Browsing by Author "Kalkan, Serpil"

Now showing 1 - 4 of 4

Citation - WoS: 1
Citation - Scopus: 1
The Ameliorative Effects of Hesperidin in Rats Developed Hepatotoxicity With Deltamethrin
(Mashhad Univ Med Sciences, 2025) Karabekir, Seda Cetinkaya; Sozen, Mehmet Enes; Ayan, Ilknur Cinar; Savas, Hasan Basri; Cuce, Gokhan; Kalkan, Serpil
Objective(s): Deltamethrin (DLM) is a widely used insecticide in agriculture; however, exposure to it can lead to serious health problems. This study aimed to evaluate the protective effects of hesperidin (HSP), a natural antioxidant, against DLM-induced liver toxicity. Materials and Methods: Thirty-two male Wistar Albino rats (250-300 g, 4 months old) were divided into four groups. The control group received 1 ml of corn oil via oral gavage for 30 days. The DLM group received 1.28 mg/kg DLM in corn oil for 30 days. The DLM+HSP 100 mg/kg and DLM+HSP 300 mg/kg groups received 1.28 mg/kg DLM followed by 100 mg/kg or 300 mg/kg HSP in distilled water, respectively, 30 min after DLM administration for 30 days. Liver tissues were examined histopathologically. Masson's trichrome staining and PCR assessed fibrosis. Caspase 3 and 9 expressions in liver tissues were determined by immunohistochemistry and PCR. Biochemical analyses were conducted on serum samples. Results: HSP supplementation led to a dose-dependent decrease in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. DLM exposure decreased antioxidant capacity, while HSP supplementation increased it dose-dependently. Histopathological evaluations showed increased liver damage in the DLM group, while HSP administration reduced liver toxicity. Masson's trichrome staining and analysis of collagen I (COL1A1) and collagen III (COL3A1) gene expression revealed increased fibrosis in the DLM group, which was attenuated with HSP treatment. Conclusion: The potential prevention of DLM-induced liver toxicity and apoptosis by HSP may be an alternative protective strategy.
Citation - WoS: 12
Citation - Scopus: 12
Protective Effect of Astaxanthin on Histopathologic Changes Induced by Bisphenol a in the Liver of Rats
(Univ Agriculture, Fac veterinary Science, 2024) Karabekir, Seda Cetinkaya; Gultekin, Burcu; Ayan, Ilknur Cinar; Savas, Hasan Basri; Cuce, Gokhan; Kalkan, Serpil
Bisphenol A (BPA) has several potential uses, including in polycarbonate plastics and epoxy resins, which could expose humans to it. Recognized for its hepatotoxicity and ability to accumulate in organs. We prompted this study to explore the hepatoprotective potential of astaxanthin (ASTX), an antioxidant against BPA toxicity. We used 32 male Wistar Albino rats and randomly assigned them as: Control, Sham (olive oil), BPA, and BPA+ASTX. At the end of the experiment, Native Thiol, Total Thiol, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were measured in serum samples. Histopathological scoring was performed to evaluate the changes caused by ASTX in the liver. Caspase 3 and caspase 9 expression in liver tissues was demonstrated immunohistochemically and by PCR. Collagen I (COL1A1) and collagen III (COL3A1) mRNA levels were measured by PCR in the tissue samples. The BPA group showed elevated AST and ALT with decreased Thiol levels. ASTX administration reversed these changes as observed by reduced AST and ALT levels and increased Thiol levels. Histopathology indicated increased liver damage and fibrosis in the BPA group which were alleviated in the BPA+ASTX group. Gene expression analyses revealed upregulated COL1A1 and COL3A1 in BPA, which was downregulated with ASTX. Immunohistochemistry and PCR confirmed BPA-induced caspase 3 and caspase 9 expression, which were attenuated by ASTX. This study underscores ASTX's hepatoprotective efficacy against BPA-induced hepatotoxicity which ultimately attributed to its antioxidant and antiapoptotic properties. Consequently, ASTX emerges as a promising therapeutic agent for preventing and treating BPA-related liver diseases.
