THE EFFECT OF QUERCETIN AND QUERCETIN-3-D-XYLOSIDE ON BREAST CANCER PROLIFERATION AND MIGRATION

Background and Purpose: The aim of this study is to investigate the migration, wound healing, colony formation, and cytotoxic effects of Quercetin-3-D-xyloside (reynoutrin), a quercetin derivative, in breast cancer cells Methods: In the present study, CRL-4010, MCF7 and MDA-MB-231 cells were used to evaluate the cytotoxic, antiproliferative and migration effects of reynoutrin on breast cancer. The IC50 concentration (400 mu g/ml) of reynoutrin, quercetin and cisplatin in the cells was determined. For cytotoxicity assessments, varying concentrations of quercetin, reynoutrin and cisplatin were applied and incubated 24h and 48h. In addition, to examine effects of reynoutrin on migration, cells were seeded in 6-well plates and incubated for 24 hours. For the colony formation assay cells were seeded to 12-well plates at a concentration of 1000 cells/well and incubated overnight. Results: These results indicated that reynoutrin markedly inhibit the cell viability in breast cancer. Conclusion: We have demonstrated for the first time with the present study that reynoutrin suppressed the progression of breast cancer cell proliferation induction and may provide a potential therapeutic target for breast cancer treatment. However, these results should be further confirmed by future more comprehensive studies

Effects of Phloretin and Phlorizin on Glutamate-Induced Neuron Injury: in Vitro Study

Aim:In this study, we aimed to investigate the effects of phloretin and phlorizin which are potent antioxidants, anti inflammatory and antiapoptotic agents on the prevention of glutamate-induced neurotoxicity which is an excitatory neurotransmitter.Materials and Methods:In our study, the newly born rat cortex was used. Glutamate was applied in concentration 3x10-3 and 6x10-3 M 2 hours after application of phloretin in concentrations 10-5 M and 2x10-5 M and phlorizin in concentrations 10-5 and 2x10-5 M. mRNA isolation was performed from the cells 6 hours after glutamate administration. 24 hours later, metiltiazol difenil tetrazolium (MTT) test, total oxidant and antioxidant capacity measurements were performed.Results:In our study, phloretin and phlorizin showed the best neuroprotective effect in high dose, while glutamate reduced cell viability in increased doses. Increased total oxidant capacity due to toxicity has been significantly improved by phloretin and phlorizin. Decreased antioxidant capacity in the toxicity group showed improvement with the application of phloretin and phlorizin. When phloretin and phlorizin were applied alone, they did not affect cell viability significantly, they increased antioxidant capacity and decreased oxidant capacity. İncreased tumor necrosis factor-alpha (TNF-α) mRNA expression after glutamate administration decreased significantly with the application of phloretin and phlorizin. Increased caspase 9 and caspase 3 mRNA expression due to glutamate showed improvement with the application of phloretin and phlorizin.Conclusion:These findings suggest that phloretin and phlorizin, potent antioxidant, antiinflammatory and antiapoptotic agents, may be protective in glutamate-induced neurotoxicity and can be used as therapeutic agents for preventing glutamate-induced neurological disorders

Potential therapeutic effect of pomegranate seed oil on ovarian ischemia/reperfusion injury in rats

Objective(s): The aim of this study is to determine the therapeutic effects of pomegranate seed oil, which is a powerful antioxidant and anti-inflammatory agent, on ovarian-ischemia and reperfusion injury in rats.Materials and Methods: Fifty-six  female albino Wistar rats were divided into 7 equal groups. Group 1; Sham Operation, Group 2; Ischemia, Group 3; Ischemia + Reperfusion, Group 4; Ischemia + Pomegranate 0,32 ml / kg (IP), Group 5; Ischemia + Pomegranate 0.64 ml / kg, Group 6; Ischemia + Pomegranate 0,32 ml / kg + reperfusion, Group 7; Ischemia + Pomegranate 0,64 ml / kg + reperfusion. Three hours after ischemia and 3 hours after reperfusion, the study was terminated. Results: While NADPH oxidase activity, MDA and TNF-α levels were significantly increased, SOD activity and GSH levels were reduced in ischemia and I/R groups. Low dose pomegranate seed oil  application reduced significantly oxidative stress and NADPH oxidase activity in both ischemic and ischemic/reperfusion groups. At the same time, low-dose pomegranate seed oil extract reduced TNF-α levels and significantly increased antioxidant activity.Conclusion: PSO demonstrated an important therapeutic effect in the treatment of ovarian ischemia and reperfusion injury

