a type II synthetic pyrethroid, has been widely used in households, agriculture, public health, and gardening to control insect pests. Despite its widespread usage, it is known to induce a variety of adverse effects, including hepatotoxicity and nephrotoxicity. The goal of this study was to investigate the protective effect of carvacrol, which has antioxidant, anti-inflammatory, anti-apoptotic, and some other properties, on ?-Cyhalothrin-induced hepatotoxicity and nephrotoxicity 35 male Sprague–Dawley rats were randomly divided into five groups for this purpose: I-Control group: II-CRV group (50 mg/kg carvacrol), III-LCT group (6.23 mg/kg LCT), IV-LCT + CRV 25 group (6.23 mg/kg LCT + 25 mg/kg carvacrol), and V-LCT + CRV 50 group (6.23 mg/kg LCT + 50 mg/kg carvacrol). Using biochemical, real-time PCR, and western blotting methods, the collected tissues were analyzed. While ?-Cyhalothrin treatment increased MDA levels, which are indicated of lipid peroxidation, but reduced SOD, CAT, GPx activities, and GSH levels. After receiving carvacrol therapy, the degree of oxidative stress reduced as the values of these parameters approached those of the control group. Increased inflammation, apoptosis, endoplasmic reticulum stress, and autophagy with ?-Cyhalothrin administration reduced with carvacrol co-administration, and liver and kidney tissues were protected from damage, depending on the degree of oxidative stress. After considering all of these data, it was discovered that ?-Cyhalothrin-induced oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress, and autophagy in the liver and kidneys; however, carvacrol protected the tissues from damage. Our findings indicate that carvacrol may be a promising protective agent in ?-Cyhalothrin-induced hepatotoxicity and nephrotoxicity.Öğe Carvacrol Reduces Mercuric Chloride-Induced Testicular Toxicity by Regulating Oxidative Stress, Inflammation, Apoptosis, Autophagy, and Histopathological Changes(Springer, 2024) Şimşek, Hasan; Gür, Cihan; Küçükler, Sefa; İleritürk, Mustafa; Akaras, Nurhan; Öz, Mehmet; Kandemir, Fatih MehmetMercuric chloride (HgCl2) is a heavy metal that is toxic to the human body. Carvacrol (CAR) is a flavonoid found naturally in plants and has many biological and pharmacological activities including anti-inflammatory, antioxidant, and anticancer activities. This study aimed to investigate the efficacy of CAR in HgCl2-induced testicular tissue damage. HgCl2 was administered intraperitoneally at a dose of 1.23 mg/kg body weight alone or in combination with orally administered CAR (25 mg/kg and 50 mg/kg body weight) for 7 days. Biochemical and histological methods were used to investigate oxidative stress, inflammation, apoptosis, and autophagy pathways in testicular tissue. CAR treatment increased HgCl2-induced decreased antioxidant enzyme (SOD, CAT, and GPx) activities and GSH levels. In addition, CAR reduced MDA levels, a marker of lipid peroxidation. CAR decreased the levels of inflammatory mediators NF-?B, TNF-?, IL-1?, COX-2, iNOS, MAPK14, MAPK15, and JNK. The increases in apoptotic Bax and Caspase-3 with HgCl2 exposure decreased with CAR, while the decreased antiapoptotic Bcl-2 level increased. CAR reduced HgCl2-induced autophagy damage by increasing Beclin-1, LC3A, and LC3B levels. Overall, the data from this study suggested that testicular tissue damage associated with HgCl2 toxicity can be mitigated by CAR administration.Öğe Chemopreventive effects of hesperidin against paclitaxel-induced hepatotoxicity and nephrotoxicity via amendment of Nrf2/HO-1 and caspase-3/Bax/Bcl-2 signaling pathways(Elsevier Ireland Ltd, 2022) Gür, Cihan; Kandemir, Fatih Mehmet; Çağlayan, Cüneyt; Satıcı, EminePaclitaxel (PTX) is a widely used chemotherapeutic drug particularly effective against lung, breast, and ovarian cancer, though its usefulness is limited due to its multi-organ toxicity. The mechanisms underlying PTX toxicity are currently not yet known and there are no approved treatments for its control or prevention. This study aimed to investigate whether hesperidin (HSP) had a protective effect on paclitaxel-induced hepatotoxicity and nephrotoxicity from biochemical, and molecular perspectives. The rats were administered PTX 2 mg/kg, b.w. intraperitoneally for the first 5 consecutive days, then 100 or 200 mg/kg b.w. HSP orally for 10 consecutive days. Our results demonstrated that HSP decreased the PTX