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Several in‐vitro and in‐vivo ethnopharmacological studies carried out with plants of the genus Wedeliahave already demonstrated hepatoprotective effects in chemically‐induced liver injury, including those induced by paracetamol. Here, the effects of the crude extract from Wedelia paludosaon paracetamol‐induced hepatotoxicity in mice was investigated. Intraperitoneal injection of paracetamol (1000 mg kg−1) caused 80% death after 24 h in mice, which was significantly reduced by oral pretreatment with W. paludosa(500 mg kg−1). Hepatotoxicity was observed 24 h after an intraperitoneal injection of paracetamol (600 mg kg−1), as evidenced by an increase in plasma activity of aspartate and alanine aminotransferases. That hepatotoxicity was significantly attenuated by W. paludosapretreatment (100–500 mg kg−1) in a dose‐response manner. Paracetamol (1000 mg kg−1) drastically depleted total glutathione levels and decreased glutathione peroxidase and δ‐aminolevulinate dehydratase activity in the liver, such effects not being prevented by pretreatment with W. paludosa.Neither paracetamol treatment alone nor pretreatment with W. paludosaaltered glutathione reductase and glutathione S‐transferase activity or the levels of end‐products of lipid peroxidation. In conclusion, we found that W. paludosaprotected against paracetamol‐induced hepatotoxicity, an effect not observed over oxidative stress‐related parameters. Hepatoprotection is likely mediated by some terpenes present in W. paludosaextract. However, further studies will be required to explain the mechanisms involved in the hepatoprotection afforded by W. paludosa.

Several in-vitro and in-vivo ethnopharmacological studies carried out with plants of the genus Wedeliahave already demonstrated hepatoprotective effects in chemically-induced liver injury, including those induced by paracetamol. Here, the effects of the crude extract from Wedelia paludosaon paracetamol-induced hepatotoxicity in mice was investigated. Intraperitoneal injection of paracetamol (1000 mg kg−1) caused 80% death after 24 h in mice, which was significantly reduced by oral pretreatment with W. paludosa(500 mg kg−1). Hepatotoxicity was observed 24 h after an intraperitoneal injection of paracetamol (600 mg kg−1), as evidenced by an increase in plasma activity of aspartate and alanine aminotransferases. That hepatotoxicity was significantly attenuated by W. paludosapretreatment (100–500 mg kg−1) in a dose-response manner. Paracetamol (1000 mg kg−1) drastically depleted total glutathione levels and decreased glutathione peroxidase and δ-aminolevulinate dehydratase activity in the liver, such effects not being prevented by pretreatment with W. paludosa.Neither paracetamol treatment alone nor pretreatment with W. paludosaaltered glutathione reductase and glutathione S-transferase activity or the levels of end-products of lipid peroxidation. In conclusion, we found that W. paludosaprotected against paracetamol-induced hepatotoxicity, an effect not observed over oxidative stress-related parameters. Hepatoprotection is likely mediated by some terpenes present in W. paludosaextract. However, further studies will be required to explain the mechanisms involved in the hepatoprotection afforded by W. paludosa.