Protective Effects of Berberis Vulgaris Plant Extract on Paracetamol-induced Liver Toxicity in Rats

INTRODUCTION: Berberis vulgaris extract is known to be protective against many damages due to its anti-inflamatory and antioxidant properties. Paracetamol toxicity is one of the most common toxicities. In our study, we aimed to reduce the damage caused by paracetamol toxicity with the beneficial effects of Berberis vullgaris extract. METHODS: In our study, 42 Sprague Dawley 8-week-old rats were used. 7 groups were formed with 6 female animals in each group. At the 24th hour of the study, all groups underwent laparotomy under anesthesia and liver dissection was performed. Hematoxylin and Eosin (H&E) staining was used to evaluate liver histopathology, and PAS staining was used to show glycogen and basement membrane staining in liver tissue. In addition, scoring was done by showing apoptotic cells with TUNEL stain RESULTS: Hepatic degeneration and peritubular inflammation were quite evident in the groups to which we applied paracetamol. In this study, we observed that the number of positive cells increased in the group given paracetamol in TUNEL staining. As a result of the PAS staining we performed, glycogen accumulation in the hepatocytes of the group we induced with paracetamol was remarkable. DISCUSSION AND CONCLUSION: Berberis vulgaris plant extract appears to reduce Paracetamol-induced hepatic toxicity. As a result of the PAS staining, glycogen accumulation in the hepatocytes was remarkable in the group which was induced with paracetamol. Further studies are required for the use of determined molecules of Berberis vulgaris plant extract against the hepatotoxic effect of paracetamol in paracetamol toxicity

Effects of Phloretin and Phlorizin on Glutamate-Induced Neuron Injury: in Vitro Study