induced lipid peroxidation, improved the serum hepatic and renal functions (by decreasing the levels of AST, ALT, ALP, urea, and creatinine), and restored the liver and kidney antioxidant armory (SOD, CAT, GPx, and GSH). HSP also significantly reduced mRNA expression levels of NF-?B, TNF-?, IL-1?, IL-6, MAPK 14, Caspase-3, Bax, LC3A, LC3B, MMP2, and MMP9 whereas caused an increase in levels of Nrf2, HO-1, and Bcl-2 in the kidney and liver of PTX-induced rats. In addition, caspase-3, Bax, and Bcl-2 protein levels were examined by Western blot analysis, and it was determined that HSP decreased caspase-3 and Bax protein levels, but increased Bcl-2 protein levels. The findings of the study suggest that HSP has chemopreventive potential against PTX-induced hepatorenal toxicity plausibly through the attenuation of oxidative stress, inflammation, apoptosis, and autophagy.Öğe Chrysin Counteracts Sodium Hydroxide-Induced Alkali Esophageal Burn by Regulating Beclin-1/HO-1/NQO1, PERK/IRE1-α/ATF-6, Oxidative Stress, Inflammation, Apoptosis Signaling Pathways and Ki-67, EGF Expressions in Rats(Springer Nature, 2025) Öztürk, Ayşe Betül; Şimşek, Hasan; Akaras, Nurhan; Kandemir, Fatih MehmetAim Alkali-esophageal burn due to ingestion of corrosive substances is an important clinical entity that can be seen in all age groups, especially children. Chrysin is a natural favonoid compound with a wide range of biological activities, including antioxidant, anti-infammatory, antiapoptotic, and anticancer efects. This study aimed to ascertain the preventive efcacy of chrysin in the treatment of alkali-esophageal burns. Materials and Methods Rats were administered 0.2 ml of 25% NaOH orally and CHR at 25 and 50 mg/kg intraperitoneally for four days. The levels of oxidative stress, ER stress, infammation, damage, and apoptotic and autophagic cell death in esophageal tissues were analyzed using biochemical and molecular methods. Additionally, esophageal tissue structure and function were examined using histological methods. Results Chrysin alleviated NaOH-induced increased oxidative stress by decreasing MDA and increasing antioxidants. Chrysin alleviated infammation damage by inhibiting the NF-κB signaling pathway. Chrysin decreased apoptotic Caspase-3, and Bax and increased antiapoptotic Bcl-2. Moreover, Chrysin reduced autophagic death damage and ER stress damage. Chrysin facilitated the restoration of impaired structural integrity of esophageal tissue and increased Ki-67 and EGF levels, contributing to the healing process. Conclusion Chrysin exhibited antioxidant, antiapoptotic, anti-autophagic, anti-infammatory, and anti-oxidant properties in alkali esophageal burns, as well as an efect on reducing ER stress injury. Additionally, chrysin facilitates esophageal tissue healing and maintains tissue integrity.Öğe Chrysin mitigates diclofenac-induced hepatotoxicity by modulating oxidative stress, apoptosis, autophagy and endoplasmic reticulum stress in rats(Springer Science and Business Media B.V., 2023) Varışlı, Behçet; Çağlayan, Cüneyt; Kandemir, Fatih Mehmet; Gür, Cihan; Ayna, Adnan; Ayna, Adnan; Genç, Aydın; Taysı, SeyithanDiclofenac (DF) is a non-steroidal anti-inflammatory drug (NSAID) generally prescribed for the treatment of pain. In spite of the widespread use of DF, hepatotoxicity has been reported after its administration. The current study discloses new evidence as regards of the curative effects of chrysin (CHR) on DF-induced hepatotoxicity by regulating oxidative stress, apoptosis, autophagy, and endoplasmic reticulum (ER) stress. Methods: The animals were separated into five different groups. Group-I was in control. Group-II received CHR-only (50 mg/kg bw, p.o.) on all 5 days. Group-III received DF-only (50 mg/kg bw, i.p.) on 4th and 5th day. Group-IV received DF (50 mg/kg bw) + CHR (25 mg/kg, bw) and group-V received DF (50 mg/kg, bw) + CHR (50 mg/kg, bw) for 5 days. Results: DF injection was associated with increased MDA while reduced GSH level, activities of superoxide dismutase, glutathione peroxidase, and catalase and mRNA levels of HO-1 and Nrf2 in the liver. DF injection caused apoptosis and autophagy in the liver by up-regulating caspase-3, Bax, LC3A, and LC3B levels and down-regulating Bcl-2. DF also caused ER stress by increasing mRNA transcript levels of ATF-6, IRE1, PERK, and GRP78. Additionally, it was observed that DF administration up-regulated MMP2 and MMP9. However, treatment with CHR at a dose of 25 and 50 mg/kg considerably ameliorated oxidative stress, apoptosis, autophagy, and ER stress in liver tissue. Conclusion: Overall, the data of this study indicate that liver damage associated with DF toxicity could be ameliorated by CHR administration.