The aim of this study was to investigate the effects of red dragon fruit (Hylocereus polyrhizus) extract (DFE) on the stomach in ulcer model induced by indomethacin in rats. Effects of DFE were evaluated in indomethacin-induced gastric damage model on Sprague-Dawley rats. Experimental model: all rats were fasted for 24 h. At the end of this period, DFE was administered to the ulcer-induced groups. One hour after this application, a dose of 25 mg/kg of indomethacin was applied by oral gavage to all groups except the HEALTHY and DFE1000 groups. Six hours after indomethacin administration, the rats were euthanized with high-dose anesthesia and the experiment was terminated. Macroscopic and microscopic analyses for investigating ulcerative area, molecular and biochemical analyses for oxidative damages investigation and molecular analyses for the effect mechanism of indomethacin and DFE were conducted on stomach tissues in the study. While oxidative stress-associated markers such as MDA, BAX, and Caspase 3 increased dramatically in the indomethacin group, GSH antioxidant levels decreased. It was observed that these parameters were significantly improved in DFE 500 mg/kg and DFE 1000 mg/kg groups compared to ulcer group, and the results of especially DFE 1000 mg/kg group were similar to famotidine group.We observed that our histopathological findings also supported all our other findings.Dragon fruit extract was protected against indomethacin-induced ulcer damage by decreased MDA levels, increased GSH levels, and inhibition of Caspase 3, BAX, and Cox-2, and activation of Cox-1.

Background:Diabetes mellitus (DM) is a metabolic disorder that occurs as a result of absolute or relative insufficiency of insulin release and/or insulin effect due to impairment of carbohydrate, fat and protein metabolism, and it is characterized by hyperglycemia and leads to various complications.Objective:In this study, it was aimed to investigate the effects of hesperidin (HP) and quercetin, which are natural flavonoids, on serum malondialdehyde (MDA), glutathione (GSH), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) levels in rats with streptozotocin (STZ)-induced diabetes.Materials and Methods:The experimental animals were divided into four groups, each group comprising ten rats designated as follows: Group 1 served as control rats (C); Group 2 served as diabetic rats (DM); Group 3 served as diabetic rats administered HP (DM + HP) (100 mg/kg b. w.); and Group 4 served as diabetic rats administered quercetin (DM + Q) (100 mg/kg b. w.).Results:Serum MDA and GSH levels were significantly higher in STZ-induced DM group than control group (P < 0.05). In DM + HP and DM + Q groups, MDA levels were significantly decreased compared to DM groups (P < 0.05), but there was no significant difference GSH levels between DM, DM + HP, and DM + Q groups (P > 0.05). TNF-α levels in STZ-induced DM group were significantly decreased compared to control group (P < 0.05), and groups of DM + HP and DM + Q had higher serum TNF-α levels than STZ-induced DM group (P < 0.05). In STZ-induced DM group, serum IL-6 levels were decreased compared to control group (P < 0.05).Conclusion:As a result, in this study, we determined that HP and quercetin may play an effective role in regulating insulin metabolism metabolism in diabetes. However, considering the incompatibility of various results in the literature as well as our own results, we think that the actual role of cytokines in the pathogenesis of diabetes is one of the issues that need to be clarified in further studies.SUMMARY Hesperidin (HP) and quercetin reduced the insulin, total cholesterol, triglyceride, low-density lipoprotein cholesterol, and malondialdehyde (MDA) serum levels and raised the glutathione (GSH) levels compared to diabetes mellitus (DM) groupSZT-induced DM increased the MDA serum levels and decreased the GSH levels compared to control groupHP and quercetin-treated rats showed higher interleukin-6 and tumor necrosis factor alpha cytokine levels than DM groupHP and quercetin may play an effective role in regulating insulin metabolism in diabetes. Abbreviations used: DM: Diabetes mellitus, MDA: Malondialdehyde, GSH: Glutathione; IL-6: Interleukin-6, TNF-α: Tumor necrosis factor alpha, HP: Hesperidin, Q; Quercetin, STZ: Streptozotocin, TC: Total cholesterol, TG: Triglyceride, HDL-C: High density lipoprotein cholesterol, LDL-C: Low density lipoprotein cholesterol, VLDL-C: Very-low-density lipoprotein cholesterol.

