Diabetic neuropathy is one of the most frequent complications of diabetes. Despite some studies, the exact mechanism of glucose neurotoxicity has not been fully elucidated. Increased reactive oxygen species (ROS) has proposed as a possible mechanism. Crocus sativus L. (saffron) has been known as a source of antioxidants. Therefore, neuroprotective effect of saffron extract, its active component crocin and gamma-glutamylcysteinylglycine (GSH) was studied in glucose-induced neurotoxicity, using PC12 cells as a suitable in vitro model of diabetic neuropathy. Cell viability was quantitated by MTT assay. ROS was measured using DCF-DA by flow cytometry analysis. The result showed that glucose (13.5 and 27 mg/ml) reduced the cell viability of PC12 cells after 4 days. Saffron extract (5 and 25 mg/ml), crocin (10 and 50 muM) and GSH (10 muM) could decrease this toxicity. Glucose toxicity was consistent with increased ROS production which reduced by saffron, crocin and GSH pretreatment. These results suggest saffron and its carotenoid crocin could be potentially useful in diabetic neuropathy treatment.
Chemical investigation on the CH 2 Cl 2 fraction of the Scutellaria litwinowii Bornm. & Sint., Lamiaceace, root extract for the fi rst time resulted in the isolation of wogonin, and neobaicalein. These compounds were evaluated for their cytotoxicity towards HeLa cell lines and lymphocytes. Meanwhile, the role of apoptosis was explored in this toxicity. The cells were cultured in RPMI medium and incubated with different concentrations of isolated fl avonoids. Cell viability was quantifi ed by MTS assay. Apoptotic cells were determined using propidium iodide staining of DNA fragmentation by fl ow cytometry (sub-G1peak). Wogonin, and neobaicalein inhibited the growth of malignant cells in a dose-dependent manner. The IC50 values of 46.62 and 79.34 µM were, respectively, found for neobaicalein and wogonin against HeLa cells after 48 h of treatment. Neobaicalein induced a sub-G1 peak in the fl ow cytometry histogram of treated cells compared to control cells indicating that apoptotic cell death is involved in neobaicalein toxicity. Neobaicalein exerts cytotoxic and pro-apoptotic effects in HeLa cell lines and could be considered as a potential chemotherapeutic agent in cancer treatment.
1 Bovine aortic endothelial cells were cultured in vitro, and shown to release both prostacyclin (PGI2; Kact = 24.1 nM) and endothelium-derived relaxing factor (EDRF, NO; K., = 0.7 nM) in a concentrationdependent manner when exposed to bradykinin.
Alzheimer's disease (AD) is one of the most common causes of dementia in the elderly. Recently, a great attention has been paid to the possible role of vascular changes in the pathogenesis of AD. Reduced microvascular density and degeneration of the endothelium are of structural cerebrovascular changes in AD. Acetylcholinesterase (AChE) inhibitors are widely used for the improvement of AD symptoms. Until now, however, the effects of AChE inhibitors on vascular changes including angiogenesis and endothelial cell apoptosis are not fully understood. In the present work, the effects of three AChE inhibitors (donepezil, rivastigmine, and galantamine) were tested on H2O2-induced apoptosis in human umbilical vein endothelial cells (HUVECs) and on angiogenesis in chicken chorioallantoic membrane model. Incubation of HUVEC with H2O2 led to a significant decrease in cell viability and an increase in the percentage of apoptotic cells. The tested drugs, at concentrations of 1–100 μM, significantly inhibited the H2O2-induced toxicity. Also, all donepezil, rivastigmine and galantamine significantly increased the number of vessels in the chorioallantoic membrane when injected into fertilized eggs. In conclusion, AChE inhibitors possess angiogenesis-accelerating properties and have antiapoptotic effects on endothelial cells. These effects of AChE inhibitors may be involved in their beneficial effects on AD.
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