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Aim: Enterococcus faecalis has surface adhesion proteins that enable it to attach to human intestinal and vaginal tissue cells with antibiotic-resistant strains in patients. Due to these properties, boron and its derivatives are preferred as therapeutic agents due to their antibacterial, antifungal, antiparasitic and antifungal activities. In this study, we aimed to evaluate the synergistic effect of boron compounds and their effect on biofilms in an infection model created with Enterococcus faecalis 29212 on the HepG2 liver cell line. Materials and Methods: It was determined that sodium perborate monohydrate + zinc borate had the lowest values as a result of the minimum inhibitory concentration and fractional inhibitor concentration studies. It has also been shown that these doses reduce cytotoxic effects. In addition, 32 µg/ml Etidote + 256 µg/ml Sodium Perborate Monohydrate showed the highest biofilm effect. Results: we show that boron compounds effectively reduce biofilm formation and cause the death of bacteria.

Aim: Klebsiella pneumoniae causes hospital-acquired pneumonia, urinary tract infection and bacteremia in immunocompromised patients. Klebsiella pneumoniae, which has become more common recently, causes antibiotic resistance as well as pyogenic liver abscesses and hematogenous metastatic spread in humans. Developing antibiotic resistance complicates the treatment of liver infections. In our study, we aimed to evaluate the effect of boron compounds in an infection model created by Klebsiella pneumoniae 700603. Materials and Methods: Minimum inhibitory concentration and fractional inhibitory concentration studies, resistance gene levels, and HepG2 cell analyses were performed and evaluated. Results: We determined the low and high minimum inhibitory concentration values of boron components, sodium perborate monohydrate and etidote, respectively. In addition, sodium perborate monohydrate is also effective on biofilm formation and resistance genes. Our findings have shown that boron compounds are more effective when used in a combination. In the toxicity model created in the cellular study, the boron compounds cytotoxic effect decreased due to their antibacterial effects. Conclusion: İt seems that boron compounds are effective, and the positive effect increases when used together.

Aim: Recently, although studies have shown that biomaterials containing graphene oxide (GO) in biomedicine stand out for their positive effects, the effect of GO on dental tissues when used with dental materials is not well known. The aim of this study was an evaluation of the cytotoxic effects of GO on gingival fibroblasts when it is combined in two different ratios with Mineral Trioxide Aggregate (MTA). Materials and Methods: In this in-vitro study, a homogenous mixture of adding +0.1 weight (wt)% and +0.3 wt% GO to Angelus MTA was created (two experimental groups) and compared with pure Angelus MTA and negative control groups. The materials were mixed according to the manufacturer’s instructions, and Teflon molds were used to form 24 disc-shaped samples for each group. The samples were divided into groups according to the simple random sampling method. The cytotoxic effect of samples was determined on gingival fibroblast cells by using the MTT test, and total oxidant status (TOS) and total antioxidant capacity (TAC) kits in 24 and 72 hours. The data were statistically analyzed using one-way ANOVA and Tukey tests. Results: A significant difference was found between the material-applied groups and the control group at the TAC 24 and 72 hours and between the groups containing GO and the control group at the MTT 72 hours and TAC and TOS 24 and 72 hours ( p < .05). Conclusion: The addition of GO to MTA increased the dose and time-based toxicity and oxidant amount, and decreased antioxidant capacity.

(1) Background: Doxorubicin (DOX) is extensively used for cancer treatments; however, its clinical application is limited because of its cardiotoxic adverse effects. A combination of DOX and agents with cardioprotective properties is an effective strategy to ameliorate DOX-related cardiotoxicity. Polyphenolic compounds are ideal for the investigation of novel cardioprotective agents. Chlorogenic acid (CGA), an essential dietary polyphenol found in plants, has been previously reported to exert antioxidant, cardioprotective, and antiapoptotic properties. The current research evaluated CGA’s in vivo cardioprotective properties in DOX-induced cardiotoxicity and the probable mechanisms underlying this protection. (2) Methods: CGA’s cardioprotective properties were investigated in rats that were treated with CGA (100 mg/kg, p.o.) for fourteen days. The experimental model of cardiotoxicity was induced with a single intraperitoneal (15 mg/kg i.p.) injection of DOX on the 10th day. (3) Results: Treatment with CGA significantly improved the DOX-caused altered cardiac damage markers (LDH, CK-MB, and cTn-T), and a marked improvement in cardiac histopathological features accompanied this. DOX downregulated the expression of Nrf2/HO-1 signaling pathways, and the CGA reversed this effect. Consistently, caspase-3, an apoptotic-related marker, and dityrosine expression were suppressed, while Nrf2 and HO-1 expressions were elevated in the cardiac tissues of DOX-treated rats after treatment with the CGA. Furthermore, the recovery was confirmed by the downregulation of 8-OHdG and dityrosine (DT) expressions in immunohistochemical findings. (4) Conclusions: CGA demonstrated a considerable cardioprotective effect against DOX-induced cardiotoxicity. One of the possible mechanisms for these protective properties was the upregulation of the Nrf2/HO-1-dependent pathway and the downregulation of DT, which may ameliorate oxidative stress and cardiomyocyte apoptosis. These findings suggest that CGA may be cardioprotective, particularly in patients receiving DOX-based chemotherapy.

