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(1 ? 3)-?-d-glucan enhances the toxicity induced by Bortezomib in rat testis
(Blackwell Publishing Ltd, 2020) Abuç, Özlem Özgül; Koç, Kübra; Bal, Tuğba; Geyiko?lu, Fatime; Atilay, Hilal; Erol, Hüseyin Serkan; Yiğit, Serdar; Gül, Murat; Akaras, Nurhan
We aimed to determine the possible effects of the antioxidant agent (1 ? 3)-?-D-glucan on bortezomib-induced rat testis damage. We used five groups of rats; control, (1 ? 3)-?-D-glucan (75 mg/kg), bortezomib group, bortezomib + (1 ? 3)-?-D-glucan groups (injection of (1 ? 3)-?-D-glucan after bortezomib and sacrificed at 48th or 72nd h). The effects of these substances were assessed by measuring the levels of the antioxidant enzymes and LPO, and by performing immunohistochemical analysis with NF-?B. The histology of testis was evaluated using aniline blue staining. (1 ? 3)-?-D-glucan leads to significant reductions in the levels of antioxidant enzymes and increased levels of LPO in testes. Moreover, it increased the NF-?B immunopositivity significantly in testis, especially in Bortezomib + (1 ? 3)-?-D-glucan group at 48th h. The histological changes were observed in the bortezomib and/or (1 ? 3)-?-D-glucan groups. Our results demonstrated that testis damage caused by the treatment with bortezomib was not eliminated by (1 ? 3)-?-D-glucan and shockingly it increased the damage. Practical applications: The testis damage caused by the treatment with bortezomib was not eliminated by (1 ? 3)-?-D-glucan and as a result, ?-1,3-(D)-glucan enhanced the toxicity by leading a decrease in the levels of GSH, SOD, and CAT, thus caused an elevation in the immunoreactivity of NF-?B and altered the histopathological changes by enhancing the toxic effects of bortezomib. The findings of the previous studies about the antioxidative activity of (1 ? 3)-?-D-glucan are controversial. So, it is necessary to consider the cytotoxicity of (1 ? 3)-?-D-glucan in testis tissue. Thus, more studies on testis tissue are necessary to confirm that (1 ? 3)-?-D-glucan is safe as an antioxidant.
A histological and biochemical study of cumulus cells and the oocyte microenviroment in in vitro fertilization patients
(Association of Clinical Biochemistry Specialists (Klinik Biyokimya Uzmanları Derneği), 2021) Akaras, Nurhan; Demirci, Tuba; Abuç, Özlem Özgül; 0000-0001-9852-8839; Halıcı, Mesut Bünyamin; Kaşali, Kamber
Objectives: The aim of this study was to investigate the effect of chemical changes in the follicular fluid and histological changes in the cumulus cells of the oocyte microenvironment on the number of oocytes in infertile patients. Methods: A total of 50 female patients aged 18-35 who presented at the Atatürk University Research Hospital Infertility Clinic and for infertility treatment were included. The patients were divided into 3 groups: Patients with fewer than 5 oocytes were classified as Group 1, patients with 5-20 oocytes comprised Group 2, and Group 3 was made up of patients with >20 oocytes. During the oocyte collection process, follicular fluid was aspirated from the follicles and the cumulus cells were collected. The follicular fluid was stored at -80°C for use in biochemical analysis of malondialdehyde (MDA), total antioxidant status (TAS), total oxidant status (TOS), superoxide dismutase (SOD), glutathione (GSH). Immunohistochemical staining was performed to examine caspase-3 and mechanistic target of rapamycin (mTOR) immunoreactivity at the stereological level. Results: The MDA level and total oxidant capacity (TOC) in the follicular fluid were higher in Group 1 patients than in the other 2 groups, while the SOD was lower (p<0.05). In Group 2 patients, the MDA level and TOS were higher than those of Group 3, while the SOD level was lower (p<0.05). The total antioxidant capacity (TAC) and GSH levels did not vary significantly according to the number of oocytes (p<0.05). Immunohistochemical staining showed that mTOR and caspase-3 immunoreactivity were more intense in Group 1 than in the other groups. Conclusion: The increase in mTOR expression may activate the caspase-3 pathway, which could lead to oxidative stress. The mTOR pathway may affect the oocyte count
