Anti-Hypertensive Effects of Anthocyanins from Hibiscus sabdarifa Calyx on the Renin-Angiotensin-Aldoslestrone System in Wistar Rats.

Hibiscus sabdariffa (HS) has gained attention as an anti-hypertensive agent. In the present study, we hypothesized that anthocyanins from HS may attenuate salt-induced hypertension in rats by suppressing the components of renin-angiotensin-aldoslestrone system (RAAS). Hypertension was induced in the rats by adding 8% NaCl in their diet for six weeks. Wistar rats (n=5 each) were randomly divided into seven groups. Group 1 was the normentensive control group and was fed with normal rat chew and water ad libitum; groups 2 and 3 served as hypertensive control (negative untreated and positive treated with captopril 30mg/kg respectively); groups 4, 5, and 6 served as treatment groups and were administered with graded doses of anthocyanins( 50, 100, 200mg/kg respectively) while group 7 received both 100mg anthocyanins and 30mg captopril per day for 4 weeks. Using HPLC, anthocyanins were isolated from HS calyx following standard protocol. Anthocyanins significantly (p<0.05) reduced blood pressure and heart rate in hypertensive rats in a dose dependent manner. The blood pressure reduction by anthocyanins was associated with a reduction in serum ACE and plasma aldosterone in the hypertensive rats. The effects of anthocyanins on blood pressure and on biomarkers of RAAS were similar to those of captopril, a reference anti-hypertensive drug. The results suggest that anthocyanins exerts a significant (p<0.05) anti-hypertensive potency on rats, probably mediated by the reduction in components of the RAAS. Keywords: hypertension, anthocyanins, renin, aldosterone, rats.

Preventive putative mechanisms involved in the psychopathologies of mice passively coping with psychosocial defeat stress by quercetin.

Derangements of neuroimmune, neurotrophic and neurochemical homeostasis have important implications in psychosocial stress-induced psychopathologies. Whether quercetin, a neuroactive compound, protects against psychosocial stress-induced psychiatric disturbances particularly via neurochemical mechanisms remain less well elucidated. Therefore, we further investigated the putative neurochemical as well as other cellular mechanisms of quercetin on social-defeat stress (SDS) model of psychosocial impairments. Saline (10 mL/kg,i.p.), quercetin (25, 50 and 100 mg/kg,i.p.) and ginseng (50 mg/kg,i.p.) were given to intruder mice for 14 days. From days 7-14, ten minutes of aggressive-resident-induced SDS (physical and psychological) were conducted thirty minutes after treatments. Subsequently, behavioral assessments: open-field, light/dark board, Y-maze, novel-object recognition, social-interaction and tail-suspension tests were conducted on day 14. Adrenal weight and glucose levels were measured. Monoamines, brain-derived neurotrophic factor (BDNF), corticosterone, inflammatory cytokines (TNF-α, IL-6) and executioner caspase-3 concentrations were determined in specific brain regions by ELISA. Oxidative/nitrergic stress and cholinergic markers were determined with UV-spectrophotometry. Psychosocial stress-induced anxiety, depression and cognitive defects were improved by quercetin. The decreased serotonin in the prefrontal-cortex and dopamine in the striatum, elevated levels of noradrenaline and acetylcholinesterase in the prefrontal-cortex and hippocampus with corresponding decrease in BDNF were reversed by quercetin. Quercetin reduced SDS-induced increased neuronal inflammation, caspase-3 activity, malondialdehyde, nitrite levels, but increased antioxidant activities in the three brain regions. Adrenal hypertrophy, increased serum glucose and corticosterone release were reduced by quercetin. Our findings showed that quercetin attenuates psychosocial stress-induced passive coping behavior via normalization of HPA-axis, modulation of neurochemical release, enhancement of BDNF, and inhibition of brain oxidative/nitrergic stress, neuroinflammation and apoptotic pathway.