Dönmez, Muhammet Oğuzhan
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Donmez, Muhammet Oguzhan
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Araştırma Görevlisi
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oguzhan.donmez@fbu.edu.tr
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Eczacılık Meslek Bilimleri Bölümü
Eczacılık Meslek Bilimleri Bölümü
Eczacılık Meslek Bilimleri Bölümü
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3
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3
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Now showing 1 - 3 of 3
Article Evaluation of the Neuroprotective Effects of Korean Ginseng Root Extract in an Experimental Model of Multiple Sclerosis(Marmara Univ, Fac Medicine, 2025) Donmez, Muhammet Oguzhan; Sener, Goksel; Akbay, Tugba Tunali; Sivas, Guzin Goksun; Akakin, Dilek; Unlu, Hilal; Goren, Mehmet Zafer; Goksun Sivas, Guzin; Tunali Akbay, TugbaObjective: Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system characterised by demyelination. The aim of this study was to evaluate the neuroprotective effects of Korean ginseng root extract (KGE) using a cuprizone-induced demyelination model. Materials and Methods: C57BL/6 mice were divided into control, demyelination and remyelination groups and each group was treated with KGE. Demyelination was induced with 0.2% cuprizone in the diet for four weeks. KGE (100 mg/kg) was administered by gavage during or after the cuprizone exposure. Body weight, food and water intake, and motor performance parameters were investigated. In addition, glutathione (GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD) malondialdehyde (MDA), oligodendrocyte transcription factor-2 (OLIG2) and myelin basic protein (MBP) levels were measured in brain samples, while MBP and glial fibrillary acidic protein (GFAP) expression was assessed by immunohistochemistry and myelin status was examined using Luxol Fast Blue staining. Results: Korean ginseng root extract prevented myelin loss, promoted remyelination, and improved motor performance. It reduced oxidative stress by increasing GSH, GST, and SOD levels while decreasing MDA. KGE also suppressed demyelination by reducing astrogliosis and restoring OLIG2 and MBP levels. Conclusion: Korean ginseng root extract exhibits neuroprotective properties during demyelination and promotes remyelination, highlighting its therapeutic potential for MS.Article Protective Effects of Lactobacillus Rhamnosus GG Against Methotrexate-Induced Oxidative Renal Toxicity(Springer, 2026) Yanardag, Refiye; Bayrak, Bertan Boran; Sener, Goksel; Almurad, Bade; Donmez, Muhammet OguzhanMethotrexate (MTX) is commonly prescribed for various malignant and autoimmune conditions, but it can cause significant oxidative and functional impairment in renal tissue. Lactobacillus rhamnosus GG. (LGG) is a well-known probiotic with biological activities that support antioxidant balance. This study investigated the impact of LGG on MTX-induced kidney damage. Male Sprague-Dawley rats were divided into four groups: physiological saline-treated control group; a group receiving MTX alone; a group receiving MTX alongside a low dose of LGG; and a group receiving MTX alongside a high dose of LGG. MTX was administered as single dose (20 mg/kg/bw) intraperitoneally and LGG (low dose 1 x 10(9) CFU/day and high dose 5 & times; 10(9) CFU/day, respectively) orally for five days. On day six, blood and kidney samples were collected and examined for oxidative indicators, enzymatic antioxidant responses, and renal functional markers. MTX significantly increased in glomerular filtration markers in serum and elevated key indicators of oxidative stress in renal tissues. More so, MTX demonstrated to disrupt renal ionic homeostasis, such as declined sodium/potassium-ATPase, paraoxonase, and increased lactate dehydrogenase, carbonic anhydrase, xanthine oxidase, myeloperoxidase, and arginase activities. In contrast, LGG supplementation has been shown to effectively reverse all MTX-induced biochemical alterations in both serum and renal tissue. We can suggest that LGG can provide significant protection against oxidative renal toxicity induced by MTX in rats.Article Protective Effects of L-Theanine against Bisphenol A-Induced Oxidative Stress and Gut Microbiota Disruption in Wistar Rats(Springer, 2026) Sener, Azize; Marzi, Mahdi; Sener, Goksel; Donmez, Muhammet OguzhanBackground Gut microbiota homeostasis plays a central role in maintaining intestinal redox balance and immune regulation. Bisphenol A (BPA), a widely distributed environmental contaminant, has been associated with oxidative stress, inflammatory responses, and disturbances in intestinal microbial communities. L-theanine (LTN), a bioactive amino acid naturally present in green tea, possesses well-documented antioxidant and anti-inflammatory properties; however, its potential protective role against BPA-induced intestinal injury has not been fully clarified. Methods and Results In the present study, female Wistar albino rats were randomly allocated into three groups: control, BPA (50 mg/kg/day), and BPA + LTN (100 mg/kg/day) and treated for 30 days. Oxidative stress and inflammatory responses in intestinal and colonic tissues were assessed by measuring malondialdehyde (MDA), reduced glutathione (GSH) levels and myeloperoxidase (MPO), catalase (CAT) activities. BPA exposure significantly increased MDA (p < 0.001) level and MPO (p < 0.001) activity while reducing GSH content (p < 0.001) and CAT activity (p < 0.001) compared with the control group. Compared to the BPA group, LTN treatment led to significant changes in MDA, MPO, and GSH levels in both tissues. MDA and MPO levels were significantly reduced in the intestine and colon tissues of the BPA + LTN group (p < 0.001). GSH and CAT levels were significantly increased in both the intestine and colon compared to the BPA group (p < 0.001). In addition, fecal microbiota composition was analyzed using 16 S rRNA gene sequencing, with taxonomic profiling performed at the phylum, genus and species levels. BPA exposure was associated with reduced microbial stability and compositional shifts within the gut microbiota, whereas LTN treatment partially restored microbial richness and community structure. Conclusions Collectively, these findings indicate that LTN alleviates BPA-induced intestinal oxidative stress and microbiota dysbiosis, suggesting its potential as a protective dietary compound against environmental toxicant-related intestinal injury.