A histological and biochemical study of the protective role of hesperidin in testicular ischemia-reperfusion injury
(Ali Cangül, 2023) Akaras, Nurhan; Şimşek, Hasan; Ordu, Melike
This study aimed to investigate the possible effects of hesperidin on ischemia-reperfusion (IR) injury applied to rat testis. Methods: Twenty-eight Wistar albino rats were used and divided into four groups of seven each. Group 1: Sham surgery was performed on the right testis. Group 2: Hesperidin 100 mg/kg was administered intraperitoneally to rats. Group 3: After 1 h of ischemia and 4 h of reperfusion, the testicles were removed. Group 4: 100 mg/kg hesperidin was given 30 min before reperfusion. Biochemical, immunohistochemical, and histopathological analyzes were performed on testicles obtained from each group. Results: Total oxidant status (TOS) and oxidative stress index (OSI) levels increased significantly in the IR and IR-He groups (respectively, p=0.016, p=0.041; p=0.01, and p=0.024). TOS and OSI values in the hesperidin group decreased, although not statistically significant, compared to the IR group. Tumor necrosis factor-alpha (TNF-?) and nuclear factor kappa B (NF-kB) values were decreased in the hesperidin group compared to the IR group, although it was not statistically significant. Caspase-3 levels in testicular tissue were significantly increased in the IR group compared to the hesperidin group (p<0.05). While there were degenerative changes in the testicular tissue in the IR groups, a decrease in bleeding, congestion, edema, and degenerative changes was observed in the hesperidin-administered groups. Conclusion: Hesperidin reduced oxidative stress (decreased total oxidant level and OSI), inflammation (TNF-?), and apoptosis (NF-kB and caspase-3). According to these results, it was observed that hesperidin application had a protective effect on IR injury.
Acacetin ameliorates acetylsalicylic acid-induced gastric ulcer in rats by interfering with oxidative stress, inflammation, and apoptosis
(Ali Cangül, 2023) Şimşek, Hasan; Akaras, Nurhan
Gastric ulcer (GU) is a benign lesion in which excessive acid and pepsin activity affects the mucosal ep- ithelium and is common worldwide. Gastrointestinal disturbances come to the fore among the side effects observed in the treatment with drugs such as aspirin. Acacetin is a plant-derived flavonoid with intriguing properties such as anti-inflammatory, antioxidant, and anticancer. The aim of the study is to investigate the effects of acacetin in GU model caused by aspirin active ingredient acetylsalicylic acid. Methods: Thirty-two Wistar albino rats were divided into four groups: Control, GU, acacetin, and GU +acacetin. Acetyl- salicylic acid (150 mg/kg) and acacetin (25 mg/kg) were administered intraperitoneally as a single dose. Gastric lesions were examined microscopically and macroscopically. TNF-a, cyclooxygenase-2 (COX-2), and nuclear factor kappa B (NF-kB) for inflammation; Caspase-3 and Bcl-2 for apoptosis, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) for oxidative stress were analyzed. Results: Bcl-2 and TAS values were decreased, while Tumor necrosis factor-alpha (TNF-?), COX-2, NF-kB, Caspase-3, TOS, and OSI values were increased in the GU group compared to the control group. Bcl-2 and TAS values were increased and TNF-?, COX-2, NF-kB, Caspase-3, TOS, and OSI values were decreased in the GU +acacetin group compared to the GU group. The GU index (GUI) detected in the GU group decreased significantly with the administration of acacetin. Conclusion: High doses of ASA contributed to the formation of GU in the stomach tissue by increasing the levels of inflammation, oxidative stress, and apoptosis, whereas ACA reduced the ulcer damage by reducing the increase in all these pathways.
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 Mehmet
Diclofenac (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.
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 Mehmet
In 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.
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, Serpil
Long-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.
