Studies have shown that diesel exhaust particles (DEP) induced oxidative stress and inflammation. This present study examined the molecular effects of aqueous rooibos extract (RE) on the cardiovascular toxic effect of methanol extract of DEP in exposed Wistar rats. The results showed that DEP caused significant (p < 0.001) increase in MDA and CDs levels in the aorta and heart but this increase was significantly (p < 0.001) attenuated by rooibos extract. DEP induced IL-8, TNFα, IL-1β and decreased IL-10 gene expressions, all of which were reversed in the presence of rooibos extract. The expression of NF-κB, and IκKB genes were also significantly (p < 0.001) induced by DEP in both tissues, but pre-treatment with RE attenuated these effects. In contrast, DEP repressed IκB mRNA level, which was significantly (p < 0.001) reversed by rooibos extract pre-treatment. In addition, pre-treatment with rooibos extract attenuated the increased Nrf2 and HO-1 mRNA levels caused by DEP. This indicates the potential of rooibos extract to protect against DEP-induced cardiovascular toxicity.

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Studies have shown that the translation of endothelium from the quiescent to the activated state plays a significant role in the aetiology of cardiovascular disease and atherosclerosis. The presence of excess reactive oxygen species (ROS), either due to the presence of pro-oxidant agents or in the presence of risk factors such as diabetes, hyperlipidemia, smoke etc., has been implicated in endothelium activation with the consequent dysfunctioning of the endothelium. It has been shown that the nitric oxide (NO) synthesized by the endothelium nitric oxide synthase (eNOS) plays important role in maintaining endothelium integrity by modulating the vascular tone. The presence of excessive ROS can interact with the NO with consequent production of peroxynitrite to produce other ROS and pro-inflammatory cytokines in cascade-reactions. These, together with other risk factors have been implicated in ED-mediated cardiovascular disease. In this review, the data supporting the role of oxidative stress and inflammation in ED-induced cardiovascular disease and atherosclerosis was examined. Therapeutic approaches using genetics, phytochemicals and pharmaceuticals methods, in regulating the effects of ROS in ED-mediated cardiovascular morbidity and mortality and atherosclerosis were also examined.