Abstract
Beneficial antioxidant phytochemicals are found in many medicinal plants. Pseuderanthemum palatiferum (PP), a well-known Vietnamese traditional medicinal plant in Thailand, has long been used in folk medicine for curing inflammatory diseases, often with limited support of scientific research. Therefore, this study aimed to determine antioxidant and modulation of inflammatory mediators of ethanol and water extracts of PP (EEP and WEP, resp.). WEP had significantly higher phenolic and flavonoid levels and DPPH radical scavenging activity than EEP. However, EEP exhibited greater reducing power than WEP. A greater decrease of tert-butyl hydroperoxide-induced oxidative stress in RAW264.7 macrophage cells was also observed with EEP. Modulation of inflammatory mediators of EEP and WEP was evaluated on LPS plus IFN-γ-stimulated RAW264.7 cells. EEP more potently suppressed LPS plus IFN-γ-induced nitric oxide (NO) production than WEP. Both EEP and WEP also suppressed the expression of iNOS and COX-2 protein levels. Collectively, these results suggest that PP possesses strong antioxidant and anti-inflammatory properties.
Highlights
Oxidative stress is known to cause cellular damage linked to various degenerative processes and diseases, such as aging, ischemic injury, atherosclerosis, cancer, diabetes, and various inflammatory diseases [1]
ethanol extract of PP (EEP) exhibited a percentage of recovery of 4.03%, while water extract of PP (WEP) had percentage of recovery of 3.29% based on the original weight of fresh leaves
WEP was prepared from the water fraction of EEP that was partitioned with hexane and water (1 : 1, v/v) with a percentage of recovery of 81.77% based on EEP
Summary
Oxidative stress is known to cause cellular damage linked to various degenerative processes and diseases, such as aging, ischemic injury, atherosclerosis, cancer, diabetes, and various inflammatory diseases [1]. Macrophages are key players in inflammation and their activation is crucial in inflammatory processes [2]. Excess levels of NO produced by activated macrophages reflect the inflammation process and are regulated by inducible nitric oxide synthase (iNOS) [4]. PGE2, the key player in inflammatory response, is produced from arachidonic acid by prostaglandin synthase or cyclooxygenase (COX) enzymes. COX-2 is considered as the inducible isoform and is primarily involved in inflammation [6]. Linkage and cross talk among NO, iNOS, and COX-2 during the inflammation process are well established. An agent with inhibitory effects on excess levels of NO, iNOS, and COX-2 expression would be highly beneficial and part of an effective strategy in the treatment of inflammatory diseases
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