In this study, histopathological and immunohistochemical evaluations were made on the damage to the gastric tissue in the gastric peptic ulcer model induced by indomethacin, and it was investigated whether the plantsHypericum perforatumandRosa spinosissimahave a therapeutic effect. In order to create an ulcer model, 25mg/kg indomethacin was administered orally to the rats in the other groups, except the sham control group, in 2 doses, 24 hours apart. In the treatment groups, the first dose of indomethacin was given an hour after the second dose, and the second dose of plant oils was given orally 24 hours later. Then, 1 hour later, the rats were sacrificed. In the histopathological evaluation, sections belonging to the indomethacin control group showed intense degeneration of both epithelial and mucosal glands in the gastric mucosa. Edema and bleeding were also present in the lamina propria and submucosa layers. These observed damages were significantly reduced in the RS+HP-1 and RS+HP-2 groups. As a result of the immunohistochemical evaluations, it was observed that the group with the highest Bax immunoreactivity was the indomethacin control group, and the groups with the lowest were RS+HP-1 and RS+HP-2. It was determined that the group with the lowest Bcl-2 immunoreactivity was the indomethacin control group, and the groups with the highest were RS+HP-1 and RS+HP-2. The results showed thatHypericum perforatumandRosa spinosissimaplants have therapeutic and anti-apoptotic effects on gastric injury.

Cortical neuron and SH-SY5Y cells are widely used in glutamate excitotoxicity studies, but it is unclear which one better reflects this model. Generally, glutamate induces toxicity conditions by leading to L and L/N-Ca2+channels activation and cell death via lethal Ca2+ influx. To evaluate this hypothesis, the effects of L and L/N-Ca2+ channel blockers, lacidipine, and amlodipine under excitotoxic conditions were evaluated. At the same time, in this study, we aimed to determine that these two cell lines better reflect this model. To induce excitotoxicity, cortical neuron and SH-SY5Y cells were incubated with glutamate 10-5 mM. After 30 min incubation with glutamate, different concentration (1, 2 and 4 µg lacidipine and 20, 50 and 100 µM amlodipine) were applied these cells. Possible neuroprotective roles of lacidipine and amlodipine were investigated through cell viability, oxidative stress, and apoptotic alterations. Our results showed that SH-SY5Y cells are the more ideal cell line for oxidative stress-mediated glutamate toxicity. In addition, 4 µg lacidipine and 100 µM amlodipine had significant neuroprotective roles in these cells, but the most protective effect was also determined in SH-SY5Y cells at 100 µM amlodipine. The highest viability rate on cell lines was found at 88,8 % in SH-SY5Y cells treated with 100 μM amlodipine. Results from the TAC, TOS, LDH assays, and flow cytometry analysis were correlated to our MTT results. Taken together, our results indicate that SH-SY5Y cells are more effective at reflecting glutamate-induced excitotoxicity and 100μM amlodipine has a more protective effect in treating this toxicity.

