Antidiarrhoeal Activity of the Ethyl Acetate Extract of Baphia Nitida (Papilionaceae)

In our search for plants useful in the treatment of diarrhoea, we investigated the ethyl acetate extract of Baphia nitida (BN) using intestinal transit (1,2), enteropooling (3) and gastric emptying (4) tests. In the normal intestinal transit test, peristaltic index (PI %) for the control group (distilled water 10ml/kg, p.o.) was obtained to be 83.64±4.07. BN produced a non-significant increase in intestinal propulsion with PI values of 84.37±1.72, 88.22±2.71 and 91.80±2.33 for doses of 100, 200 and 400mg/kg (p.o.), respectively. The extract effected a significant (P<0.05) dose dependent decrease in propulsion in the castor oil induced intestinal transit model. PI values were 56.85±6.76, 36.84±3.04 and 31.98±2.60, respectively for BN at 100, 200 and 400mg/kg vs. 89.33±6.28 for control. The effect at 400mg/kg was significantly lower than that of morphine, 10mg/kg s.c. (20.29±3.78), and was antagonized by isosorbide dinitrate, IDN (150mg/kg, p.o.) but not by yohimbine (1mg/kg, s.c.). This effect was not potentiated by atropine (1mg/kg, s.c.). In the castor oil induced diarrhoea test, BN produced a significant increase in onset of diarrhoea (103.40±8.74, 138.80±17.04 and 174.8±29.04min., 100 to 400mg/kg, vs. 47.60±8.76min. for control and 226.10±12.57min. for morphine). The severity of diarrhoea (diarrhoea score) was reduced (19.00±2.26, 17.04±1.89, 15.00±2.05, 100 to 400mg/kg, vs. 31.40±2.11 for control and 7.7±2.2 for morphine). This effect was not antagonized by IDN or yohimbine. The effect on severity was however potentiated by atropine. BN also reduced the number and weight of wet stools but did not have any significant effect on intestinal fluid accumulation and gastric emptying. Results obtained suggest that the ethyl acetate extract of Baphia nitida is endowed with antidiarrhoeal activity, which can be potentiated by muscarinic antagonists, due mainly to its inhibitory effect on gastrointestinal propulsion possibly mediated by interference with the nitric oxide pathway.

References: [1] Hsu, W. H. (1982) Eur. J. Pharmacol. 83: 55–60. [2] Aye-Than, J.H. et al. (1989) J. Crude Drug Res. 27: 195–200. [3] Robert, A. et al. (1976) Prostaglandins 11: 809–814. [4] Droppleman, D.A. (1980) J. Pharmacol. Methods 4: 227–230.