Öğe Effect of syringic acid on oxidative stress, autophagy, apoptosis, inflammation pathways against testicular damage induced by lead acetate.(Elsevier GmbH, 2023) Akarsu, Serkan Ali; Gür, Cihan; İleritürk, Mustafa; Akaras, Nurhan; Küçükler, Sefa; Kandemir, Fatih MehmetHeavy metals are one of the environmental pollutants. Lead (Pb) is one of the most common of these heavy metals. In this study, it was aimed at investigating the effects of syringic acid (SA) against testicular toxicity in rats administered lead acetate (PbAc). Methods: In the present study, a total of 35 Sprague-Dawley rats, 7 in each group, were used. The rats were divided into 5 groups, with 7 male rats in each group. Rats were given PbAc and SA orally for 7 days. The effects of PbAc and SA on epididymal sperm quality and apoptosis, inflammation, oxidative stress and histopathological changes in testicular tissue were determined. Results: While PbAc disrupted the seminiferous tubules and produced atrophic images, SA corrected these histological abnormalities. PbAc adminisration significantly reduced the levels of SOD, GSH, GPx, CAT, NRF-2 and NQO1 and significantly increased the levels of MDA and 8-OHdG in the testicular tissue of rats, while SA improved this situation. NF-?B, TNF-?, IL-1?, NLRP3, RAGE, ATF6, PERK, IRE1, CHOP, and GRP78 genes expression levels increased with PbAc administration, however these levels decreased with SA administration. In addition, PbAc increased the levels of apoptotic markers Bax, Caspase-3 and APAF-1 and decreased the level of Bcl-2, while SA improved this situation. It was observed that PbAc significantly reduced sperm quality in rats, while SA positively affected sperm quality. Conclusion: As a result, SA administered against PbAc-induced testicular dysfunction in rats can provide effective protection at doses of 25 mg/kg/bw and 50 mg/kg/bw.Öğe Effects of chrysin in cadmium-induced testicular toxicity in the rat; role of multi-pathway regulation(Springer Science and Business Media B.V., 2023) Tuncer, Sibel Çiğdem; Küçükler, Sefa; Gür, Cihan; Aygörmez, Serpil; Kandemir, Fatih MehmetCadmium (Cd) is a strong toxic agent and causes serious damage to testicular tissues. Chrysin (CHR) is a natural flavonoid with many effective properties, especially antioxidant, anti-inflammatory and anti-apoptotic properties. The current study describes new evidence for the ameliorative effects of CHR on oxidative stress, apoptosis, autophagy and inflammation pathways in Cd-induced testicular tissue toxicity. Methods: Thirty-five male Wistar rats were divided into five groups, control, Cd, CHR, Cd + CHR25, and Cd + CHR50. Cd was administered alone at a dose of 25 mg/kg body weight or in combination with CHR 25 mg/kg and CHR 50 mg/kg for 7 days. Cd and CHR were administered orally. Biochemical, molecular, and histological methods were used to investigate inflammation, apoptosis, autophagy, and oxidant pathways in testicular tissue. Results: Cd increased lipid peroxidation, JAK-2/STAT-3 levels, inflammation-related NF-?B, TNF-?, IL-1?, IL-6, COX-2, and iNOS levels, AKT-2, FOXO1, Bax, Apaf-1 and Caspase-3 levels, autophagic Beclin-1, LC3A and LC3B. The Cd also caused a decrease in the activities of antioxidant enzymes and GSH levels, antiapoptotic Bcl-2 levels. CHR, on the other hand, had the opposite effect of all these Cd-induced changes. Conclusions: Overall, the data of this study indicate that testicular damage associated with Cd toxicity could be ameliorated by CHR administration.