Amaç:Çalışmamızda eksitatör bir nörotransmitter olan glutamata bağlı nörotoksisitenin önlenmesi amacıyla güçlü antioksidan, antiinflamatuar ve antiapoptotik olan floretin ve florizinin etkilerini araştırmayı amaçladık.Materyal ve Metot:Çalışmamızda yeni doğan sıçan korteksi kullanıldı. 10-5 M ve 2x10-5 M konsantrasyonlarında floretin ile 10-5 M ve 2x10-5 M konsantrasyonlarında florizin ayrı ayrı uygulandıktan 2 saat sonra 3x10-3 M ve 6x10-3 M konsantrasyonlarında glutamat uygulaması gerçekleştirildi. Glutamat uygulamasından 6 saat sonra hücrelerden mRNA izolasyonu yapıldı. 24 saat sonra ise metiltiazol difenil tetrazolium (MTT) testi, total oksidan ve antioksidan kapasite ölçümleri gerçekleştirildi.Bulgular:Çalışmamızda glutamat artan dozlarda hücre canlılığını azaltırken floretin ve florizin uygulaması yüksek dozda en iyi nöroprotektif etkiyi ortaya koydu. Toksisiteye bağlı artan total oksidan düzey floretin ve florizin tarafından anlamlı derecede düzeltildi. Toksisite oluşturulan grupta azalan antioksidan kapasite floretin ve florizin uygulaması ile düzelme gösterdi. Floretin ve florizin tek başlarına uygulandığında hücre canlılığını anlamlı derecede etkilemezken, antioksidan kapasiteyi artırdı, oksidan düzeyi ise azalttı. Glutamat uygulaması sonrası artan tümör nekroz faktör-alfa (TNF-?) mRNA ekspresyonu, floretin ve florizin uygulaması ile anlamlı derecede azaldı. Glutamat uygulamasına bağlı artan kaspaz 9 ve kaspaz 3 mRNA ekspresyonu ise floretin ve florizin uygulaması ile anlamlı derecede düzelmegösterdi.Sonuç:Bu bulgular, güçlü antioksidan, antiinflamatuar ve antiapoptotik olan floretin ve florizinin glutamata bağlı gelişen nörotoksisitede koruyucu olabileceğini ve glutamatın neden olduğu nörolojik bozuklukların önlenmesi için terapötik ajanlar olarak kullanılabileceğini gösterir.Aim:In this study, we aimed to investigate the effects of phloretin and phlorizin which are potent antioxidants, anti inflammatory and antiapoptotic agents on the prevention of glutamate-induced neurotoxicity which is an excitatory neurotransmitter. Materials and Methods:In our study, the newly born rat cortex was used. Glutamate was applied in concentration 3x10-3 and 6x10-3 M 2 hours after application of phloretin in concentrations 10-5 M and 2x10-5 M and phlorizin in concentrations 10-5 and 2x10-5 M. mRNA isolation was performed from the cells 6 hours after glutamate administration. 24 hours later, metiltiazol difenil tetrazolium (MTT) test, total oxidant and antioxidant capacity measurements wereperformed. Results:In our study, phloretin and phlorizin showed the best neuroprotective effect in high dose, while glutamate reduced cell viability in increased doses. Increased total oxidant capacity due to toxicity has been significantly improved by phloretin and phlorizin. Decreased antioxidant capacity in the toxicity group showed improvement with the application of phloretin and phlorizin. When phloretin and phlorizin were applied alone, they did not affect cell viability significantly, they increased antioxidant capacity and decreased oxidant capacity. İncreased tumor necrosis factor-alpha (TNF-?) mRNA expression after glutamate administration decreased significantly with the application of phloretin and phlorizin. Increased caspase 9 and caspase 3 mRNA expression due to glutamate showed improvement with the application of phloretin andphlorizin. Conclusion:These ?ndings suggest that phloretin and phlorizin, potent antioxidant, antiinflammatory and antiapoptotic agents, may be protective in glutamate-induced neurotoxicity and can be used as therapeutic agents for preventing glutamate-induced neurologicaldisorders

Does the cardiovascular drug levosimendan prevent iodinated contrast medium nephrotoxicity with glycerol aggravation in rats?

Background We investigated whether levosimendan prevents contrast medium nephrotoxicity with glycerol aggravation in rats. Methods Forty-eight Wistar albino rats were assigned to eight groups (n = 6 x 8). No medication was administered to group I (controls); glycerol (intramuscular injection of 25% glycerol, 10 mL/kg) group II; intravenous iohexol 10 mL/kg to group III; glycerol and iohexol to group IV; iohexol and intraperitoneal levosimendan 0.25 mg/kg to group V; glycerol, iohexol, and levosimendan 0.25 mg/kg to group VI; iohexol and levosimendan 0.5 mg/kg to group VII; and glycerol, iohexol, and levosimendan 0.5 mg/kg to group VIII. One-day water withdrawal and glycerol injection prompted renal damage; iohexol encouraged nephrotoxicity; levosimendan was administered 30 min after glycerol injection and continued on days 2, 3, and 4. The experiment was completed on day 5. Serum blood urea nitrogen (BUN) and creatinine levels, superoxide dismutase (SOD) activity, glutathione (GSH), malondialdehyde (MDA) levels, tumour necrosis factor-alpha (TNF-alpha), nuclear factor kappa ss (NFK-ss), interleukin 6 (IL-6), and histopathological marks were assessed. One-way analysis of variance and Duncan's multiple comparison tests were used. Results Levosimendan changed serum BUN (p = 0.012) and creatinine (p = 0.018), SOD (p = 0.026), GSH (p = 0.012), and MDA (p = 0.011). Levosimendan significantly downregulated TNF-alpha (p = 0.022), NFK-ss (p = 0.008), and IL-6 (p = 0.033). Histopathological marks of hyaline and haemorrhagic cast were improved in levosimendan-injected groups. Conclusion Levosimendan showed nephroprotective properties due to its vasodilator, oxidative distress decreasing and inflammatory cytokine preventing belongings

