The present study was conducted to evaluate the antioxidant and anti-inflammatory activities of Jungia paniculata (DC.) A. Gray (Asteraceae), used traditionally in Peru. The dry leaves were extracted with methanol, 50% methanol, and water. The anti-inflammatory activity of this plant was studied using in vitro (nitric oxide production in RAW 264.7 macrophages and sPLA(2) inhibition assay) and in vivo (carrageenan-induced paw edema in rats and TPA-induced ear edema in mice) model systems. The antioxidant activity of extracts was studied using three in vitro model systems (DPPH(*) radical-scavenging assay, ABTS(*+) assay, and superoxide radical-scavenging activity). The results have been correlated with total phenolics and total flavonoids contents. In the NO test of the extracts of Jungia paniculata, no significant cytotoxicities were observed at the concentrations determined by MTT assay. Only the MeOH50 extract of Jungia paniculata significantly inhibited PLA(2) enzyme activity (82.3 +/- 2.6%). At 3 h, the 50% methanol extract of Jungia paniculata at an oral dose of 500 mg/kg showed significant suppression of carrageenan-induced rat paw edema (36.36%). The same extract induced a 93.99% reduction in TPA-induced edema in topical administration. The extracts exhibited a high antioxidant activity and contained high total levels of polyphenols and flavonoids. There was a significant linear correlation between total phenolics and flavonoids contents and antioxidant activity in the three models used. In conclusion, Jungia paniculata possesses anti-inflammatory and antioxidant properties, which confirm the use of this plant in folk medicine as a topical anti-inflammatory herbal.
[Show abstract][Hide abstract] ABSTRACT: This study was conducted to explore the anti-inflammatory effect of Jungia sellowii (Asteraceae) using a murine model of pleurisy induced by carrageenan (Cg). This plant is used in southern Brazil to treat inflammatory diseases. J. sellowii leaves were extracted with ethanol/water to obtain the crude extract (CE), which was fractionated with different solvents, yielding n-hexane (Hex), dichloromethane (DCM), ethyl acetate (EtOAc) and n-butanol (BuOH) fractions, and aqueous fraction (Aq). The major compounds succinic acid (SA) and lactic acid (LA) were isolated from Aq fraction, and their structures were determined by 1H and 13C NMR. Pleurisy was induced by Cg (Saleh et al. 1996). The leukocytes, exudation, myeloperoxidase (MPO) and adenosine–deaminase (ADA) activities, metabolites of nitric oxide (NO
) levels, protein levels and mRNA expression for interleukin 1 beta (IL-1β), tumour necrosis factor alpha (TNF-α), interleukin 17A (IL17A) and inducible of nitric oxide synthase (iNOs), and p65 protein phosphorylation (NF-κB) were analysed 4 h after pleurisy induction. Animals pre-treated with CE, BuOH, Aq, SA, or LA inhibited leukocytes, exudation, MPO and ADA activities, NO
, IL-1β, TNF-α, and IL-17A levels, and the mRNA expression for IL-1β, TNF-α, IL-17A, iNOS, and p65 protein phosphorylation (NF-κB) (p < 0.05). Our study demonstrated that J. sellowii can protect against inflammation induced by Cg by decreasing the leukocytes and exudation. Its effects are related to the decrease of either proinflammatory cytokines and/or NO
. The isolated compounds SA and LA may play an important role in this anti-inflammatory action by inhibiting all the studied parameters. The anti-inflammatory properties of these compounds are due to the downregulation of NF-κB.
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