TY - JOUR
T1 - Effects of acetonylgeraniin A on changes in the cAMP content and stress- induced gastric lesions in mice stomachs
AU - Tsai, L. H.
AU - Lee, Y. H.
AU - Hsu, F. L.
AU - Chen, C. F.
PY - 1996
Y1 - 1996
N2 - The effect of acetonylgeraniin A (AGA) on changes in the levels of cyclic AMP and ulcer formation in cold-restraint stress (CRS)-induced gastric lesions as well as on the pylorus-ligated gastric acid secretion were studied in mice. Gastric lesions induced by CRS (duration from 0.5 h to 2.5 h) produced a marked timedependent increase in the cAMP content of the stomach. AGA (0.2 mg/kg and 0.4 mg/kg, i.p.) significantly attenuated the increase in the cAMP content of CRS-induced stomachs. AGA administered intraperitoneally (i.p.) and orally (p.o.) to mice at doses of 0.1-0.4 mg/kg and 0.8-1.6 mg/kg, respectively, exhibited a protective effect on the development of gastric lesions induced by CRS. AGA at 0.2 mg/kg (i.p.) or 1.6 mg/kg (p.o.) prevented the development of gastric ulcers by about 95 %. A high correlation (r = 0.715, p <0.001, i.p.; r = 0.882, p <0.001, p.o.) between AGA-treatment and reduction of CRS-induced ulcers was observed. AGA (0.1-2 mg/kg, p.o.) decreased total acidity and peptic activity in a dose-dependent manner in pylorus-ligated mice. These results suggest that 1) the changes in the cyclic AMP levels observed in CRS-induced stomachs may be associated with the formation of mucosal damage, 2) AGA effectively reduced gastric mucosal ulcerations in response to CRS, 3) the antiulcer activity of AGA may be related to a decrease in the cyclic AMP content and acid secretion in the stomach of mice. Thus, AGA may protect against the development of CRS- induced gastric lesions by regulating cAMP levels and acid secretion in the stomach.
AB - The effect of acetonylgeraniin A (AGA) on changes in the levels of cyclic AMP and ulcer formation in cold-restraint stress (CRS)-induced gastric lesions as well as on the pylorus-ligated gastric acid secretion were studied in mice. Gastric lesions induced by CRS (duration from 0.5 h to 2.5 h) produced a marked timedependent increase in the cAMP content of the stomach. AGA (0.2 mg/kg and 0.4 mg/kg, i.p.) significantly attenuated the increase in the cAMP content of CRS-induced stomachs. AGA administered intraperitoneally (i.p.) and orally (p.o.) to mice at doses of 0.1-0.4 mg/kg and 0.8-1.6 mg/kg, respectively, exhibited a protective effect on the development of gastric lesions induced by CRS. AGA at 0.2 mg/kg (i.p.) or 1.6 mg/kg (p.o.) prevented the development of gastric ulcers by about 95 %. A high correlation (r = 0.715, p <0.001, i.p.; r = 0.882, p <0.001, p.o.) between AGA-treatment and reduction of CRS-induced ulcers was observed. AGA (0.1-2 mg/kg, p.o.) decreased total acidity and peptic activity in a dose-dependent manner in pylorus-ligated mice. These results suggest that 1) the changes in the cyclic AMP levels observed in CRS-induced stomachs may be associated with the formation of mucosal damage, 2) AGA effectively reduced gastric mucosal ulcerations in response to CRS, 3) the antiulcer activity of AGA may be related to a decrease in the cyclic AMP content and acid secretion in the stomach of mice. Thus, AGA may protect against the development of CRS- induced gastric lesions by regulating cAMP levels and acid secretion in the stomach.
KW - Acetonylgeraniin A
KW - Cold- restraint stress
KW - Cyclic AMP
KW - Gastric lesion
KW - Peptic activity
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M3 - Article
AN - SCOPUS:0029945791
SN - 1016-1015
VL - 48
SP - 91
EP - 102
JO - Chinese Pharmaceutical Journal
JF - Chinese Pharmaceutical Journal
IS - 1
ER -