AIM: To identify the autophagy mechanism T98 glioma cells. MATERIAL and METHODS: Three groups were created with T98 human glioblastoma cells; Group 1: T98 glioma cells without treatment (Control group). Group 2: T98 glioma cells treated with 3 Nl/ml JWO. Group 3: T98 glioma cells treated with 6 Nl/ml JWO. The cell proliferation, oxidative stress, types of cell death were studied at IC50 dose of JWO. RESULTS: The proliferation of glioma cells was inhibited in 5.296 Nl/ml dose. JWO induced apoptosis in T98 glioma cells in comparison with the control and there was statistically significant difference (p<0.001). Apoptosis was analyzed via TUNEL method and results were checked by flow cytometry. We also investigated the effects of JWO on autophagy in T98 glioma cells by immunostaining LC3-II and MDC fluorescent stainings. The differences between JWO treated and control group were notably significant (p<0.001). The immunofluorescence staining resultsof LC3-II was confirmed by Western blotting analysis. CONCLUSION: JWO seems to be an effective treatment agent for glioblastoma. Not only does it induce apoptosis via oxidative stress but also affects the autophagy. The use of JWO in combination with other treatment options may increase the efficacy of treatment.
Diabetes (DB)-related sperm damage is one of the most significant issues contributing to infertility. Mesenchymal Stem Cells (MSCs) are an important product that has recently gained clinical relevance. The medium composed of MSC secretions after 48 h of culture is called Conditioned Medium (CM), and its effectiveness has been demonstrated in experimental studies. Platelet-Rich Plasma (PRP) and Stromal Vascular Fraction (SVF) are products commonly used in clinical settings with proven efficacy. However, there is limited research on the combined use of these products in treatment. This study examined the effectiveness of combined therapy (CT) compared to individual treatments in sperm damage induced by DB damage (DBD) simulated using a high glucose medium (HGM) in culture. Sperm obtained from male Wistar Albino rats were placed in 6-well flasks and divided into 6 different groups: Control (CG), DBD with high glucose (HG), HG + MSC, HG + CM, HG + PRP, HG + SVF, and HG + MSC + CM (CT). After one hour of treatment, the samples were evaluated for viability, motility, and morphology. Slides prepared from these samples were analyzed immunohistochemically for oxidative stress using endothelial Nitreous Acide Syntease (eNOS) and for apoptosis using Caspase 3. The damage to sperm caused by HG led to significant increases in eNOS and Caspase 3, as well as significant reductions in viability, motility, and morphological abnormalities. Although all single treatments reversed all parameters, the most effective treatment was found to be the combined application of MSC and CM. The DB in vitro model demonstrated that sperm damage can occur and that this damage can potentially be prevented with cell therapy treatments, highlighting the importance of exploring other treatment possibilities. The combination of MSC and CM was shown to be quite beneficial by reducing oxidative stress and apoptosis. Cellular therapy, a cost-effective and newly developed regenerative method, could offer hope to families wishing to have children, especially in the context of the high prevalence and increasing incidence of male infertility. Validation of these findings through studies in experimental animals and humans, as well as clarification of the underlying mechanisms, will facilitate their clinical application.
BACKGROUND:The gut microbiota modulates nervous system function. In the literature, it has been shown that this modula-tion is used in many nervous system injuries through oxidative stress (OS) and apoptosis mechanisms. In this study, it was aimed to investigate the neuroprotective effects of probiotic (PB) treatment in a rat traumatic brain injury (TBI) model with histological and electroencephalographic (EEG) data.METHODS:Forty male Wistar albino rats were divided into four groups. Group 1 was the control group (CONTROL, n=10) and no trauma was applied. Group 2 was the trauma group with the weight-drop technique (TBH, n=10). Group 3 was the sham group (SHAM), (TBH+sterile saline [SS], n=10) rats were given 500 µL of SS per day by oral gavage. Group 4 was the PB treatment group, (TBH+PB, n=10) rats were treated daily for 7 days with 500 µL of PB oral gavage. Brain samples were collected 7 days after trauma. Histopathological evaluation of brain samples was done with HE. OS with Endothelial nitric oxide synthase, vascularization with Vas-cular Endothelial Growth Factor, gliosis with S100, and apoptosis with caspase 3 were evaluated immunohistochemically. Apoptotic index was determined with TUNEL. In addition, EEG and somatosensory evoked potential (SEP) recording findings were compared.RESULTS:It was determined by HE staining that there was a significant (P<0.001) damage in the TBI and sham groups compared to the control group. It was found that PB treatment provided a significant (P<0.01) improvement in the damage created. While OS (P<0.01), gliosis (P<0.01), and apoptosis (P<0.05) decreased with PB treatment, angiogenesis (P<0.01) increased. In support of these findings, in the software-mediated EEG and SUP examination; Delta wave power and theta/alpha ratio increased with TBI and de-creased with PB treatment.CONCLUSION:The results showed that PB treatment provided a significant improvement in rats by reducing OS, apoptosis, and gliosis and increasing vascularity. To the best of our knowledge in the literature, it was shown for the 1st time that histological results for the treatment of PB were supported by software-mediated EEG and SEP analysis.
Amaç: Barsak mikrobiyatası ile beyin arasında iki yönlü bir ilişki olup özellikle travmatik beyin hasarı (TBH) sonrası hasarda oksidatif stres ve enflamatuvar aşama önemli bir role sahiptir.Barsakta oluşan patoloji bu hasarın tedavisinde problem oluşturmaktadır.Probiyotikler (PB) bunu düzenleyerek oluşan oksidatif stres ve gliozisi azaltabilme potansiyelindedir.Bu çalışmada sıçan modelinde TBH oluşturulup PB için bu olası etki
Giriş ve Amaç: Diyabetik deri yarası kronik, tedavisi zor ve maliyetli bir patolojidir Probiyotikler (PB) yeni ürünler olup barsak mikrobiyotasını düzenleyerek cilt yaralarının iyileşme sürecini olumlu yönde etkilerler. Ancak mekanizmaları bilinmemektedir. Bu çalışmada diyabetik sıçan deri yarasına PB katkısı morfolojik parametreler, oksidatif stres, apoptoz, damarlanma, inflamasyon ve bağ doku açısından mekanizmalar araştırıldı. Gereç ve Yöntemler: Sıçanlar 50 mg/kg intraperitoneal Streptozotosin kullanılarak diyabetik hale getirildi. Sırt bölgesinde 1x1cm tam kat deri defekti yapıldı ve NBL Probiotic Gold preparatı PB olarak oral gavaj ile uygulandı. Yara iyileşmesinin 7. gününde örnekler alındı. Histokimyasal olarak HE boyamaları ile morfolojik inceleme ve skorlama yapıldı. Örnekler, immünohistokimyasal yöntem ile eNOS, Kaspas 3, IL-10, VEGF ve Kollagen1 ile boyandı ve H-skor ile değerlendirildi. Bulgular: Tam kat deri defekti ile oluşan yaranın iyileşmesinde PB kullanımı morfometrik skorlamada anlamlı bir hızlanma ve olgunlaşma sağladı. Yara yerinde hasara bağlı oluşan eNOS, Kaspas 3 ve IL-10 artışı ile VEGF ve Kollagen1 azalışının PB ile anlamlı bir şekilde geri döndürüldüğü izlendi. Sonuç: PB için deride kronik, zor ve maliyetli yara iyileşmesi üzerindeki olumlu etkisinin klinikte hasta yaşam kalitesini arttıracağı düşünülmektedir.