Antioxidant Effects of Bromelain on Paracetamol-Induced Renal Injury in Rats
(AVES Yayıncılık, 2023) Akaras, Nurhan; Tokyay, Erdem; Aydemir Celep, Nevra; Yüce, Neslihan; Şimşek, Hasan; Özkan, Halil İbrahim
Bromelain, a natural antioxidant, is the active ingredient of pineapple. Paracetamol is a nonsteroidal drug that is used worldwide as a pain reliever and causes kidney damage in high doses. This study was conducted to investigate the potential effects of bromelain on paracetamol-induced kidney damage. Methods: 56 Sprague–Dawley rats were randomly divided into 7 groups, namely (1) control, (2) N-acetylcysteine (140 mg/kg), (3) bromelain (100 mg/kg), (4) paracetamol (2 g/kg), (5) paracetamol (2 g/kg) + N-acetylcysteine (140 mg/kg), (6) paracetamol (2 g/ kg) + bromelain (50 mg/kg), (7) paracetamol (2 g/kg) + bromelain (100 mg/kg). At the end of the experiment, creatinine and urea levels from blood serum, malondialdehyde (MDA) and glutathione (GSH) levels from kidney tissue, and superoxide dismutase (SOD), glutathione peroxidase (GPx) activities were measured. Additionally, the kidney was evaluated histopathologically. Results: It was determined that serum creatinine, urea levels, and kidney tissue MDA levels were significantly increased in rats in the paracetamol group compared to the control group, while SOD, GSH, and GPx activities were decreased (P < .050). N-acetylcysteine and bromelain applications were determined to decrease serum creatinine and urea levels and kidney tissue MDA levels caused by paracetamol and increased SOD, GSH, and GPx activities (P< .050). When the histopathological scores were examined, it was found that paracetamol-induced renal tissue damage was reduced by Bro50, Bro100, and N-acetylcysteine applications, and especially Bro100 application was more effective in reducing damage than N-acetylcysteine and Bro50 (P < .050). Conclusion: It was determined that increased serum urea and creatine, tissue oxidative stress markers, and histopathological changes due to paracetamol have decreased thanks to the antioxidant property of bromelain. Additionally, it was determined that the Bro100 dose was more effective than the N-acetylcysteine treatment. It is thought that the obtained data will support different studies to be conducted on the usability of bromelain-supportive treatment in preventing paracetamol-induced kidney damage.
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 Mehmet
Cadmium (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.
Carvacrol Ameliorates Cisplatin-Induced Cardiotoxicity By Regulating Notch/Hes1 Signaling Pathway, Oxidative Stress and Cell Death In Rat Cardiac Tissue
(Bingöl Üniversitesi Fen Bilimleri Enstitüsü, 2024) Akaras, Nurhan; Kandemir, Özge; Şimşek, Hasan
Cisplatin is one of the most active cytotoxic agents used mainly in the treatment of solid tumors. High doses and long-term use of Cisplatin are known to cause cardiotoxicity. In recent years, the antiapoptotic and antioxidant effects of Carvacrol in cardiovascular diseases have attracted attention. In this study, the effects of Carvacrol on Cisplatin-induced cardiotoxicity in a rat model were investigated using biochemical and histological methods. Twenty-eight rats were divided into 4 groups: 1. Control group, 2. Carvacrol group, 3. Cisplatin group, 4. Cisplatin + Carvacrol group. The expression of antioxidant enzymes, proinflammatory cytokines, apoptotic, and autophagic proteins was examined in heart tissue obtained from rats sacrificed after the last drug administration. Additionally, heart tissue was evaluated histopathologically. Cisplatin has been observed to cause oxidative stress and inflammatory damage in animal heart tissue. Carvacrol administration significantly increased antioxidant enzyme (superoxide dismutase and glutathione peroxidase) activities while suppressing inflammatory markers (NF-κB, TNF-α, IL-1β). Additionally, Cisplatin induced apoptotic (caspase-3, Bax, Bcl-2) and autophagic (Beclin-1, LC3A, LC3B) markers. It has been determined that carvacrol can protect heart tissues from the destructive effects of cisplatin by exerting anti-apoptotic and anti-autophagic effects. The expression levels of Notch1 and Hes1, which were decreased by cisplatin administration, were upregulated after administration of Carvacrol. H&E staining results showed that Carvacrol preserved myocardial tissue integrity. In conclusion, Carvacrol showed a cardioprotective effect against cisplatin-induced cardiotoxicity.