Öğe Effects of Morin on the Wnt, Notch1/Hes1, KI-67/3-Nitrotyrosine and Damage Signaling Pathways in Rats Subjected to Experimental Testicular Ischemia/Reperfusion(Springer International Publishing, 2025) Öztürk, Ayşe Betül; Şimşek, Hasan; Akaras, Nurhan; Kandemir, Fatih MehmetTesticular torsion, which occurs when the testicle rotates around the axis of the spermatic cord, is a serious cause of hospital admission, mostly in newborns and children, but also in adults. Oxidative stress is an important mediator of the development of complications. Morin has anti-inflammatory, anti-autophagic, and anti-apoptotic activities and especially strong antioxidant activity. This study aimed to determine the effects of Morin on testicular torsion injury. Methods: 35 Wistar rats were divided into 5 groups (n = 7): Control, Morin, I/R, I/R + MRN50, and I/R + MRN100. Parameters are effective in oxidative stress, inflammation, endoplasmic reticulum stress, apoptosis, and autophagy damage and Wnt pathway parameters, KI-67, and 3-NT levels were analyzed by biochemical, molecular, and histological methods. Results: I/R injury significantly increased oxidative stress (MDA, p < 0.001) and reduced antioxidant activity (GSH, SOD, CAT, GPx; p < 0.001). MRN administration reversed these effects, with higher doses showing greater improvement (p < 0.01 for CAT, p < 0.001 for others). Inflammation markers (NF-kB, IL-1β, TNF-α, COX-2, iNOS) were elevated in the I/R group, but MRN reduced their expression (p < 0.001). MRN also mitigated ER stress and reactivated the Wnt signaling pathway, particularly at 100 mg/kg (p < 0.001). Additionally, MRN reduced apoptosis (Caspase-3, Bax, p < 0.001) and autophagy (Beclin-1, LC3A, LC3B, p < 0.001), and improved testicular histology and sperm parameters. MRN treatment restored sperm density, motility, and viability (p < 0.05), with higher doses proving more effective. Conclusion: MRN has effects properties in testicular I/R injury by inhibiting many damage pathways and activating protective mechanisms.Öğe Effects of sinapic acid on lead acetate-induced oxidative stress, apoptosis and inflammation in testicular tissue(John Wiley and Sons Inc, 2023) Tuncer, Sibel Çiğdem; Akarsu, Serkan Ali; Küçükler, Sefa; Gür, Cihan; Kandemir, Fatih MehmetIn this study, the effect of lead acetate (PbAc) and sinapic acid (SNP) administration on oxidative stress, apoptosis, inflammation, sperm quality and histopathology in testicular tissue of rats was tried to be determined. PbAc was administered at a dose of 30 mg/kg/bw for 7 days to induce testicular toxicity in rats. Oral doses of 5 and 10 mg/kg/bw SNP were administered to rats for 7 days after PbAc administration. According to our findings, while PbAc administration increased MDA content in rats, it decreased GPx, SOD, CAT activity and GSH content. NF-kB, IL-1?, TNF-?, and COX-2, which are among the inflammation parameters that increased due to PbAc, decreased with the administration of SNP. Nrf2, HO-1, and NQO1 mRNA transcript levels decreased with PbAc, but SNP treatments increased these mRNA levels in a dose-dependent manner. RAGE and NLRP3 gene expression were upregulated in PbAc treated rats. MAPK14, MAPK15, and JNK relative mRNA levels decreased with SNP treatment in PbAc treated rats. While the levels of apoptosis markers Bax, Caspase-3, and Apaf-1 increased in rats treated with PbAc, the level of Bcl-2 decreased, but SNP inhibited this apoptosis markers. PbAc caused histopathological deterioration in testis tissue and negatively affected spermatogenesis. When the sperm quality was examined, the decrease in sperm motility and spermatozoon density caused by PbAc, and the increase in the ratio of dead and abnormal spermatozoa were inhibited by SNP. As a result, while PbAc increased apoptosis and inflammation by inducing oxidative stress in testicles, SNP treatment inhibited these changes and increased sperm quality.Öğe Effects of zingerone on rat induced testicular toxicity by sodium arsenite via oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, and autophagy pathways(Mashhad University of Medical Sciences, 2024) Tuncer, Sibel Çi?dem; Gür, Cihan; Küçükler, Sefa; Akarsu, Serkan Ali; Kandemir, Fatih MehmetThis study aimed to investigate the effects of zingerone (ZNG) treatment on testicular toxicity in rats induced by sodium arsenite (SA). Materials and Methods: In the study, five groups were formed (n=7) and the experimental groups were designated as follows; Vehicle group, ZNG group, SA group, SA+ZNG 25 group, and SA+ZNG 50 group. While SA was administered orally to rats at 10 mg/kg/bw, ZNG was given to rats orally at 25 and 50 mg/kg/bw doses for 14 days. Results: As a result of the presented study, an increase was observed in the MDA contents of the testicular tissue of the rats administered SA, while significant decreases were observed in GSH levels, SOD, CAT, and GPx activities. The mRNA transcript levels of the pro-inflammatory genes NF-?B, TNF-?, IL-1?, and IL-6 