ABSTRACT
BACKGROUND: This study investigated the effect of n-perfluorooctane (PFC) on hypoxia/reoxygenation (H/R) injury in human umbilical vein endothelial cells (HUVECs). METHODS: In this study, the H/R models were prepared by chemical methods (using dithionite solution). The experimental groups included the control group, the PFC group with a culture volume ratio of 10%, the H/R model group, and treatment groups with various doses of PFC + H/R (i.e., 5%, 10%, or 20% PFC by volume). The cell counting kit-8 (CCK-8) method was used to assay cell viability. Colorimetric assays were used to estimate the leakage of lactate dehydrogenase (LDH) in the medium, the levels of intracellular malondialdehyde (MDA) and nitric oxide (NO), and the activity of superoxide dismutase (SOD). Western blot was used to analyze the expression of the apoptosis-related protein cystine aspartate proteolytic enzyme 3 (caspase-3). RESULTS: Compared with the control group, every detected index of 10% PFC group had no statistical significance (p > 0.05). Compared with the model group, 10% and 20% PFC treatment groups could increase cell viability A, decrease the content of NO and reduce caspase-3 expression (p < 0.05); Every PFC treatment group could significantly reduce the release of LDH and the contents of MDA, and also increase the activities of SOD (p < 0.01). CONCLUSIONS: PFC has a significant protective effect on HUVEC H/R injury, which may be related to the inhibition of oxidative stress and inflammation and further enhance cell antioxidant and anti-apoptotic characteristics.
ABSTRACT
OBJECTIVE: The aims of this study were to search for the role of glucose in the regulation blood pressure of rats and to investigate the effects of glucose on the production of vascular aldosterone and corticosterone in rats. METHODS: Male Wistar rats received glucose 15.0 g x kg(-1) x d(-1) (glucose-treated group 1) or 25.0 g x kg(-1) x d(-1) (glucose-treated group 2) or 35.0 g x kg(-1) x d(-1) (glucose-treated group 3), orally, for 3 months, and blood pressure was monitored by a pressure transducer. Mesenteric artery perfusion ex vivo was performed and pressor responses to norepinephrine were determined in Wistar rats. The perfusate from the mesenteric arteries was collected and applied to a Sep-Pak C 18 cartridge column for reverse phase high-performance liquid chromatography and levels of both aldosterone and corticosterone were determined by radioimmunoassay. Reverse transcriptase polymerase chain reaction was used to measure the expression of 11beta-HSD2 and CYP11B2 mRNA in mesenteric arteries. RESULTS: Blood pressure increased in Wistar rats treated with glucose compared to control rats. The pressor responses to norepinephrine in mesenteric arteries treated with glucose were significantly increased. Levels of aldosterone were decreased but those of corticosterone increased in the perfusate from arteries treated with glucose. Reverse transcriptase polymerase chain reaction showed that glucose inhibited the expression of 11beta-HSD2 and CYP11B2 mRNA in mesenteric arteries. CONCLUSION: These results reveal that glucose able to induce hypertension and provide evidence that glucose inhibits the transcriptions of both 11beta-HSD2 and CYP 11B2 in vasculature, leading to lower aldosterone and higher corticosterone production in vessels, and increased vasoconstrictor responses to norepinephrine.