ÖzPurpose: In this study, our aim was to investigate the potential effects of strong antioxidant daidzein (DZ) on ovarian ischemia and reperfusion injury. Materials and Methods: A total of 42 female Sprague-Dawley rats were randomly divided into seven groups. For the experimental model, the clamps were removed after 3 hours of ischemia, and blood flow was provided again. Then, reperfusion process was terminated for 3 hours. Daidzein was orally administered to animals at doses of 35 and 70 mg/kg 30 minutes before ischemia (I) and ischemia and reperfusion (I/R) procedures. Results: Severe immunoreactivity of the IL-1β, IL-6 and Caspase-3 were detected in I and I/R groups. Moderate immunoreactivity of IL-1β, IL-6 and Caspase-3 was detected in I+DZ35 and I/R+DZ35 groups, and slightly positivity was detected in I+DZ70 and I/R+DZ70 groups. The SOD activity level increased in the groups treated with Daidzein, while MDA levels decreased. In addition, hemorrhage areas and inflammatory cell migration decreased in I/R+DZ70 and I/R+DZ35 groups, when compared to I/R group in a dose dependent manner. Conclusion: Daidzein has a strong protective role in the treatment of ovarian ischemia-reperfusion injury and can be used as a therapeutic agent.Amaç: Bu çalışmada, güçlü antioksidan daidzeinin (DZ) over iskemi ve reperfüzyon hasarı üzerindeki potansiyel etkisini araştırdık. Gereç ve Yöntem: Toplam 42 adet dişi Sprague-Dawley sıçan rastgele yedi gruba ayrıldı. Deney modeli için, 3saatlik iskeminin ardından klempler çıkarıldı ve tekrar kan akışı sağlandı. Reperfüzyon 3 saatin sonunda sonlandırıldı. Daidzein, iskemi (I) ve iskemi ve reperfüzyon (I/R) işlemlerinden 30 dakika önce hayvanlara ağızdan 35 ve 70 mg/kg dozlarında uygulandı. Bulgular: I ve I/R gruplarında IL-1β, IL 6 ve Caspase 3'ün şiddetli immünoreaktivite görüldü. I+DZ35 ve I/R+DZ35 gruplarında IL-1β, IL 6 ve Kaspaz 3'ün immünreaktivitesi orta düzeyde iken, I+DZ70 ve I/R+DZ70 gruplarında hafif pozitiftir. Daidzein ile tedavi edilen gruplarda SOD aktivite seviyesi artarken, MDA seviyeleri azaldı. Ayrıca I/R + DZ70 ve IR+DZ35 gruplarında I/R grubuna göre doza bağlı olarak kanama alanları ve inflamatuar hücre göçü azaldı. Sonuç: Daidzein, over iskemi-reperfüzyon hasarının tedavisinde güçlü bir koruyucu role sahiptir ve terapötik bir ajan olarak kullanılabilir.

Cisplatin is one of the most general chemotherapeutic agents used to treat various cancers, including colorectal and breast cancer. because cisplatin has some adverse effects including cardiotoxicity and hepatoxicity, it is usage limited. Melatonin is a natural product that responsible for regulator of circadian rhythms and has anti-cancer potential. However, its synergistic effects with melatonin and cisplatin, its efficacy in cancer cell death, its mechanisms and biological targets are not well understood. In this study, it was aimed to determine the synergistic activity of cisplatin with melatonin in colon cancer cell death through apoptotic and autophagic mechanisms. In the present study, we found that melatonin with cisplatin treatment did not affect the cytotoxicity, but cisplatin increased in 24 h incubation period. Melatonin and combined treatment of melatonin and cisplatin also increased the cytotoxicity in 48h incubation period. It was observed that cisplatin treatments used together with melatonin and melatonin inhibited the mitogen activity of colon cancer cells. In addition, combined treatment of cisplatin and melatonin and single treatment of cisplatin increased both apoptosis and autophagic cell death. The results revealed that the use of melatonin with combined cisplatin has been shown to increase the apoptosis and autophagic cell deaths via P53 gene activation.