Tani S, Tanaka T, Kudo Y, Takahagi M
Chem Pharm Bull (Tokyo). 1989 Aug;37(8):2188-90. doi: 10.1248/cpb.37.2188.
Rat gastric mucosal cells were isolated with the aid of 0.1% collagenase and Dispase. Pepsinogen secretion from these cells was stimulated by carbachol, cholecystokinin octapeptide (CCK(S)-8) and pentagastrin, but not by histamine. Attempts to obtain a sufficient number of cells using a higher concentration of Dispase resulted in disappearance of the responses to secretagogues. However, when gastric mucosal cells thus prepared were cultured for 24 h in a CO2 incubator, they were found to respond not only to carbachol, CCK(S)-8 and pentagastrin, but also to histamine, resulting in an increase in pepsinogen secretion. The secretagogue-induced pepsinogen secretion was inhibited by its antagonist in a dose-dependent manner. These results suggest that the receptor present in chief cells for pepsinogen secretion was destroyed during the isolation procedure and regenerated during culture.
借助0.1%的胶原酶和分散酶分离大鼠胃黏膜细胞。这些细胞的胃蛋白酶原分泌受到卡巴胆碱、八肽胆囊收缩素(CCK(8))和五肽胃泌素的刺激,但不受组胺的刺激。尝试使用更高浓度的分散酶获得足够数量的细胞导致对促分泌剂的反应消失。然而,当如此制备的胃黏膜细胞在二氧化碳培养箱中培养24小时时,发现它们不仅对卡巴胆碱、CCK(8)和五肽胃泌素产生反应,而且对组胺也产生反应,导致胃蛋白酶原分泌增加。促分泌剂诱导的胃蛋白酶原分泌被其拮抗剂以剂量依赖的方式抑制。这些结果表明,在分离过程中,主细胞中存在的用于胃蛋白酶原分泌的受体被破坏,并在培养过程中再生。