Inhibitory effect of fluvastatin on ileal ulcer formation in rats induced by nonsteroidal antiinflammatory drug

Table 1 Effect of HMG-CoA reductase inhibitors on BFMeT-induced ulcer formation in rat small intestines(mean±SD).

HMG-CoA reductase inhibitor	Number of rats	Total length of ulcers	Length of the small intestine	Ulcer index (%)
None (control)	7	7.1±2.84	78.8±10.5	9.2±4.10
Fluvastatin 5 mg/kg	5	6.0±3.71	83.4±4.6a	7.0±4.13
Fluvastatin 25 mg/kg	5	2.4±0.77a	97.4±12.5a	2.6±1.00a
Pravastatin 5 mg/kg	5	5.4±2.38	87.9±15.9	6.6±3.76
Pravastain 25 mg/kg	4	8.0±2.88	87.9±11.4	9.6±4.47
Atorvastatin 5 mg/kg	5	11.3±3.28a	82.8±14.2	14.0±4.79
Atorvastatin 25 mg/kg	5	6.8±4.56	85.9±17.2	9.3±7.48

All rats were administered BFMeT at a dose of 1000 mg/kg of body weight. Ulcer index was calculated as the percentage of total length of ulcers in the whole length of the small intestine. There was no ulcer formation in small intestines of rats treated with a solvent only and the length of the small intestine was 104.8±4.2 cm. Significantly different from the control group at

^aP<0.05 (ANOVA).

Table 2 Reducing power of HMG-CoA reductase inhibitors(mean±SD).

HMG-CoA reductase inhibitor	Dose (mmol/L)	Absorbance at 510 nm (as the reducing power)
Solvent only	0	0.182±0.019
Fluvastatin	0.01	0.545±0.0162
Pravastatin	0.01	0.182±0.021
Atorvastatin	0.01	0.308±0.0162
Gallic acid	0.005	0.709±0.0101

The intensity of the absorbance at 510 nm reflected antioxidative activity as the reducing power.

¹Gallic acid was not a HMG-CoA reductase inhibitor and used as a positive control of this test.

²Significantly different from the solvent at P<0.0001 (ANOVA).