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    Cannabidiol mitigates methotrexate-induced hepatic injury via SIRT-1/p53 signaling and mitochondrial pathways: reduces oxidative stress and inflammation
    (Taylor & Francis Ltd, 2025) Ilhan, Ilter; Asci, Halil; Candan, Ibrahim Aydin; Savran, Mehtap; Imeci, Orhan Berk; Sevuk, Mehmet Abdulkadir
    Methotrexate (MTX), a widely used chemotherapeutic agent, often induces hepatotoxicity, limiting its clinical utility. Cannabidiol (CBD), derived from hemp, possesses antioxidant, anti-inflammatory, and antiapoptotic properties. This study aims to investigate CBD's protective effects against MTX-induced liver injury and elucidate the underlying mechanisms. Thirty-two female Wistar Albino rats were divided into four groups: control, MTX (20 mg/kg intraperitoneally [i.p.] once), MTX+CBD (20 mg/kg i.p. once + 5 mg/kg i.p. for seven days), and CBD (5 mg/kg, i.p. for seven days). Biochemical analyses of serum and liver tissues were performed to assess oxidative stress markers (total oxidant status, total antioxidant status, oxidative stress index), liver function tests (AST, ALT), and antioxidant enzyme activities (glutathione peroxidase, superoxide dismutase). Histopathological and immunohistochemical examinations were conducted to evaluate liver tissue damage and TNF-alpha expression. Genetic analyses were performed to measure the expression levels of SIRT-1, p53, Bcl-2, and Bax genes using RT-qPCR. MTX administration increased oxidative stress markers, liver enzymes, TNF-alpha, p53, and Bax levels while decreasing antioxidant defenses and SIRT-1 expression. CBD administration reversed these alterations effectively. CBD mitigated MTX-induced hepatotoxicity by reducing oxidative stress, inflammation, and apoptosis. It activates antioxidant defenses via SIRT-1 upregulation, suppresses inflammation by reducing TNF-alpha, and prevents apoptosis by modulating p53, Bcl-2, and Bax gene expressions. These findings suggest CBD could be a promising therapeutic agent for chemotherapy-induced liver damage. Further research is warranted to explore additional pathways and broader molecular mechanisms.
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    Investigation of cardioprotective effect of lercanidipine on doxorubicin-induced cardiotoxicity
    (Springer, 2023) Karakuyu, Nasif Fatih; Savran, Mehtap; Candan, Ibrahim Aydin; Buyukbayram, Halil Ibrahim; Erzurumlu, Yalcin
    Although doxorubicin (DOX) is an effective anti-neoplastic drug for many types of cancer, particularly dose-related cardiotoxicity limits the use of the drug. In this study, it was aimed to investigate the protective effect of lercanidipine (LRD) against DOX-induced cardiotoxicity. In our study, 40 Wistar albino female rats were randomly divided into 5 groups as control, DOX, LRD 0.5 (DOX + 0.5 mg/kg LRD), LRD 1 (DOX + 1 mg/kg LRD), and LRD 2 (DOX + 2 mg/kg LRD). At the end of the experiment, the rats were sacrificed, and their blood, heart, and endothelial tissues were examined biochemically, histopathologically, immunohistochemically, and genetically. According to our findings, necrosis, tumor necrosis factor alpha activity, vascular endothelial growth factor activity, and oxidative stress were increased in the heart tissues of the DOX group. In addition, DOX treatment caused the deteriorations in biochemical parameters, and levels of autophagy-related proteins, Atg5, Beclin1, and LC3-I/II were detected. Significant dose-related improvements in these findings were observed with LRD treatment. Besides, Atg5, LC3-I/II, and Beclin1 levels evaluated by western blot revealed that LRD exerts a tissue protective effect by regulating autophagy in endothelial tissue. LRD treatment, which is a new-generation calcium channel blocker, showed antioxidant, anti-inflammatory, and anti-apoptotic properties in heart and endothelial tissue in a dose-dependent manner and also showed protective activity by regulating autophagy in endothelial tissue. With studies evaluating these mechanisms in more detail, the protective effects of LRD will be revealed more clearly.
