The nutrient composition of Myrothamnus flabellifolius leaf tea extract (MLTE) and its protective effect against oxidative hepatic cell injury were evaluated. Gallic acid, caffeic acid, ferulic acid, methyl gallate, and epicatechin were identified in MLTE by high‐performance liquid chromatography (HPLC). The tea extract showed an appreciable nutritional content of proximate, sugar, vitamin E, monounsaturated fatty acids, omega 6 and 9 unsaturated fatty acids, as well as considerable amounts of various mineral elements. Nineteen amino acids were found. Moreover, MLTE exhibited potent in vitro antioxidant activities, presumably because of its richness in polyphenols (gallic acid and ferulic acid) and vitamin E. In Chang liver cells, pretreatment with MLTE suppressed oxidative lipid peroxidation (IC50 = 113.11 μg/ml) and GSH depletion (IC50 = 70.49 μg/ml) without causing cytotoxicity. These data support the local consumption of M. flabellifolius herbal tea, which may be used against oxidative stress‐induced diseases while providing the body with necessary nutrients.
Practical application
Herbal teas are one of the most consumed beverages in the world today, due to their refreshing taste and additional health benefits. Myrothamnus flabellifolius herbal tea is a widely used traditional herbal tea in Southern Africa with potentials for commercialization due to its pleasant flavor. This study, for the first time, reported the nutritional composition of the leaf decoction of M. flabellifolius and its protective effect on hepatic oxidative insults. These results can inform the dietary and nutritional use of the tea for optimum benefits, as well as provide preliminary scientific validation of the use of the herbal tea as an antioxidant beverage with good nutritional value.
Cardiotoxicity leading to cardiovascular dysfunction and ultimately cardiac failure remains a major global health issue irrespective of race, age and country. Several factors including lipotoxicity, oxidative imbalance, exacerbated angiotensin-converting enzyme (ACE) activity and altered bioenergetics have been implicated in the pathophysiology of cardiovascular diseases. Turbina oblongata (E. Mey. ex Choisy) A. Meeuse is among the medicinal plants commonly used traditionally in the treatment and management of various ailments including cardiovascular dysfunctions in South Africa. In the present study, T. oblongata was investigated for its cardioprotective mechanism on oxidative-mediated cardiotoxicity by determining its effect on redox imbalance, purinergic and cholinergic dysfunction, and ACE activity as well as lipid dysmetabolism and pathways in iron-induced oxidative cardiac injury. Oxidative injury was induced ex vivo in freshly isolated heart by incubating with 0.1 mM FeSO4. Treatment was done by co-incubating with T. oblongata extract or gallic acid which served as the standard antioxidant. Induction of oxidative cardiac injury led to significant depleted levels of glutathione, triglyceride, HDL-cholesterol, superoxide, catalase and ENTPDase activities, with concomitant elevated levels of malondialdehyde, cholesterol, LDL-cholesterol, ACE, acetylcholinesterase, ATPase and lipase activities. These levels and activities were significantly reversed following treatment with T. oblongata. Induction of oxidative injury also caused alterations in lipid metabolites, with concomitant activation of beta oxidation of very long chain fatty acids, plasmalogen synthesis and mitochondrial beta-oxidation of long chain saturated fatty acids pathways. Some of the altered metabolites were restored following treatment with T. oblongata, with concomitant inactivation of beta oxidation of very long chain fatty acid pathway. These results indicate the cardioprotective effect of T. oblongata against oxidative-mediated cardiotoxicity. This is evidenced by its ability to mitigate lipotoxicity and modulate dysregulated cardiometabolic activities as portrayed by its antioxidative activity and suppressive effects on ACE, acetylcholinesterase and lipase activities, while modulating cardiac lipid dysmetabolism.
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