Long-term consumption of fermented rooibos herbal tea offers neuroprotection against ischemic brain injury in rats.

Stroke is the second leading cause of death worldwide, affecting about 240 people a day in South Africa and leaving survivors with residual disabilities. At the moment, there is no clinically approved neuroprotective product for stroke but the consumption of plant polyphenols has been suggested to offer some protection against stroke. In this study, we investigated the effects of long-term consumption of fermented rooibos herbal tea (FRHT) on ischemia/reperfusion (I/R)-induced brain injury in adult male Wistar rats. FRHT was administered to the animals ad libitum for 7 weeks prior to the induction of ischemic injury via a 20-minute bilateral occlusion of the common carotid arteries (BCCAO) followed by reperfusion for 24, 96 and 168 hours respectively. Neurobehavioural deficits, brain oedema, blood-brain barrier (BBB) damage, apoptosis, lipid peroxidation and total antioxidant capacity were subsequently evaluated using standard methods. Our results showed that long-term consumption of FRHT by Wistar rats signi icantly reduced brain oedema and neuronal apoptosis, but did not attenuate BBB damage following cerebral ischemia. Analysis of whole-brain homogenates showed significantly reduced lipid peroxidation levels, increased total antioxidant capacity and resulted in improved neurobehavioural outcomes in FRHT-treated rats when compared with untreated animals. Taken together, our results tend to suggest that continuous consumption of FRHT could confer some protection against ischemic brain injury (IBI) and is therefore highly recommended for patients with stroke-predisposing conditions.

Effects of hippadine on the blood pressure and heart rate in male spontaneously hypertensive Wistar rats.

ETHNOPHARMACOLOGICAL RELEVANCE: Hippadine is an alkaloid isolated from Crinum macowanii. Crinum macowanii is used in South Africa to treat oedema, 'heart disease', rheumatic fever, cancer and skin diseases, and belongs to the plant family Amaryllidaceae, assumed to have originated in the South African region. The aim of this study was to evaluate the effect of hippadine, an alkaloid extracted from Crinum macowanii, on the blood pressure (BP) and heart rate (HR) in anaesthetized male spontaneously hypertensive Wistar rats (SHR); and to find out if α1 and⧸or ß1 adrenoceptors contribute to its effects. MATERIALS AND METHODS: Hippadine (2.5-12.5mg/kg), adrenaline (0.05-0.20mg/kg), atenolol (0.5-40mg/kg) and prazosin hydrochloride (100-500µg/kg) were infused intravenously, and the BP and HR measured via a pressure transducer connecting the femoral artery and the PowerLab. Adrenaline increased the systolic, diastolic and mean arterial BP, while hippadine, atenolol and prazosin respectively decreased the systolic, diastolic and mean arterial BP. Increases in HR were observed with both adrenaline and prazosin, while reductions in HR were observed with atenolol and hippadine. Infusion of adrenaline in rats pre-treated with atenolol (30mg/kg), prazosin (400µg/kg), and hippadine (10mg/kg) led to similar increases in BP and HR in all groups. All changes in HR or BP were significant (p<0.05) and dose dependent. CONCLUSION: Hippadine decreases the BP and HR in SHR, and these effects may be due to α1 and ß1 adrenoceptor inhibition.

Early cardiovascular changes occurring in diet-induced, obese insulin-resistant rats.

The metabolic syndrome is recognized as a cluster of disturbances associated with obesity, type 2 diabetes and hypertension. Over the past two decades, the number of people with the metabolic syndrome has increased at an alarming rate. This increase is associated with the global epidemic of both obesity and diabetes. Cardiovascular mortality is increased among diabetics and obesity-related insulin-resistant patients, and obesity is currently recognized as independent risk factor for cardiovascular disease. We aimed to establish the effects of a short period of an altered diet on the heart using a rat model of hyperphagia-induced obesity (diet supplemented with sucrose and condensed milk for 8 weeks = DIO) compared to age-matched controls. Isolated, perfused hearts were subjected to global or regional ischaemia/reperfusion. Function on reperfusion was recorded and infarct size determined. A plasma lipid profile was established via HPLC-based methods and proteins involved in metabolic signalling determined either by western blotting or RT-PCR. 8 weeks of diet resulted in whole-body but not myocardial insulin resistance, increased plasma triglyceride and phospholipid levels as well as increased lipid peroxidation. Despite the similar baseline function, hearts from DIO animals showed significantly poorer postischaemic recovery than controls (41.9 % RPP recovery vs 57.9 %, P < 0.05, n = 7-11/group) but surprisingly, smaller infarct size (24.95 ± 1.97 vs 47.26 ± 4.05 % of the area at risk, P < 0.005, n = 8/group). Basal phosphorylation of PKB/Akt was elevated but IRS-1 and SERCA-2 expression severely downregulated. In conclusion, after only 8 weeks of a slight change in diet, the rat heart shows signs of metabolic remodelling. Some of these changes may be protective but others may be detrimental and eventually lead to maladaptation.