Daidzein is a water-insoluble phytoestrogenic isoflavone of the Leguminosae family, mainly found in soy and soy-derived foods. Daidzein has a broad spectrum of physiological and pharmacological functions. It has anti-cancer, anti-inflammatory, antioxidant, enzyme inhibitor properties and causes a decrease in low-density lipoprotein levels. Glioblastoma Multiforme (GBM) is the most common, rapidly progressing, and fatal primary brain tumor. It accounts for more than 51% of all gliomas. For this reason, much scientific research is being done to treat brain tumors. This study aims to prepare daidzein-loaded PLGA and PLGA-Gelucire® 44/14 nanoparticles for the treatment of GBM and to evaluate their characteristics, neurotoxicity, and cytotoxicity in vitro. The PLGA and PLGA-Gelucire® 44/14 nanoparticles were prepared by using the non-modified and modified emulsion-solvent diffusion method. The surface morphology, particle size, zeta potential (ZP), encapsulation efficiency (EE) and in vitro release characteristics of nanoparticles were investigated. Furthermore, FT-IR, DSC and SEM were used to characterize these systems. The neurotoxicity on neurons and cytotoxicity against the U-87 MG cell line of the chosen optimum nanoparticle formulations were evaluated. The mean particle size and ZP values of all prepared nanoparticles were a range of 198.52±7.04-672.78±70.95 nm (p≥0.05) and -14.70±0.36--0.50±0.34 mV (p≥0.05), respectively. SEM images of nanoparticles revealed their approximately spherical shape. The EE % values of nanoparticles were a range of % 35.79±3.43-84.85±2.20 (p≥0.05). The cumulative daidzein release from daidzein-loaded nanoparticle formulations was up to about 100 % at 19-37 days of release. It was found that the prepared nanoparticulate systems reduced the neurotoxic effects of daidzein and showed similar cytotoxic effects to those of daidzein (p0.05). The prepared nanoparticles are useful and promising systems for sustained release of daidzein, reduction of the neurotoxic effects of daidzein at high doses (200 μM and 300 μM) and maintaining of its cytotoxic activity against cancer cells.

In our study, it was aimed to create a new drug delivery system by loading the chemotherapeutic drugs into exosome vesicles. This system act as a Trojan horse to targeting GBM cancer. Exosomes were isolated from the T-98G cell line and characterized. Exosomes were encapsulated with Temozolomide. Then, the effectiveness of this new delivery system was evaluated by using MTT, LDH, TAC, TOS, GR. MTT results show a dose-dependent decrease in the TMZ and Exolimer+TMZ groups. But this rate decreased significantly in the Exolimer+TMZ groups. The lowest viability was observed at the Exolimer+TMZ 800 ng/ml concentration. Our results in LDH, GR, TAS and TOS analyzes shows correlation with MTT. Based on this study, we think that targeting the exosome to cancer by combining with special molecules and nanotechnology will bring a new perspective to cancer treatment.

Aloe Vera, one of the recently developed medicinal plants, is of interest for its multiple effects and has also been shown to have antibacterial, antimicrobial, antioxidant, anticancer properties. Although it is known that the aloe vera family has protective effects on neurons, the neuroprotective effect of the aloe barbadensis miller plant has not yet been fully explained. Glufosinate is structurally similar to glutamate and is an herbicide that blocks glutamine synthetize. Glutamate has been shown to induce cyclooxygenase-2 (COX-2), which causes toxicity. It is also known to induce oxidative stress in neurons. In our study, we exposed neuron culture to Aloe Vera Barbadensis Miller plant (25, 50, 100, 200, 400, 800, and 1600 µgr/ml doses) for 24 hours against glufosinate (200 mM) and glutamate (10-5 mM) toxicity. After 24 hours, MTT, TAC, and TOS analyzes were performed and the results were revealed.In our study, it was seen that the aqueous extract of aloe barbadensis miller plant, glufosinate, and glutamate, could preserve the vitality of neurons (89% protection in AVB 400 µgr/ml group). At the same time, it was seen that while increasing the antioxidant level in neurons, it decreased the oxidant level. The group that increases the antioxidant value best is AVB 400 µgr/ml (the group that increases it 1.4 times). According to the results we obtained, it was revealed that aloe vera and its components may have an effect on neuroprotection., Son zamanlarda geliştirilen şifalı bitkilerden biri olan Aloe Vera, çoklu etkileri ile ilgi görmekte ve ayrıca antibakteriyel, antimikrobiyal, antioksidan, antikanser özelliklere sahip olduğu da bilinmektedir. Aloe vera ailesinin nöronlar üzerinde koruyucu etkileri olduğu bilinmesine rağmen aloe barbadensis miller bitkisinin nöroprotektif etkisi henüz tam olarak açıklanamamıştır. Glufosinat, yapısal olarak glutamata benzer ve glutamin sentetazı bloke eden bir herbisittir. Glutamatın toksisiteye neden olan siklooksijenaz-2'yi (COX-2) indüklediği gösterilmiştir. Ayrıca nöronlarda oksidatif strese neden olduğu bilinmektedir. Çalışmamızda nöron kültürünü glufosinat (200 mM) ve glutamat (10-5 mM) toksisitesine karşı koruması amacıyla Aloe Vera Barbadensis Miller bitkisine (25, 50, 100, 200, 400, 800 ve 1600 µgr/ml) 24 saat süreyle maruz bıraktık. 24 saat sonra MTT, TAC ve TOS analizleri yapıldı ve sonuçlar açıklandı.Çalışmamızda aloe barbadensis miller bitkisinin sulu ekstresinin, glufosinat ve glutamat toksisitesine karşı nöron canlılığını koruyabildiği görüldü (AVB 400 µgr/ml grubunda 89% koruma). Aynı zamanda nöronlarda antioksidan seviyesini arttırırken oksidan seviyesini azalttığı görüldü. Antioksidan değerini en iyi artıran grup AVB 400 µgr/ml'dir (1.4 kat artıran grup). Elde ettiğimiz sonuçlara göre aloe vera ve bileşenlerinin nöroproteksiyon üzerinde etkisi olabileceği ortaya çıktı.

