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May 15, 2026

In Vivo Evaluation of the Analgesic Effects of Orientin With Possible Underlying Mechanisms

Key Points

This study aims to assess the acute antinociceptive effects of orientin and the mechanisms involved.
Mice received orientin at doses of 50, 100, or 200 mg/kg intraperitoneally.
Central and peripheral antinociceptive activities were assessed using hot-plate, tail-immersion, and acetic acid-induced writhing tests.
Mice were pretreated with various antagonists to investigate the mechanisms involved in orientin's effects.
Orientin significantly reduced nociceptive responses in all tests.
Yohimbine, naloxone, AM251, and AM630 reversed the antinociceptive effects, while glibenclamide did not.
Findings indicate that α2-adrenoceptors, μ-opioid receptors, and cannabinoid receptors are involved in orientin's pain relief.

Abstract

Orientin is a water-soluble flavonoid C-glycoside present in various medicinal plants and known for its diverse pharmacological activities. The present study aimed to evaluate the acute antinociceptive effects of orientin and to investigate the involvement of adrenergic, opioidergic, cannabinoid systems, and ATP-sensitive potassium channels in these effects. Orientin (50, 100, and 200 mg/kg, i.p.) was administered to mice. Central antinociceptive activity was assessed using the hot-plate and tail-immersion tests, while peripheral activity was evaluated using the acetic acid-induced writhing test. To explore the underlying mechanisms, mice were pretreated with yohimbine (α2-adrenoceptor antagonist), naloxone (μ-opioid receptor antagonist), AM251 (CB1 receptor antagonist), AM630 (CB2 receptor antagonist), or glibenclamide (KATP channel blocker) prior to orientin administration. Orientin significantly reduced nociceptive responses in all experimental models at the tested doses. All antagonists except glibenclamide significantly reversed the spinal, supraspinal, and peripheral antinociceptive effects of orientin to varying degrees. These findings suggest that α2-adrenoceptors, μ-opioid receptors, and cannabinoid CB1 and CB2 receptors contribute to the analgesic effect of orientin, whereas KATP channels do not appear to be directly involved.

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