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    Investigation of the efficiency of pulsed electromagnetic field treatment and stretching exercise in experimental skeletal muscle injury model
    (Bmc, 2025) Ergan, Mesut; Keskin, Tahir; Candan, Ibrahim Aydin; Erzurumlu, Yalcin; Asci, Halil; Comlekci, Selcuk; Baskurt, Ferdi
    Objective Pulsed electromagnetic fields (PEMF) and stretching exercises are safe and noninvasive methods that could have a therapeutic effect on tissue healing. This study aimed to assess the effectiveness of these methods in treatment of muscle injury (INJ). Method Rats were divided into 5 groups (Control, INJ, INJ + Exercise, INJ + PEMF, INJ + Exercise + PEMF). At the end of the experiment, genetic, histopathological, and immunohistochemical evaluations were made in the muscle tissue. Results Mononuclear cell infiltration, muscle degeneration, atrophy, and necrosis were found to be higher in the INJ group than in all groups (p < 0.001). On the 7th day, fibroblast growth factor (FGF) was found to be higher in the INJ group compared to both the control and the INJ + Exercise group (p < 0.05). On the 14th day, Vascular endothelial growth factor values were found to be higher in the injury group than the other groups except for the PEMF group (p < 0.05), and FGF values were higher in the injury group compared to all groups (p < 0.001). The expressions of transforming growth factor beta 1 (TGF-beta 1) and endothelial nitric oxide synthase (eNOS) on the 7th and 14th days showed a significant increase in the INJ group compared to the other groups (p < 0.001). Conclusion In this study, it has been shown that PEMF and stretching exercise is effective in the treatment of muscle injuries as they balance the inflammatory process in the muscle, have a positive effect on muscle development, accelerate healing, prevent fibrosis development by reducing TGF-beta 1 signaling, and inhibit inflammatory-induced eNOS activity.
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    Investigation of the Neuroprotective Effect of Riluzole on Matrix Metalloproteinases in an Experimental Model of Glaucoma
    (Wolters Kluwer Medknow Publications, 2024) Yildiz, Fatma; Sahinoglu-Keskek, Nedime; Yilmaz, Isil Tan; Candan, Ibrahim Aydin; Korkmaz, Orhan Tansel
    Purpose: To investigate the neuroprotective effect of riluzole through matrix metalloproteinase-2 (MMP-2) and MMP-9 in rats, in an experimental glaucoma model. Methods: A total of 28 Wistar albino rats, 3-4 months old, weighing 250-300 g, were divided into four groups; Group I (control), Group II (glaucoma), Group III (glaucoma + corn oil + dimethyl sulfoxide (DMSO), and Group IV (glaucoma + corn oil + DMSO + riluzole). A glaucoma model was created by episcleral vein cauterization in the left eyes of Group II, III, and IV subjects. After the formation of the model, daily intraperitoneal riluzole (5 mg/kg) administration was started. At the end of 7 weeks, retinal tissues were taken and some parts of them were stained with hematoxylin and eosin for histopathological examinations. In the other part, MMP-2 and MMP-9 expressions were determined using real-time quantitative PCR and immunohistochemical techniques. Results: As a result, a statistically significant increase in intraocular pressures (IOP) was found in Groups II, III, and IV when compared with the control eyes after 7 weeks (P < 0.001). There was a decrease in IOP in the riluzole group compared to the glaucoma group. Expression levels in both genes decreased slightly with riluzole administration. In the histopathological evaluation of the groups, it was observed that there were no significant differences between the findings of degeneration in ganglion cells, hemorrhage, and differentiation in layers. Conclusions: MMP-2 and MMP-9 exhibited decreased expression levels in both Group III (glaucoma + corn oil + DMSO) and Group IV (glaucoma + corn oil + DMSO + 5 mg/kg riluzole) compared to the glaucoma groups in Group II. Given that both Group III and Group IV received injections of corn oil + DMSO, this conclusion was drawn.
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    Melatonin receptor agonist ramelteon alleviates experimental acute ocular inflammation via HIF-1?/VEGF/E-NOS signaling
    (Sage Publications Ltd, 2023) Sofu, Gulsah Usta; Erzurumlu, Yalcin; Karaca, Umut; Candan, Ibrahim Aydin; Savran, Mehtap; Asci, Halil; Hasseyid, Nursel
    Purpose: Ramelteon (RML) is a potent, selective agonist of the high-affinity melatonin receptor 1 and 2 receptors. In addition, RML is known to have antioxidant and anti-inflammatory effects. In this study, we aimed to investigate the effects of RML on HIF-1 alpha, VEGF and e-NOS signaling pathway in a rat model of endotoxin-induced uveitis (EIU). Methods: Twenty-eight Wistar albino rats were divided into 4 groups as controls, lypopolysaccharide (LPS) group (5 mg/kg i.p.), LPS + RML group (5 mg/kg i.p and 8 mg/kg orally, respectively) and RML group (8 mg/kg orally). EIU was induced by a single intraperitoneal LPS injection. Histopathological and genetical analyses were performed. Results: In histopathological analysis, LPS caused mild anterior uveitis characterized by increased surface area of iris leaflets and ciliary body due to edema, mild to moderate congestion, and inflammatory infiltrate 6 h following the injection. The pathological findings were reduced by RML. Higher inflammation levels seen in LPS group were significantly reduced in LPS + RML group. Also, HIF-1 alpha, eNOS and VEGF expressions increased in LPS and decreased in LPS + RML group. Conclusion: RML treatment reversed the changes in the HIF-1 alpha /eNOS/ VEGF signaling pathway in LPS-induced uveitis in rats, preventing the progression of the damage and showed positive effects.