Opioid and Nitrergic Pathways Mediate Antinociception by Pectis elongata Kunth. Essential Oil

Abstract

In the present study, we aimed to evaluate the antinociceptive potential of the Pectis elongata essential oil (PeEO) and to understand its mechanism of action by identifying possible pain inhibition pathways. PeEO was analyzed using gas chromatography coupled with mass spectrometry. Male Swiss mice were subjected to the hot plate test to assess analgesic activity, determine the effective dose, and elucidate the pharmacological pathways involved, using specific blockers of the opioid, cholinergic, and nitric oxide pathways. Chemical analysis identified 23 compounds accounting for 95.57% of the sample, with citral (86.4%-Geranial and Neral) as the major constituent. The antinociceptive activity of PeEO was observed at a dose of 600 mg/kg, and this effect was mediated by the opioid and nitrergic pathways, as evidenced by pretreatment with L-NAME and naloxone. These findings reinforce the analgesic potential of PeEO, possibly related to its high citral content.

Keywords: citral; essential oil; inflammation; mechanism of action; pain.

FIGURE 1

Antinociceptive effect of Pectis elongata essential oil (PeEO) in a hot plate test at different time points. Mice were treated with PeEO at doses of 200, 400, and 600 mg/kg (PO) and compared to control groups: positive control (morphine 10 mg/kg, IP), vehicle control (mineral oil), and negative control (distilled water). Latency to nociceptive response was measured at 30, 60, 90, and 120 min after administration. Data are expressed as mean ± SEM (n = 6). *p ≤ 0.05 versus negative control. Statistical analysis: one‐way ANOVA followed by Dunnett's Multiple Comparison test.

FIGURE 2

Effect of naloxone, atropine, and L‐NAME on the antinociceptive activity of Pectis elongata essential oil (PeEO) in the hot plate test at T30. Mice were pre‐treated intraperitoneally with naloxone (1 mg/kg), atropine (1 mg/kg), or L‐NAME (3 mg/kg) 30 min before administration of PeEO (600 mg/kg, PO) or morphine (10 mg/kg, IP). Nociceptive latency was assessed 30 min after treatment. Data are expressed as mean ± SEM (n = 6). *p ≤ 0.05 versus negative control; *p ≤ 0.05 versus PeEO alone. Statistical analysis: one‐way ANOVA followed by Dunnett's Multiple Comparison test.