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 Mehmet
This 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.
Carvacrol reduces abnormal and dead sperm counts by attenuating sodium arsenite-induced oxidative stress, inflammation, apoptosis, and autophagy in the testicular tissues of rats
(Wiley, 2023) Gür, Cihan; Akarsu, Serkan Ali; Akaras, Nurhan; Tuncer, Sibel Çiğdem
Arsenic (As) is a highly toxic metalloid. Carvacrol (CAR) is the active ingredient of Lamiaceae plants and has various biological and pharmacological properties. The present study investigated the protective effects of carvacrol (CAR) against testicular toxicity induced by sodium arsenite (SA). Rats were given SA (10 mg/kg) and/or CAR (25 or 50 mg/kg) for 14 days. Semen analyzes showed that CAR increased sperm motility and decreased the percentage of abnormal 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 inflammation triggered by SA in testicular tissue were alleviated by suppressing the expressions of LC3A, LC3B, MAPK-14, NF-?B, TNF-?, IL-1?, iNOS, and COX-2 biomarkers in rats given CAR. Also, CAR treatment suppressed SA-induced apoptosis by inhibiting Bax and Caspase-3 expressions in testicles and up-regulating Bcl-2 expression. Histopathological analyzes showed that rats given SA had deterioration in tubule structure and spermatogenesis cell line, especially a serious loss of spermatogonia cells, atrophy of seminiferous tubules, and deterioration of germinal epithelium. In the group given CAR, the germinal epithelium and connective tissue were in normal morphological structure and an increase in seminiferous tubule diameters was observed. As a result, it was determined that oxidative stress, inflammation, autophagy, and apoptosis induced by SA were suppressed by CAR, thus protecting the testicular tissue from damage and increasing semen quality.
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 Mehmet
Mercuric 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.
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 Mehmet
Aim 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.
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 Mehmet
Heavy 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.
Effects of Bromelain on Oxidative Stress and Lung Tissue Histopathology in an Experimental Rat Sepsis Model
(Afyon Kocatepe University, 2023) Akaras, Nurhan; Toktay, Erdem; Şimsek, Hasan; Celep Aydemir, Nevra; Yüce, Neslihan
Sepsis is an inflammatory syndrome that targets the lung tissue. Bromelain (BRO) is an enzyme complex known for its anti-inflammatory properties. In this study, the protective effect of BRO on lung injury due to sepsis induced by cecal ligation and puncture (CLP) in Sprague-Dawley rats was investigated by biochemical and histopathological methods. Forty Sprague dawley rats were randomly divided into five groups as control, CLP, BRO, CLP+BRO 50 and CLP+BRO 100. In the study, after oral administration of 50 and 100 mg/kg BRO (total of 7 applications for 7 days) to rats, laparotomy and CLP were performed.
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 Mehmet
Testicular 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.
Effects of Quercetin on Cypermethrin-Induced Stomach Injury: The Role of Oxidative Stress, Inflammation, and Apoptosis
(Gümüşhane Üniversitesi, 2023) Akaras, Nurhan; Gür, Cihan; Şimşek, Hasan; Tuncer, Sibel Çiğdem
This study was conducted to investigate the effects of quercetin (QUE) on cypermethrin (CYP) induced gastrotoxicity in rats. 35 Sprague-Dawley rats were randomly divided into five groups, 7 in each group. In the study, 25 and 50 mg/kg QUE were administered orally 30 min after 25 mg/kg cypermethrin was administered to rats for 28 days. Oxidative stress, inflammation, ER stress, apoptosis and autophagy markers were biochemically analyzed in gastric tissues. Additionally, histological analysis was performed for microscopic evaluation of gastric tissue. The results revealed that QUE prevented tissue damage by reducing CYP-induced lipid peroxidation (MDA) and increasing GSH, SOD, CAT and GPx activities. It also showed anti-inflammatory effect by suppressing inflammatory markers such as NF- B, IL-1?, TNF-?, iNOS and COX-2. QUE administration down-regulated CYP-induced increased PERK, ATF6, Caspase-3 and Beclin-1 markers. In addition, administration of QUE ameliorated the pathological tissue damage in gastric tissue due to CYP. The data of this study show that Que suppresses CYP-induced gastric toxicity by reducing oxidative stress, inflammation, ER stress, apoptosis a autophagy.