(1) Background: Various epidemiological studies suggest that oxidative stress and disrupted neuronal function are mechanistically linked to neurodegenerative diseases (NDs), including Parkinson’s disease (PD) and Alzheimer’s disease (AD). DNA damage, oxidative stress, lipid peroxidation, and eventually, cell death such as NDs can be induced by nitrosamine-related compounds, leading to neurodegeneration. A limited number of studies have reported that exposure to diethylnitrosamine (DEN), which is commonly found in processed/preserved foods, causes biochemical abnormalities in the brain. Artichoke leaves have been used in traditional medicine as a beneficial source of bioactive components such as hydroxycinnamic acids, cynarine, chlorogenic acid, and flavonoids (luteolin and apigenin). The aim of this study is to investigate the favorable effects of exogenous artichoke (Cynara scolymus) methanolic leaf extract supplementation in ameliorating DEN-induced deleterious effects in BALB/c mouse brains. (2) Methods: This study was designed to evaluate DEN (toxicity induction by 100 mg/kg) and artichoke (protective effects of 0.8 and 1.6 g/kg treatment) for 14 days. All groups underwent a locomotor activity test to evaluate motor activity. In brain tissue, oxidative stress indicators (TAC, TOS, and MDA), Klotho and PPARγ levels, and apoptotic markers (Bax, Bcl-2, and caspase-3) were measured. Brain slices were also examined histopathologically. (3) Results: Artichoke effectively ameliorated DEN-induced toxicity with increasing artichoke dose. Impaired motor function and elevated oxidative stress markers (decreasing MDA and TOS levels and increasing TAC level) induced by DEN intoxication were markedly restored by high-dose artichoke treatment. Artichoke significantly improved the levels of Klotho and PPARγ, which are neuroprotective factors, in mouse brain tissue exposed to DEN. In addition, caspase-3 and Bax levels were reduced, whereas the Bcl-2 level was elevated with artichoke treatment. Furthermore, recovery was confirmed by histopathological analysis. (4) Conclusions: Artichoke exerted neuroprotective effects against DEN-induced brain toxicity by mitigating oxidant parameters and exerting antioxidant and antiapoptotic effects. Further research is needed to fully identify the favorable impact of artichoke supplementation on all aspects of DEN brain intoxication.

