Hypertension is one of the risk factors for cardiovascular diseases and has been associated with about 13% of global deaths
worldwide. Oxidative stress and reduced nitric oxide (NO) bioavailability contribute to the development of endothelial
dysfunction and subsequently hypertension. Nɷ-nitro-L-arginine methyl ester hydrochloride (L-NAME) inhibits NO synthesis;
leading to hypertension. Piper sarmentosum (PS) is an herb with antioxidant, antiatherosclerosis and antiinflammation
properties. PS also stimulated NO production by endothelial cells. The aim of this study was to determine the effects of
aqueous extract of Piper sarmentosum (AEPS) on blood pressure, oxidative stress and the level of nitric oxide in L-NAMEinduced hypertensive rats. Hypertension was induced by oral administration of L-NAME (100 mg/L) in drinking water for
four weeks. The rats were concurrently treated with AEPS by oral gavage in serial doses (125, 250 and 500 mg/kg/day).
Blood pressure was measured using non-invasive tail-cuff method at baseline and fortnightly thereafter. Serum level of
NO and an oxidative stress marker, malondialdehyde (MDA) were measured at baseline and at the end of treatment. The
results showed that treatment with three different doses of AEPS successfully reduced systolic blood pressure (p<0.001),
diastolic blood pressure (p<0.05) and mean arterial pressure (p<0.05) in L-NAME-induced hypertensive rats. Treatment
with AEPS also reduced MDA level (p<0.001) and increased serum NO (p<0.001) in L-NAME-induced hypertensive rats.
The findings showed that AEPS decreased blood pressure by protecting against oxidative stress and increasing NO in
L-NAME-induced hypertensive rats.
Endothelial cell death due to increased reactive oxygen species (ROS) may contribute to the initial endothelial injury, which promotes atherosclerotic lesion formation. Piper sarmentosum (PS), a natural product, has been shown to have an antioxidant property, which is hypothesized to inhibit production of ROS and prevent cell injury. Thus, the present study was designed to determine the effects of PS on the hydrogen peroxide (H(2)O(2))-induced oxidative cell damage in cultured human umbilical vein endothelial cells (HUVECs). In this experiment, HUVECs were obtained by collagenase perfusion of the large vein in the umbilical cord and cultured in medium M200 supplemented with low serum growth supplementation (LSGS). HUVECs were treated with various concentrations of H(2)O(2) (0-1000 micromol/L) and it was observed that 180 micromol/L H(2)O(2) reduced cell viability by 50% as denoted by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Using the above concentration as the positive control, the H(2)O(2)-induced HUVECs were concomitantly treated with various concentrations (100, 150, 250 and 300 microg/ml) of three different extracts (aqueous, methanol and hexane) of PS. Malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) levels showed a significant increase (P<0.05) in HUVECs compared to the negative control. However, PS extracts showed a protective effect on HUVECs from H(2)O(2)-induced cell apoptosis with a significant reduction in MDA, SOD, CAT and GPX levels (P<0.05). Furthermore, PS had exhibited ferric reducing antioxidant power with its high phenolic content. Hence, it was concluded that PS plays a beneficial role in reducing oxidative stress in H(2)O(2)-induced HUVECs.