Gossypin protects against renal Ischemia-Reperfusion Injury in rats
(Kafkas University, 2020) Tanyeli, Ayhan; Eraslan, Ersen; Güler, Mustafa Can; Kurt, Nezahat; Akaras, Nurhan
Renal injury occurring as a result of renal ischemia-reperfusion may lead to renal failure or even death. The aim of this study is to investigate possible protective effects of Gossypin on tissue damage occurred due to ischemia-reperfusion in rat kidney tissue. A total of 48 male Wistar albino rats were used in the study. These rats were randomly divided into 6 groups equally (n = 8). The created groups were control (C), sham (S), ischemia-reperfusion (I/R), I/R + DMSO, I/R + 400 mu g/kg gossypin and I/R + 4 mg/kg gossypin. In the rats of sham group, the right nephrectomy was performed. In the rats of other groups rather than sham, the left renal artery was clamped after performing the right nephrectomy. Gossypin was administered intraperitoneally before the reperfusion. 24 h reperfusion was applied to the left renal after 1 h of ischemia. TNF-alpha, IL-1 beta, IL-6 and IL-10 levels were measured with spectrophotometric methods in the kidney tissues after the procedures were completed. Apoptosis and inflammatory pathways were evaluated histopathologically using Caspase 3 and NF-kappa B antibodies. There was a statistically significant decrease in IL-1 beta and IL-6 levels of the gossypin groups compared to the I/R group (P<0.05). As the level of TNF-alpha was decreased in the gossypin administered groups compared to the I/R group although not statistically significant, the level of IL-10 was increased. In the present study, we aimed to show that gossypin in renal I/R model is effective on inflammatory process and apoptosis and that it can be used in routine treatment to decrease the damage in all reasons that may cause I/R. In addition, this study can shed light on the studies to be done in this field in the future.
Hesperidin ameliorates vancomycin-induced kidney injury via multipathway modulation: Nrf-2/HO-1, Caspase-3/Bax/Bcl-2, ATF-4, KIM-1 and improved renal tissue function
(Elsevier Inc., 2025) Gencer, Selman; Şimşek, Hasan; Akaras, Nurhan; Gür, Cihan; İleritürk, Mustafa; Kandemir, Özge; Küçükler, Sefa; Kankılıç, Nazım Abdülkadir; Kandemir, Fatih Mehmet
Vancomycin (VCM) is a therapeutic agent used to treat drug-resistant gram-positive bacteria. However, its high-dose use is associated with nephrotoxicity, limiting its clinical application. Hesperidin (HES), a flavonoid naturally found in citrus fruits, exhibits various biological and pharmacological activities, including anti-inflammatory, antioxidant, and anticancer effects. While HES has been shown to exert protective effects in several organ systems, its potential role in preventing VCM-induced nephrotoxicity remains unclear. This study investigates whether HES can mitigate VCM-induced renal damage through its antioxidant and anti-inflammatory properties. VCM was administered intraperitoneally at a dose of 200 mg/kg for seven days. HES (100 mg/kg and 200 mg/kg) was administered orally for seven days. Biochemical, and molecular methods were used to investigate indicators of oxidative stress, ER stress damage, apoptotic and autophagic death in kidney tissue. Additionally, histological methods were used to determine the structural and functional characteristics of kidney tissue. HES treatment alleviated VCM-induced oxidative stress by increasing antioxidants (SOD, CAT, GPx, GSH) and reducing increased MDA levels, a marker of lipid peroxidation. In addition, HES increased antioxidant activity by activating the Nrf2 signaling pathway. VCM-induced increases in apoptotic Bax, Caspase-3, and P53 were reduced by HES, while the decreased level of antiapoptotic Bcl-2 was increased. HES reduced VCM-induced ER stress damage by reducing the levels of ATF-4, ATF-6, eIF2-α, and CHOP. HES treatment attempted to preserve kidney function and structural integrity. Overall, HES was effective in reducing VCM-induced nephrotoxicity damage and may be an effective treatment option.

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