Excessive release of the excitatory neurotransmitter glutamate is thought to be a major contributor to the pathophysiology of numerous neurodegenerative including epilepsy and Alzheimer's disease. Therefore, it is important to investigate for compounds that protecting neuronal cells against glutamate-induced cytotoxicity. Pycnogenol®, a standardized French maritime pine bark extract, has strong antioxidant activity which primarily comprises phenolic compounds and flavonoids. Therefore, in the present study, inducing glutamate toxicity in primary cultured cortical neurons, we studied the neuroprotective effects of bioflavonoid compound Pycnogenol an extract of Pinus maritime bark. The cortical neuron cells were exposed to 10-5 mM glutamate for 30 min to induce excitotoxicity. Then, different concentrations (10-1 - 10-5) of PYC were added to the cells for 24 hours. The cell viability was determined using MTT assay. To investigate oxidative damage, the total antioxidant status (TAS)- total antioxidant status (TOS) analysis were used. According to MTT analysis results, it was found that 10-1 and 10-2 pycnogenol groups significantly attenuated the glutamate excitotoxicity induced cell damage. Furthermore, TAS-TOS analysis showed a correlation with MTT result. According to the results of this study, pycnogenol has the potential to be used as a therapeutic agent against glutamate excitotoxicity., Eksitatör bir nörotransmitter olan glutamatın aşırı salınımı epilepsi ve Alzheimer gibi birçok nörodejeneratif hastalığın patogenezinde yer almaktadır. Bu nedenle nöronal hücreleri glutamata bağlı toksisiteye karşı koruyan bileşiklerin araştırılması oldukça önemlidir. Pinus maritima'dan elde edilen piknogenol® içerdiği fenolik bileşikler ve flavonoidlerden dolayı güçlü antioksidan özelliğe sahiptir. Bu çalışmada Pinus maritime'den elde edilen bioflavonoid yapısında olan pignogenolün nöroprotektif etkilerini glutamat toksisitesi oluşturulan kortikal nöron kültüründe araştırmayı amaçladık. Kortikal nöron hücreleri 30 dakika süre ile 10-5 mM glutamata maruz bırakılarak glutamat eksitotoksisitesi indüklendi. Sonrasında faklı konsantrasyonlarda (10-1 - 10-5) PYC ile 24 saat boyunca inkübe edilmiştir. Hücre canlılık testi MTT yöntemi ile belirlendi. Oksidatif hasarı göstermek için total antioksidan seviyesi (TAS)- - total oksidan seviyesi (TOS) analizleri kullanılmıştır. MTT sonuçlarına göre 10-1 ve 10-2 piknogenol konsantrasyonlarının glutamat eksitotoksisitesine bağlı hücre ölümünü azalttığı görüldü. Aynı zamanda TAS-TOS sonuçları MTT sonuçları ile korelasyon saptandı. Bu çalışma sonuçlarına göre piknogenolün glutamat eksitotoksisitesine karşı teropatik ajan olarak kullanılabileceği düşünülmüştür.

Epilepsy is a neurological disorder resulting from abnormal neuronal firing in the brain. Glutamate transporters and the glutamate-glutamine cycle play crucial roles in the development of seizures. In the present study, the correlation of epilepsy with glutamate transporters and enzymes was investigated. Herein, male Wistar rats were randomly allocated into four groups (six animals/group); 35 mg/kg pentylenetetrazole (PTZ) was used to induce a kindling model of epilepsy. Once the kindling model was established, animals were treated for 15 days with either valproic acid (VPA, 350 mg/kg) or ceftriaxone (CEF, 200 mg/kg) in addition to the control group receiving saline. After treatment, electrocorticography (ECoG) was performed to record the electrical activity of the cerebral cortex. The glutamate reuptake time (T80 ) was also determined in situ using an in vivo voltammetry. The expression levels of glutamate transporters and enzymes in the M1 and CA3 areas of the brain were determined using a real-time polymerase chain reaction (RT-PCR). ECoG measurements showed that the mean spike number of the PTZ + VPA and PTZ + CEF groups was significantly lower (p

Glutamate, one of the most important excitatory neurotransmitters, acts as a signal transducer in peripheral tissues and endocrine cells. Excessive glutamate secretion has been shown to cause excitotoxicity and neurodegenerative disease. Cerebrolysin is a mixture of enzymatically treated peptides derived from pig brain including neurotrophic factors, like brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and ciliary neurotrophic factor (CNTF). The present study investigated the protective effects of cerebrolysin on glutamate transporters (EAAT 1, EAAT 2) and cytokines (IL-1β and IL-10) activity in glutamate-mediated neurotoxicity. Primary cortex neuron culture was exposed to glutamate and successively treated with various cerebrolysin concentrations for 24 and 48 h. Our data showed that cerebrolysin primarily protects neurons by decreasing glutamate concentration in the synaptic cleft. In addition, Cerebrolysin can decrease oxidative stress and neuron cell damage by increasing antioxidant activity and decreasing inflammation cytokine levels.

