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Improved modulation of the endogenous antioxidant system and inflammatory responses in male wistar rats by rooibos (Aspalathus linearis) and red palm oil (Elaeis guineensis)
Oxidative stress and chronic (low-grade) inflammation are inseparably interconnected and both have been implicated in the aetiology of many disease states. The use of plant extracts for disease prevention and therapeutic purposes, is gaining more attention because of the health benefits of the bioactive phytochemicals in these extracts. This thesis reports on the antioxidant status, the oxidative stress modulation and anti-inflammatory properties of fermented rooibos (Aspalathus linearis) and red palm oil (RPO) from the oil palm plant (Elaeis guineensis) using a long-term and two short-term in vivo models. In the first (long-term) study, the effect of chronic feeding of rooibos, RPO or their combination on the endogenous antioxidant system was investigated. Data from this study provided: The first scientific evidence that chronic feeding of rooibos, RPO or their combination for 22 weeks did not adversely affect the liver or kidney function parameters. The first scientific evidence that chronic feeding of rooibos alone, or together with RPO for 22 weeks modulated the endogenous antioxidant system by inhibiting MDA formation and augmenting the reduced glutathione status. The first scientific evidence of an additive or synergistic interaction in the ability of rooibos and RPO to modulate the endogenous antioxidant system. The second (short-term) study investigated the protective effects of rooibos, RPO or their combination on tert-butyl hydroperoxide (t-BHP)-induced oxidative hepatotoxicity, and results from this study provided: The first evidence of the ability of the two extracts, either alone or in combination to protect against t-BHP induced hepatotoxicity. Supplementation of rooibos, RPO or their combination for eight weeks reversed the hepatic damage induced by t-BHP. The changes induced by t-BHP in the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GR) were reversed by these plant extracts. The extracts, supplemented alone or combined prevented lipid peroxidation as shown by the decreased levels of conjugated dienes iv (CD) and malondialdehyde (MDA) and reversed the t-BHP.-induced impairment of the glutathione redox status. The third (short-term) study provided the first scientific evidence of the in vivo anti-inflammatory properties of rooibos and RPO. The properties were demonstrated using a lipopolysaccharide (LPS)-induced hepatic endotoxemic model by: Providing the first evidence of an additive or synergistic interaction in the ability of the combined rooibos extract and RPO supplementation to reverse LPS-induced hepatic damage. Providing the first evidence for the modulation of the inflammatory responses by rooibos extract, RPO or their combination. Supplementation of rooibos extract, RPO or their combination for four weeks, modulated LPS-induced inflammatory responses by inhibiting the synthesis of pro-inflammatory cytokines, tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Providing evidence that the observed anti-inflammatory effects of rooibos and RPO may be related to their ability to modulate oxidative stress. Supplementation of rooibos extract, RPO or their combination for four weeks, prevented hepatic lipid peroxidation induced by LPS by decreasing CD and MDA formation in the liver. Changes induced in the activities of antioxidant enzymes were reversed and the glutathione redox status was augmented. Based on these study results, it is proposed that the ability of rooibos and RPO to protect the liver, modulate endogenous antioxidant system and inhibit inflammatory responses may be associated with the unique combination of antioxidant phytochemicals in both plant extracts. The study suggested possible mechanism(s) for the observed health effects, and the development of rooibos and RPO as nutraceuticals, which may be beneficial in the prophylactic management of oxidant-induced liver injury.