Effects of Carvacrol on Oxidative Stress and Fibrosis in Streptozotocin-Induced Diabetic Nephropathy: Histological, Gene Expression, and Biochemical Insights
(MDPI, 2025) Canbaz, Halime Tuba; Sozen, Mehmet Enes; Cinar Ayan, Ilknur; Savas, Hasan Basri; Canbaz, Furkan Adem; Cuce, Gokhan; Kalkan, Serpil
Diabetes mellitus (DM) leads to renal damage through oxidative stress. Carvacrol (CAR), a monoterpenoid phenol, possesses anti-inflammatory and antioxidant properties. We investigated the potential effects of CAR on histological, gene expression, and biochemical parameters in a rat model of DM. Four groups were created: group 1, control; group 2 (n = 9), DM; group 3 (n = 9), DM + dimethyl sulfoxide (DMSO); and group 4 (n = 9), DM + CAR. DM was created by injecting streptozotocin (STZ). CAR (20 mg/kg) was prepared through dissolution in 0.1% DMSO. CAR and 0.1% DMSO were administered daily for 4 weeks to groups 4 and 3, respectively. At the end of this study, urea, creatinine, paraoxonase-1 (PON-1), and arylesterase (ARES) were measured in serum samples. Histopathological changes and expression of Nuclear factor erythroid 2-related factor 2 (Nrf-2) in renal tissues were assessed. Immunohistochemical(ihc) staining and RT-qPCR analysis were performed to evaluate apoptosis, focusing on Bax and Bcl-2gene expression. Masson's trichrome(MT) staining and RT-qPCR analysis of COL1A1 and COL3A1 mRNA levels were used to assess fibrosis. Increased urea and creatinine levels in DM were significantly decreased after CAR administration. CAR application also improved reduced levels of PON 1 and ARES, which are associated with diabetes. Both immunohistochemistry and RT-qPCR analyses revealed that CAR therapy mitigated the diabetes-induced elevation in Bax and reduction in Bcl-2 expression. CAR treatment improved histopathological findings and renal Nrf-2 immunofluorescence(if) intensity. Furthermore, gene expression analysis demonstrated that COL1A1 and COL3A1 were upregulated in DM, while CAR administration downregulated them. In conclusion, CAR has a protective role in decreasing renal impairment linked to DM by regulating Bax and Bcl-2 levels and rectifying histological damage.
Protective Role of Astaxanthin Against Bisphenol A Induced Biochemical and Histopathological Alterations in Rat Kidneys
(Mashhad Univ Med Sciences, 2025) Gultekin, Burcu; Karabekir, Seda Cetinkaya; Ayan, Ilknur Cinar; Sava, Hasan Basri; Kalkan, Serpil
Objective(s): This study investigates the ability of astaxanthin (ASTX), a powerful anti-oxidant, to protect kidney tissue from oxidative and cellular damage resulting from bisphenol A (BPA) toxicity, a widespread global toxin associated with chronic kidney disease. Materials and Methods: We used 32 male Wistar Albino rats, 16 weeks old, and weighing 250-300 g. The rats were randomly divided into four groups: Control, Sham, BPA, and BPA+ASTX. Following the experiment, serum samples were assessed for Paraoxonase 1 (PON1), Arylesterase (ARE), urea, and creatinine levels. Changes in kidney tissue induced by BPA were examined using histopathological methods. Also, the levels of apoptosis and collagen content were evaluated. Results: ASTX treatment reversed the BPA-induced inhibition of PON1 and ARE levels, restoring them to control levels, and reduced the BPA-induced increase in urea levels. Creatinine levels showed no significant differences across the groups. BPA exposure in kidney tissue caused vacuolization, congestion, tubular dilatation, desquamation, infiltration, and increased collagen around glomeruli and blood vessels. However, ASTX treatment significantly improved these pathological findings. While BPA induced apoptosis as indicated by Bax and Bcl-2 analysis, ASTX treatment partially inhibited this process. Conclusion: These findings indicate that ASTX may protect against BPA-induced renal injury. However, the study's limitations include the use of a single dose and a focus solely on kidney tissue. Additionally, the lack of dose-response data and evaluations of other organs or long-term effects are significant drawbacks. Future research should explore multiple doses and longer observation periods for a better understanding of ASTX's protective efficacy.