Berberine decreases intestinal activity by activating alpha-2-adrenoceptors and reducing cyclic adenosine monophosphate (cAMP) (Hui et al 1991). Berberine also inhibits intestinal ion secretion and inhibits toxin formation from microbes (Birdsall & Kelly 1997).
Berberine has demonstrated efficacy in vitro for many bacteria that cause infective diarrhoea, including E. coli, Shigella dysenteriae, Salmonella paratyphi, Clostridium perfringens and Bacillus subtllus (Mahady & Chadwick 2001). It has also demonstrated activity in vitro against parasites that cause diarrhoea, including Entamoeba histolytica, Glardia lamblla and Trichomonas vaginalis.
The effects of berberine on cholera toxin-induced water and electrolyte secretion were investigated in an experimental in vivo model (Swabb 1981). Secretions of water, sodium and chlorine were reduced 60-80 minutes after exposure to berberine.
Berberine did not alter ileal water or electrolyte transport in the control model. It produced a significant reduction in fluid accumulation caused by infection with E. coli in vivo (Khin-Maung & Nwe Nwe 1992). Oral doses of berberine before the toxin was introduced and intragastric injection after infection were both effective. Berberine was shown to inhibit by approximately 70% the secretory effects of Vibrio cholerae and E. coll in a rabbit ligated intestinal loop model (Sack & Froehlich 1982). As in the other study, the drug was effective when given either before or after enterotoxin binding. In an investigation using pig jejunum, berberine demonstrated a reduction in water and electrolyte secretion after intraluminal perfusion with E. coli (Zhu & Ahrens 1982).
Berberine significantly slowed small intestine transit time in an experimental in vivo model (Eaker & Sninsky 1989). Berberine inhibited myoelectric activity, which appears to be partially mediated by opioid and alpha-adrenergic receptors. The antidiarrhoeal properties of berberine may be partially due to the constituents' ability to delay small intestinal transit time.
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