Abstract P080: New Strategy, Old Remedy: Elucidating the Effect of Hibiscus Sabdariffa in a Neuronal Model of Oxidative Stress
Introduction: Neurogenic hypertension is characterized by increased blood pressure, neuroinflammation, and neuronal oxidative stress. Thus, its pathophysiology dictates a unique therapeutic strategy. It is established that Hibiscus sabdariffa (HS) plays a beneficial role in decreasing blood pressure, yet the role of HS as an anti-oxidant defense system in neurogenic hypertension has not been investigated. Our objective was to generate an in vitro model of neuronal oxidative stress to test the hypothesis that HS creates a neuroprotective antioxidant defense system.
Methods: To create a model of oxidative stress, SY5Y, neuroblastoma cells, were treated with 32uM hydrogen peroxide. To determine the effect of methanol-extracted HSE (50 and 100ug n ≥ 8) in this model of oxidative stress, SY5Y cells were treated with vehicle-PBS, HSE (24hrs), pretreated with HSE (24hrs) and then treated with H2O2 (8hrs). Using molecular techniques markers of oxidative stress were measured and percentages were out of 100. Data was normalized to the control and analyzed by one way ANOVA (p value < .05 was considered significant).
Results: HSE significantly increases cell viability (50 or 100ug > 99%) compared to H2O2 alone (43%). HSE significantly decreases ROS generation (113%-50ug versus 89%-100ug) compared to H2O2 (120%). HSE significantly decreases lipid peroxidation (11.3%-50ug versus 10.2%-100ug) compared to H2O2 (135%). HSE significantly increases GSH content (72%-50ug versus 91%-100ug) compared to H2O2 (58%). HSE significantly increases catalase activity (31%-50ug versus 51%,-100ug) compared to H2O2 (23%). HSE significantly increases mitochondrial complex 1 activity (125%-50ug versus 229%-100ug) compared to H2O2 (26.2%). There was no significant change in superoxide dismutase activity amongst groups.
Conclusion: These observations suggest that HSE creates an antioxidant defense system that provides cytoprotection against H2O2-induced neuronal oxidative stress. Thus, HS, a known anti-hypertensive should be revisited to investigate its in vivo role in neurogenic hypertension.
Author Disclosures: A. Shalgum: None. P. Jones: None. A. Angajala: None. J. Glenn: None. J. Dobbs: None. P. Bowers: None. G. Griffin: None. W. Collier: None. M. Dhanasekaran: None. C.N. Bradford: None.
- © 2015 by American Heart Association, Inc.