were triggered after SA administration. Additionally, SA administration caused inflammation by increasing RAGE, NLRP3, and JAK-2/STAT3 gene expression. Moreover, endoplasmic reticulum (ER) stress occurred in the testicular tissues of SA-treated rats and thus ATF-6, PERK, IRE1, and GRP78 genes were up-regulated. SA caused apoptosis by up-regulating Bax and Caspase-3 expressions and inhibiting Bcl-2 expression in testicles. SA caused histological irregularities in the testicles, resulting in decreased sperm quality. Conclusion: ZNG treatment reduced SA-induced oxidative stress, ER stress, inflammation, apoptosis, and histological irregularities in the testicles while increasing sperm quality. As a result, it was observed that ZNG could alleviate the toxicity caused by SA in the testicles.Öğe Evaluation of protective effects of quercetin against cypermethrin-induced lung toxicity in rats via oxidative stress, inflammation, apoptosis, autophagy, and endoplasmic reticulum stress pathway(John Wiley and Sons Inc, 2022) İleritürk, Mustafa; Kandemir, Özge; Kandemir, Fatih MehmetCypermethrin (CYP), a type II synthetic pyrethroid, is the most widely used insecticide worldwide. Inhalation of it may cause side effects. This study is aimed to examine potential protection of quercetin (QUE) which is a well-known antioxidant in CYP-induced lung toxicity. Accordingly, 35 Spraque Dawley male rats were divided into five equal groups as follows: I-Control group, II-QUE group (50 mg/kg/b.w. QUE), III-CYP group (25 mg/kg/b.w. CYP), IV-CYP + QUE 25 (25 mg/kg/b.w. CYP + 25 mg/kg/b.w. QUE), V-CYP + QUE (25 mg/kg/b.w. CYP + 50 mg/kg/b.w. QUE) were treated with oral gavage throughout 28 days. CYP intoxication was associated with increased malondialdehyde level while glutathione concentration, activities of glutathione peroxidase, superoxide dismutase, and catalase reduced. CYP adminisitration caused of apoptosis in the lung by up-regulating caspase-3 and Bax levels and down-regulating Bcl-2. CYP also caused of endoplasmic reticulum (ER) stress by increasing mRNA transcript levels of PERK, IRE1, ATF6, and GRP78. Additionally, it was observed that CYP administration activated IL-6/JAK2/STAT3/MAPK14 signaling pathway and levels of IL-1?, NF-?B, TNF-?, and iNOS in the lung tissue. Therefore, it was determined that CYP administration triggered autophagy by upregulating LC3A and LC3B mRNA transcript levels. Moreover, the protein levels of NF-?B, caspase-3, Bax, Bcl-2, and cytochorme-c were examined by Western blot analysis. However, co-treatment with QUE at a dose of 25 and 50 mg/kg considerably protective oxidative stress, inflammation, apoptosis, ER stress, autophagy, and IL-6/JAK2/STAT3/MAPK14 signaling pathway in lung tissue. Overall, the findings of this study suggest that lung damage associated with CYP toxicity could be protected by QUE administration.Öğe Evaluation of the levels of metalloproteinases as well as markers of oxidative stress and apoptosis in lung tissues after malathion and rutin administrations to rats(Bingöl Üniversitesi Fen Bilimleri Enstitüsü, 2022) Gür, Cihan; Kandemir, Fatih MehmetMalathion (MLT) is an important environmental pollutant in the organophosphate class. Rutin (RUT), on the other hand, is one of the flavonoid family members whose effectiveness against various toxic agents has been extensively studied. In the present study, the effects of MLT and RUT treatments on oxidative stress, apoptosis and metalloproteinases in lung tissues of rats were investigated. In the study, MDA, GSH, Nrf2, HO-1, MMP2, MMP9 and caspase-3 levels in lung tissues were analyzed by biochemical or RT-PCR method after rats received MLT and/or RUT treatment for 28 days. The data showed that MLT-induced MDA levels decreased after RUT treatment. In addition, it was determined that Nrf2 and HO-1 mRNA transcript levels and GSH levels suppressed by MLT approached the control group levels after RUT treatment. MLT up-regulated the expression of metalloproteinases (MMP2 and MMP9) in lung tissues, while RUT down-regulated the expression of these genes. In addition, it was observed that MLT triggered caspase-3 expression, while RUT exerted an anti-apoptotic effect by suppressing caspase-3. As a result, it was determined that while MLT showed toxic effects in the lung tissues of rats through oxidative stress, apoptosis and metalloproteinases, RUT could alleviate these toxic effects.