Hypertension, as a primary risk factor for many fatal disorders, is prevalent in the elderly. There is wide literature on hypertension dealing with its biological and/or biochemical aspects; however, limited research is available on the multifactorial nature of hypertension from a mechanobiological standpoint. This study intended to study in parallel histopathological alterations and deviated protein expressions with the mechanical behavior of the hypertensive tissues. The Goldblatt (2K1C) method was chosen for induction of renovascular hypertension in rabbits. The microstructural and immunohistological characteristics of the aortic, pancreatic, and brain vasculature were investigated. The mechanical properties of the aortic tissue were also evaluated using biaxial tensile tests. Our findings indicated severe hypertrophy of the hypertensive vessels and declined content of intact smooth muscle cells. Most of the collagen I content of the wall was compromised and less functional type III collagen was highly expressed. Reversed collagen I to collagen III ratio was the main contributor to the hypertrophic and less stiff hypertensive vessel walls. The multifactorial nature of hypertension is illustrated, and smooth muscle cell detachment is identified as the sign of described degenerative cascades all along the arterial tree.

Background: Pain is one of the common experiences which is unpleasant feeling that originates from any part of the body, is associated with real or possible tissue damage and linked to human past experiences. Momordica Charantia (MC) or bitter melon mainly is used all around the world for the treatment of diabetes, cancer and inflammation- associated conditions due to the existence of many bioactive ingredients which have vigorous biologic effect. The aim of our study is to investigate how low and high doses of MC plant affect foot inflammation and animal's behavior. Materials and Methods: Sixteen male rats randomly divided into 4 experimental groups. Formaldehyde was (hind-paw formalin injection) administered for inducing pain model. After 24 hours MC (50 mg/kg, 200 mg/kg) was administered every day for five days. During the experiment, the pain thresholds, motor cortex measurements and inflamed foot volume, Locomotor Activity Test and Water Overflow Method in sequence. Results: According to our result, when we consider the foot volume, pain threshold and motor cortex data of our control group, there is no significant difference between the beginning and the last day, while On the 7th day, the pain threshold continues to decrease as the foot volume of our animals in our positive control group does not decrease. 200 mg concentration of MC has provided a great treatment by reducing the increasing foot volume at the same time pain threshold and motor activity was in highest level at 4th day. Conclusion: Our experiment shows that MC (200 mg/ml MC ) has high analgesic activity provides significant pain reduction and improvement in symptoms

Aim: The aim of our study is to the evaluation of melatonin (MLT) and Momordica charantia (MC) combination on PC-3 and HT-29 cancer lines and to address the question of where or not MLT increases MC antitumor effect in the PC-3 and HT-29 cancer lines. Material and Method: The PC-3 and HT-29 cell lines were grown in a manufacturer-specified culture medium. Cisplatin, MLT, increasing concentrations of MC, 40 μg/ml MLT + increasing concentrations MC were applied to PC-3 and HT-29 cell lines for 72 hours. 3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium Bromide (MTT) cell viability, Total Antioxidant Capacity (TAC), Total Oxidant Status (TOS), Cellular Migration (Wound Healing test), and Lactate Dehydrogenase (LDH) tests were done 72 hours after drug administration.Results: The combination of MLT 40 μg/ml + MC 100 µg/ml reduced cell viability in both PC-3 and HT-29 cells. Besides, TAC and TOS levels showed a correlation with LDH and MTT assays and were found to be statistically significant (P, Amaç: Çalışmamızın amacı, PC-3 ve HT-29 kanser hatlarında melatonin (MLT) ve Momordica charantia (MC) kombinasyonunun değerlendirilmesi ve MLT'nin PC-3 ve HT-29 kanser hatlarında MC antitümör etkisini nerede artırdığı sorusunu ele almaktır. Gereç ve yöntem: PC-3 ve HT-29 hücre çizgileri, üreticinin belirlediği bir kültür ortamında büyütüldü. Sisplatin, MLT, artan MC konsantrasyonları, MLT 40 μg / ml + artan konsantrasyonlar MC, PC-3 ve HT-29 hücre hatlarına 72 saat süreyle uygulandı. 3- (4,5-Dimetiltiyazol-2-Yl) -2,5-Difeniltetrazolyum Bromür (MTT) hücre canlılığı, Toplam Antioksidan Kapasitesi (TAC), Toplam Oksidan Durumu (TOS), Hücresel Göç (Yara İyileştirme testi) ve Laktat Dehidrojenaz (LDH) testleri, ilaç uygulamasından 72 saat sonra yapıldı.Bulgular: MLT 40 ug / ml + MC 100 ug / ml kombinasyonu, hem PC-3 hem de HT-29 hücrelerinde hücre canlılığını azalttı. Ayrıca TAC ve TOS seviyeleri LDH ve MTT testleri ile korelasyon gösterdi ve istatistiksel olarak anlamlı bulundu (P