Sıçanlarda CYP2E1 İnihibisyonu İle Parasetamol İntoksikasyonunda Punica granatum çekirdek yağı ektraktının hepatoprotektif etkisi

Punica granatum seed oil enriched by punikalagins has been shown to have a therapeutic effect against antidiabetic, anticancer, antiinflammatory and some organ toxicities. We aimed to reveal both protective and therapeutic effects of punica granatum seed oil, which has strong antioxidant and anti-inflammatory activity on paracetamol-induced hepatic toxicity via biochemically, molecularly and pathologically in our study. Our study, 64 albino wistar rats were fasted for 24 h and then divided into 8 equal groups. Group 1: Healthy, Group 2: 2 g/kg of paracetamol (2a: 24 h, 2b: 48 h) (orally), Group 3: 140 mg/kg of n-acetylcysteine (orally) + paracetamol, Group 4: 0.32 mg/mL Punica granatum (i.p) + paracetamol, Group 5: 0.64 mg/mL Punica granatum + paracetamol, Group 6: Paracetamol + 0.32 mg/mL Punica granatum, Group 7: Paracetamol + 0.64 mg/mL Punica granatum, Group 8: Paracetamol + 140 mg/kg n-acetylcysteine. The study was terminated at 24 and 48 h after paracetamol administration. Serum ALT and AST levels were significantly increased at 24th and 48th h of paracetamol administration according to toxicity. While malondialdehyde, CYP2E1 and TNF-? levels also increased in the liver, superoxide dismutase and glutathione peroxidase levels decreased significantly. Increased ALT, AST levels with malondialdehyde and TNF-? levels significantly decreased by punica granatum seed oil (low doses) application and antioxidant levels were also significantly improved. Punica granatum seed oil may be used as a potential therapeutic agent in the future by strengthening the antioxidant system and preventing inflammation, especially liver toxicity due to overdose of paracetamol in suicide- battered individuals.Punikalaginlerle zengin olan Punica granatum çekirdek yağının, antidiyabetik, antikanser, antiinflamatuar ve bazı organ toksisitelerine karşı terepötik etkileri gösterilmiştir. Çalışmamızda, parasetamol ile indüklenen hepatotoksisite üzerine güçlü antioksidan ve anti-inflamatuvar etkinliğe sahip punica granatum çekirdek yağının biyokimyasal, moleküler ve patolojik olarak koruyucu ve terapötik etkilerini ortaya koymayı amaçladık. Çalışmamızda 64 albino wistar sıçan 24 saat aç bırakıldıktan sonra 8 eşit gruba ayrıldı. Grup 1: Sağlıklı, Grup 2: Parasetamol (2a: 24 saat, 2b: 48 saat) (oral), Grup 3: 140 mg/kg n-asetilsistein (oral) + parasetamol, Grup 4: 0.32 mg/mL Punica granatum (i.p.) + parasetamol, Grup 5: 0.64 mg/mL Punica granatum + parasetamol, Grup 6: Parasetamol + 0.32 mg/mL Punica granatum, Grup 7: Parasetamol + 0.64 mg/mL Punica granatum, Grup 8: Parasetamol + 140 mg/kg n-asetilsistein. Çalışma, parasetamol uygulamasından 24 ve 48 saat sonra sonlandırıldı. Parasetamol uygulamasının 24. ve 48. saatlerinde toksisiteye göre serum ALT ve AST düzeyleri anlamlı şekilde arttı. Malondialdehit, CYP2E1 ve TNF-? düzeyleri karaciğerde de yükselirken, süperoksit dismutaz ve glutatyon peroksidaz düzeyleri anlamlı olarak azaldı. Punica granatum çekirdek yağı (düşük dozlarda) uygulaması ile artmış ALT, AST düzeyleri, malondialdehit ve TNF-? seviyeleri anlamlı derecede azalmış ve antioksidan düzeyleri önemli derecede düzelmiştir. Punica granatum çekirdek yağı, intihar girişiminde bulunan kişilerde parasetamolün aşırı dozundan dolayı oluşan karaciğer toksisitesini önleyerek ve antioksidan sistemi güçlendirerek potansiyel terapötik bir madde olarak kullanılabili