From popular use to pharmacological validation: A study of the anti-inflammatory, anti-nociceptive and healing effects of Chenopodium ambrosioides extract

Chenopodium ambrosioides (Amarantaceae) is an annual or perennial plant popularly known as ‘erva de Santa Maria’, ‘mastruço’ and ‘erva-do-formigueiro’. This herb is used in folk medicine in the form of teas, poultices and infusions for inflammatory problems, contusions and lung infections, and as an anthelmintic and anti-fungal. The aim of the present study was to further the understanding of the anti-nociceptive, anti-inflammatory and wound healing effects of ethanol extract (EE) obtained from the leaves and stems of Chenopodium ambrosioides in animal models of acute pain, inflammation and wound healing, thus supporting its medicinal use for the treatment of pain and inflammatory conditions The anti-nociceptive activity of EE (150–500mg/kg) was evaluated using the nociception induced by formalin (2.5%), prostaglandin-E2 (PGE2; 3nmol/paw), capsaicin (CAP, 1.6μg/paw) and bradykinin (BK, 10nmol/paw). The anti-inflammatory activity of EE (150–500mg/kg) was evaluated in carrageenan- (Cg, 300μg/paw), PGE2- (3nmol/paw), substance P- (SP, 20nmol/paw) and BK- (3nmol/paw) induced paw oedema. The topical anti-inflammatory activity of EE (1%, 3% and 5%) was evaluated in arachidonic acid- (AA, 2mg/ear), oil croton- (1μg/ear) and CAP- (250μg/ear) induced ear oedema. The effect of this extract in the inhibition of the influx of neutrophil, myeloperoxidase (MPO) and adenosine-deaminase (ADA) activities and nitric oxide (NO) and TNF-á levels was also determined using the mouse of pleurisy induced by Cg. The excision wound model in rats was used to evaluate the wound healing efficacy of EE (1%, 3% and 5%). To exclude the possible non-specific muscle relaxant or sedative effects of EE, mice motor performance was also evaluated with the rota-rod test. EE (5% per ear) was effective in reducing ear oedema induced by croton oil by 78.09%, CAP by 70.85% and AA by 77.02%. EE (500mg/kg; p.o.) also significantly inhibited paw oedema induced by Cg by 40%, PGE2 by 51%, SP by 56% and BK by 57%. EE (500mg/kg; p.o.) inhibited the cell influx of leucocytes by 78% and neutrophils by 53%, MPO activity by 62.22% and ADA activity by 23.07%, as well as NO by 77.77% and TNF-á levels by 50% in the fluid leakage due to the carrageenan-induced pleurisy. EE also inhibited the formalin-induced nociceptive in both phases of pain (neurogenic and inflammatory) at a dose of 500mg/kg, resulting in inhibitions of 77.39% and 95.60%, respectively. EE (500mg/kg; p.o.) was also effective in inhibiting the no