Paracetamol like antipyretic activity of lyophilized succulent of Aloe vera leaves in rats

Abstract

Aims: To evaluate the antipyretic activity of lyophilized succulent of Aloe vera (AVS) as well as its interaction with conventional antipyretic drug paracetamol (PCM) against experimentally induced pyrexia in rats. Materials and Methods: Pyrexia was induced experimentally by either Brewer’s yeast or misoprostol injection after recording basal rectal temperature in rats. Animals were treated with lyophilized AVS at the dose of 100, 200, and 300 mg kg and standard drug PCM 150 mg/kg, 18 h after injection of Brewer’s yeast suspension in one set of experiment and combination of sub‑effective dose of AVS with that of PCM 1 h after injecting misoprostol in other set of experiment. Rectal temperature was recorded at different time intervals after drug administration. AVS was also phytochemically screened for the presence of tannins, saponins, flavonoids, coumarins, sterols, reducing sugar, glycosides, starch, alkaloids, and triterpenoids. Results: Pyrexia was observed at 18 h and at 1 h after Brewer’s yeast and misoprostol injection subcutaneous, respectively. AVS (200 and 300 mg/kg) treated groups showed significant fall in rectal temperature (P < 0.05, P < 0.01, respectively) in Brewer’s yeast‑induced pyrexia as compared to control and AVS 100 mg/kg treated groups at different time intervals. The antipyretic activity of AVS at 300 mg/kg was comparable (P > 0.05) with standard drug PCM at 150 mg/kg. The combination of sub‑effective dose of AVS (100 mg/kg) with that of PCM (50 mg/kg) produced significant (P < 0.05) antipyretic activity against misoprostol‑induced pyrexia at different time intervals as compared with control, AVS 100 mg/kg and PCM 50 mg/kg treated groups when used alone. Phytochemical tests showed the presence of flavonoids, saponins, tannins, reducing sugar, glycoside, starch, and steroids. Conclusion: Lyophilized AVS possesses antipyretic activity. It enhances the antipyretic activity of PCM suggesting its role in inhibition of prostaglandin synthesis.