Objectives There are several types of pesticides to control pests and several new types coming into use that could be less toxic compared to the old ones. Pesticide-induced oxidative stress, which is one of the main mechanisms of toxicity, is the research area focused most on over the last decade. There are several different studies in the literature on whether pesticide exposure induces oxidative stress parameter-mediated toxicity. Pesticide-induced oxidative stress level depends on the biochemical features of mammalian systems. Imidacloprid is a neonicotinoid pesticide in wide use that is considered safe; however, it has been reported in different studies that it may cause changes in oxidative stress parameters. Materials and methods We investigated the dose- and time-dependent effects of imidacloprid on acetylcholinesterase (AChE), lactate dehydrogenase (LDH), and glutathione (GSH) levels in the L-929 fibroblast cell line. The effects of 1-500 μg imidacloprid dose range on AChE, GSH, and LDH were investigated. Results LDH levels were significantly increased dose dependently in the 250 and 500 ng imidacloprid groups compared to the control group. GSH levels nonsignificantly decreased dose dependently and GSH levels were lower in the 500 ng imidacloprid group compared to the control group. There were no significant differences between the groups in AChE levels. Conclusion These results indicated that high doses of imidacloprid may induce oxidative stress in fibroblast cells.

Ferula orientalis L. is a wild edible plant which belongs to the Apiaceae family. Ferula species have promising bioactive compounds and they can be used in developing drugs. This study was designed...

Living organisms have an innate ability to regulate the synthesis of inorganic materials, such as bones and teeth in humans. Cadmium sulfide (CdS) can be utilized as a quantum dot that functions as a unique light-emitting semiconductor nanocrystal. The increased use in CdS has led to an increased inhalation and ingestion rate of CdS by humans which requires a broader appreciation for the acute and chronic toxicity of CdS. We investigated the toxic effects of CdS on cerebellar cell cultures and rat brain. We employed a ‘green synthesis’ biosynthesis process to obtain biocompatible material that can be used in living organisms, such as Viridibacillus arenosi K64. Nanocrystal formation was initiated by adding CdCl2 (1 mM) to the cell cultures. Our in vitro results established that increased concentrations of CdS (0.1 μg/mL) lead to decreased cell viability as assessed using 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide (MTT), total antioxidant capacity (TAC), and total oxidant status (TOS). The in vivo studies showed that exposure to CdS (1 mg/kg) glial fibrillary acidic protein (GFAP) and 8-hydroxy-2' -deoxyguanosine (8-OHdG) were increased. Collectively, we describe a model system that addresses the process from the synthesis to the neurotoxicity assessment for CdS both in vitro and in vivo. These data will be beneficial in establishing a more comprehensive pathway for the understanding of quantum dot-induced neurotoxicity.

Aim: Glioblastoma is the best widespread and aggressive major brain tumor. Despite efforts to improve treatment and advances, the average survival of patients remains limited to 14 months after diagnosis. Recent research has shown that Moringa is widely used in traditional medicine. The purpose of our study is to show the neuroprotective effect of Moringa, which we will use in the treatment, on the neurotoxicity induced by the transwell co-culture method. Method: First of all, RN-33B, U373, and HUVEC cell lines were grown in prepared media. Then, HUVEC and U373 cell lines reaching 85% confluence were removed with trypsin EDTA. U373 was seeded on the top base of the transwell membrane and the lower base of the HUVEC. Transwell membranes were placed in the wells with neuron culture and incubated for 1 day. Afterward, 25-50-100-200 and 400 µg/ml doses of Moringa extract were added to the wells and incubated for 1 day. After 1 day, MTT, TAC, TOS, GSH, and LDH tests were performed and the results were compared with the control groups and statistically evaluated. Results: Moringa showed a dose-dependent increase in viability and cell viability was found to be 90% at the highest dose. In addition, antioxidant parameters (TAC, GSH) correlated with MTT analysis. In TOS and LDH levels, it was observed that the oxidant level decreased depending on the dose. Conclusion: It demonstrated the neuroprotective effect of Moringa by preventing neurotoxicity following short-term exposure of neurons to U373 cancer cells.