Effect of chloroform and aqueous basic fraction of ethanolic extract from Apium graveolens L. in experimentally-induced hyperlipidemia in rats.

The present study was undertaken to explore the antihyperlipidemic effect of ethanolic extract of seeds of Apium graveolens L. and its chloroform and aqueous basic fraction in olive oil induced hyperlipidemic rats. The antihyperlipidemic activity of Apium graveolens was compared with a standard drug Atrovastatin (50mg/kg). The study involved phytochemical screening and chromatographic studies of extract and fractions. The ethanolic extract and its fractions were administered orally at doses of 200 and 400 mg/kg body weight in rats. Olive oil (5ml/kg oral dose) was administered 30 min after treatment. Blood was collected by ocular puncture 2 and 4 h after olive oil treatment and centrifuged at 3000 rpm for 15-20 min. Serum samples were further subjected to biochemical analysis. The study dose dependently inhibited the total cholesterol (TC) triglycerides (TG), low density lipoproteins (LDL) level, and significantly increased high density lipoprotein (HDL) level. Phytochemical screening revealed the presence of terpenoid, tannin, alkaloid, glycoside, flavanoid and sterols. UV λmax was found to be 206 nm with a melting point of 137-138°C for the isolated component. The antihyperlipidemic effect was evaluated in olive oil loaded rats. Acute treatment caused stimulatory effect on HDL level and inhibition in TC and TG elevation induced by olive oil.

Activity of new NOP receptor ligands in a rat peripheral mononeuropathy model: potentiation of morphine anti-allodynic activity by NOP receptor antagonists.

The effect of new NOP receptor agonists and antagonists in the rat chronic constriction injury model was investigated. Intraperitoneally administered NOP receptor agonist SR14150 and antagonists SR16430 and SR14148, had no effect on mechanical allodynia when given alone. The nonselective NOP/mu-opioid receptor agonist SR16435, however, produced an anti-allodynic response, similar to morphine and reversible by naloxone. Notably, co-administration of the NOP receptor antagonists potentiated the anti-allodynic activity of both morphine and SR16435. Increased levels of the NOP receptor are implicated in the reduced efficacy of morphine in neuropathic pain. Our results suggest the utility of NOP receptor antagonists for potentiating opioid efficacy in chronic pain.