Qin Zhen, Chen Chao
Laboratory of Natural Drugs of Medical College, China Three Gorges University, Yichang 443002, Hubei Province, China.
World J Gastroenterol. 2005 Dec 7;11(45):7203-7. doi: 10.3748/wjg.v11.i45.7203.
To assess the synergistic action of famotidine (FMD) and chlorpheniramine (CPA) on acetic acid-induced chronic gastric ulcer in rats.
Chronic gastric lesions were induced in male Sprague-Dawley (SD) rats by serosal application of the acetic acid. Forty SD rats were randomly divided into blank group (n = 8), control group (n = 8), FMD group (n = 8), CPA group (n = 8), and FMD+CPA group (n = 8). Each group was given intraperitoneally (i.p.) 0.5 mL/100 g distilled water, 9 g/L NaCl saline, 4 mg/kg FMD, 10 mg/kg CPA, 4 mg/kg FMD+10 mg/kg CPA, respectively, daily for 10 d. On d 10, ulcer area was determined by planimetry. The level of myeloperoxidase (MPO) in the liver homogenization was determined by biochemical methods and the plasma levels of 6-ketoprostaglandin F1 alpha (6-keto-PGF(1a)) and IL-8 were determined by radioimmunoassay.
The synergistic effects of FMD+CPA group on the lesion, IL-8, 6-keto-PGF(1a) and MPO were confirmed. The effect of FMD+CPA group was significantly different as compared to the control and FMD groups. The lesion (mm(2)) was reduced from 40.18+/-2.6 in control group to 6.83+/-2.97 in PMD+CPA group, P<0.01, and from 32.9+/-3.27 in FMD group to 6.83+/-2.97 in PMD+CPA group, P<0.01. The plasma levels of IL-8 decreased from 0.69+/-0.11 ng/L in control group to 0.4+/-0.04 ng/L in PMD+CPA group, P<0.01, and from 0.51+/-0.08 ng/L in FMD group to 0.4+/-0.04 ng/L in PMD+CPA group, P<0.05. The level of 6-keto-PGF(1a) increased from 7.55+/-1.65 ng/L in control group to 16.62+/-0.97 ng/L in PMD+CPA group, P<0.01, and from 13.15+/-1.48 ng/L in FMD group to 16.62+/-0.97 ng/L in PMD+CPA group, P<0.05. The levels of MPO in the liver homogenate decreased from 9.12+/-2.05 u/L in control group to 4.33+/-0.95 u/L in PMD+CPA group, P<0.01, and from 8.3+/-1.29 u/L in FMD group to 4.33+/-0.95 u/L, P<0.01.
The synergistic action of FMD and CPA on acetic acid-induced chronic gastric ulcer in rats decreases the incidence of ulcer and also enhances the healing of ulcer.
评估法莫替丁(FMD)与氯苯那敏(CPA)对乙酸诱导的大鼠慢性胃溃疡的协同作用。
通过在雄性Sprague-Dawley(SD)大鼠浆膜上涂抹乙酸诱导慢性胃损伤。40只SD大鼠随机分为空白组(n = 8)、对照组(n = 8)、FMD组(n = 8)、CPA组(n = 8)和FMD+CPA组(n = 8)。每组分别腹腔注射(i.p.)0.5 mL/100 g蒸馏水、9 g/L氯化钠盐水、4 mg/kg FMD、10 mg/kg CPA、4 mg/kg FMD + 10 mg/kg CPA,每日1次,共10天。在第10天,通过平面测量法测定溃疡面积。采用生化方法测定肝匀浆中髓过氧化物酶(MPO)水平,采用放射免疫分析法测定血浆中6-酮前列腺素F1α(6-keto-PGF(1a))和IL-8水平。
证实了FMD+CPA组对损伤、IL-8、6-keto-PGF(1a)和MPO的协同作用。FMD+CPA组的效果与对照组和FMD组相比有显著差异。损伤面积(mm(2))从对照组的40.18±2.6降至FMD+CPA组的6.83±2.97,P<0.01,从FMD组的32.9±3.27降至FMD+CPA组的6.83±2.97,P<0.01。血浆IL-8水平从对照组的0.69±0.11 ng/L降至FMD+CPA组的0.4±0.04 ng/L,P<0.01,从FMD组的0.51±0.08 ng/L降至FMD+CPA组的0.4±0.04 ng/L,P<0.05。6-keto-PGF(1a)水平从对照组的7.55±1.65 ng/L升至FMD+CPA组的16.62±0.97 ng/L,P<0.01,从FMD组的13.15±1.48 ng/L升至FMD+CPA组的16.62±0.97 ng/L,P<0.05。肝匀浆中MPO水平从对照组的9.12±2.05 u/L降至FMD+CPA组的4.33±0.95 u/L,P<0.01,从FMD组的8.3±1.29 u/L降至4.33±0.95 u/L,P<0.01。
FMD与CPA对乙酸诱导的大鼠慢性胃溃疡的协同作用降低了溃疡发生率,也促进了溃疡愈合。