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This study investigated the influence of Salvia barrelieri (SBA) methanol and decocted extracts (ME and DE) on intestinal transit (IT) and gastric emptying (GE) in mice. Only the doses of ME SBA induced a strong inhibition of GE at 46.82 ± 4.34, 54.71 ± 3.29 and 48.45 ± 1.33% (P≤0.0001) for the dosages 100, 200 or 400 mg·kg-1 respectively. The extracts by themselves had no effects on intestinal movement (only a slight, non–significant increase at 400 mg·kg-1). However, blocking muscarinic receptors resulted in a decrease in IT by 10.34 and 17.53% with ME and DE extracts, respectively, compared to control. Conversely, co–administration with L–arginine (Nitric Oxide donor) significantly decreased transit (47.31 and 50.80% for ME and DE, respectively), while inhibiting Nitric Oxide Synthase (NOS) with L–Nω–Nitro–Arginine (L–NNA) had a smaller effect (12.24 and 17.24% for ME and ED, respectively). Only ME SBA extracts significantly inhibited GE (46.82–54.71% decrease across doses), mimicking atropine’s effect. DE extracts and combining ME with atropine showed no significant impact. Interestingly, L–arginine only affected emptying with DE SBA (27.8% decrease), not ME SBA. Inhibiting NOS partially blocked the effect of ME SBA. These findings suggest that ME SBA extracts primarily target GE through mechanisms involving both muscarinic and NO pathways, while DE extracts have minimal effects. This study highlights the intricate interplay of pathways in gut function and the potential influence of extract type and formulation on their effectiveness.

Senecio perralderianus belongs to the family of Asteraceae and is only found in Algeria. Some species of this family are used to heal gastrointestinal issues in conventional medicine for their antioxidant and anti-inflammatory properties. This research was performed in order to determine if methanolic extract from the leaves of S. perralderianus had any protective effects on gastroenteritis brought on by alcohol consumption. Wistar rats were fed with 100% ethanol orally to induce gastric ulcer, and pre-treated with 50, 100, and 200 mg·kg-1 of the extract in addition to 5 mg·kg-1 of Ranitidine as a positive reference drug. The extract had shown a positive effect to protect ethanol-induced gastric ulcers with a protection percentage of 71 to 88%. In addition, pretreatment of rats significantly increased levels of GSH, CAT, and SOD in vivo as non-enzymatic and enzymatic antioxidants, and also reduced the level of lipid peroxidation. Histopathological sections, which showed the action of the therapeutic extract, substantially confirmed these findings on the reduction of the inflammation zone and the reduction of immune cell filtration caused by ethanol toxicity with increased extract dosages compared to Ranitidine. The antiulcer activity is due to inhibition of oxidative stress and gastritis. It is associated with a total polyphenol, flavonoids, chlorophyll (a, b), and carotenoids substantial amounts.