Effect of Senna Is Not Mediated by Platelet-Activating Factor

Abstract

The effect of in vivo treatment with senna was examined on the ex vivo formation of platelet-activating factor (PAF) by small and large intestine of rat, mouse and guinea pig. A single or a prolonged oral administration of senna (60-240 mg/kg) to animals did not increase intestinal PAF content. Nor did senna increase the intraluminal release of acid phosphatase. A similar result was obtained in the colonic tissue of rat perfused in vitro with rhein (1-500 μg/ml) or rhein anthrone (1-500 μg/ ml). In contrast, a single oral administration of phenolphthalein (20 mg/kg), bile salts (20 mg/kg) or magnesium sulfate (30 mg/kg) to rats increased intestinal PAF content. Magnesium sulfate also increased the intraluminal release of acid phosphatase. Colonic tissue of rats perfused in vitro with calcium ionophore A23187 (10 μg/ml) formed large amounts of PAF and acid phosphatase. PAF stimulates intestinal motility and secretion and mediates gut damage while acid phosphatase is a marker of cellular damage. Therefore, our data suggest that senna is well tolerated in animals and PAF does not mediate senna-induced laxation.

Finger Clubbing Caused by Herbal Tea

“…Perhaps an analogous situation occurs in the pulmonary capillaries at the same time. Enterocyte platelet activating factor levels were not raised after chronic senna exposure in one rat study, but systemic levels were not measured (5). There are no data regarding the direct or indirect effects of the anthraquinones on platelet function or vascular tone outside the gastrointestinal tract.…”

Sennoside-lnduced Secretion and Its Relevance for the Laxative Effect

“…Stimulation of active Cl secretion seems to be the predominant mechanism of sennoside-induced secretion [20][21][22], but there is some controversy about the pathways involved. In rabbit colon it has been found that rhein stimulates Cl secretion by activat ing submucosal neurons and by release of ace tylcholine and prostaglandins [20,22] [28]. Thus, if epithelial damage plays a role in senna-induced secretion, it seems that small alterations without patholog ical significance are sufficient to activate the intestinal immune system and lead to media tor release.…”