Takeuchi K, Ohtsuki H, Okabe S
Dig Dis Sci. 1986 Apr;31(4):406-11. doi: 10.1007/BF01311677.
16,16-Dimethyl PGE2 (16,16-dmPGE2), given orally at 10-30 micrograms/kg, had no effects on gastric acid secretion, or carbonic anhydrase activity, but did increase HCO3- secretion in both the stomach and duodenum of rats. 16,16-dmPGE2, at nonantisecretory doses, potently inhibited indomethacin- and water-immersion stress-induced gastric lesions and mepirizole-induced duodenal lesions in rats. Acetazolamide, given orally at 50 mg/kg, markedly inhibited carbonic anhydrase activity, but had no effects on gastric acid secretion and the basal and 16,16-dmPGE2-stimulated HCO3- secretion. Acetazolamide, at a nonantisecretory dose, had no effects on indomethacin-induced gastric lesions and mepirizole-induced duodenal lesions, but significantly inhibited water-immersion stress-induced gastric lesions. Combined administration of 16,16-dmPGE2 and acetazolamide did not influence the protective activity of 16,16-dmPGE2 on these lesions. The mechanism of the cytoprotective activity of 16,16-dmPGE2 may involve an increase in HCO3- secretion (nonmediated by carbonic anhydrase), while mechanisms involved in the effects of acetazolamide are apparently different.
16,16-二甲基前列腺素E2（16,16-dmPGE2），以10 - 30微克/千克的剂量口服，对胃酸分泌或碳酸酐酶活性没有影响，但确实增加了大鼠胃和十二指肠中的HCO3-分泌。16,16-dmPGE2在非抗分泌剂量下，能有效抑制吲哚美辛和水浸应激诱导的大鼠胃损伤以及美吡拉佐诱导的大鼠十二指肠损伤。乙酰唑胺以50毫克/千克的剂量口服，显著抑制碳酸酐酶活性，但对胃酸分泌以及基础和16,16-dmPGE2刺激的HCO3-分泌没有影响。乙酰唑胺在非抗分泌剂量下，对吲哚美辛诱导的胃损伤和美吡拉佐诱导的十二指肠损伤没有影响，但能显著抑制水浸应激诱导的胃损伤。16,16-dmPGE2和乙酰唑胺联合给药并不影响16,16-dmPGE2对这些损伤的保护活性。16,16-dmPGE2细胞保护活性的机制可能涉及HCO3-分泌增加（非由碳酸酐酶介导），而乙酰唑胺作用的机制显然不同。
