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给大鼠自由饮用５０μｇ／ｍｌＭＮＮＧ溶液共２０周，诱发脾胃粘膜病变。实验从第３６周起，按１５０ｍｇ／ｋｇ体重，每日１次给大鼠喂服丁酸钠共８周，以后处死动物进行观察。丁酸钠治疗组大鼠腺胃粘膜肠化生、硫酸粘液阳性肠化生、中重度异型增生及胃癌的发生率（各为６０．０％、４０．０％、２０．０％、０％）显著低于未加治疗的对照组（各为８８．０％、７６．０％、４８．０％、１６．０％）（Ｐ＜０．０５）；治疗组大鼠幽门腺与胃底腺平均肠化腺体数（各为７０．３±４６．８、３９．８±２９．６）亦显著地低于治疗前对照组（各为２１６．３±９８．４、１３０．７±５９．２）和未加治疗的对照组（各为２４１．４±１１３．９、１４６．４±６６．３）（Ｐ＜０．０１）；经丁酸钠治疗后，大鼠病变胃粘膜血流量改善，泌酸功能好转，跨膜电位差及血和组织中ＬＰＯ含量恢复接近正常水平。说明丁酸钠对大鼠实验性腺胃粘膜癌前病变有部分逆转和阻断治疗作用。这为探讨人类胃癌前病变的防治提供了新的途径。
The rats were allowed to freely drink 50 μg/ml MNNG solution for 20 weeks to induce splenic and gastric mucosal lesions. From the 36th week, the rats were fed sodium butyrate at a dose of 150 mg/kg body weight once a day for 8 weeks, and the animals were sacrificed for observation. The incidence of intestinal metaplasia, acid-sulfhydric acid-positive intestinal metaplasia, moderate-severe dysplasia, and gastric cancer in the sodium butyrate treatment group (60.0%, 40.0%, 20.0%, 0%, respectively) Significantly lower than the untreated control group (88.0%, 76.0%, 48.0%, 16.0% each) (P<0.05); pyloric gland and fundus of the treatment group rats The average number of glandular intestine glands (70.3±46.8, 39.8±29.6 each) was also significantly lower than that before treatment (216.3±98.4, 130.7±each). 59.2) and untreated control groups (241.4±113.9, 146.4±66.3, respectively) (P<0.01); lesions of gastric mucosa after treatment with sodium butyrate Improved blood flow, improved oxyntic function, poor transmembrane potential, and LPO levels in blood and tissues recovered to near normal levels. It was demonstrated that sodium butyrate partially reversed and blocked the therapeutic effects of experimental gastric and gastric precancerous lesions in rats. This provides a new way to explore the prevention and treatment of human gastric precancerous lesions.