CAJ | 학술논문

胃泌素通过胃泌素受体介导,刺激胃酸的分泌,又维持胃黏膜的完整性.胃泌素与脾虚的关系密切,脾虚病理过程中胃泌素水平处于紊乱状态.本研究观察到:脾虚大鼠胃壁细胞胃泌素受体结合位点数下降而受体亲和力升高;与胃黏膜保护机制相关的一氧化氮在胃黏膜中含量下降;经五肽胃泌素腹腔注射刺激后的胃酸分泌反应性显著升高.经益气健脾复方补中益气汤治疗后,以上紊乱状态均获得一定程度的恢复.另证明体外补中益气汤含药血清给药能与胃泌素受体竞争性结合.总之,文章阐明了补中益气汤的健脾机制与调节胃泌素相关.
위비소통과위비소수체개도,자격위산적분비,우유지위점막적완정성.위비소여비허적관계밀절,비허병리과정중위비소수평처우문란상태.본연구관찰도:비허대서위벽세포위비소수체결합위점수하강이수체친화력승고;여위점막보호궤제상관적일양화담재위점막중함량하강;경오태위비소복강주사자격후적위산분비반응성현저승고.경익기건비복방보중익기탕치료후,이상문란상태균획득일정정도적회복.령증명체외보중익기탕함약혈청급약능여위비소수체경쟁성결합.총지,문장천명료보중익기탕적건비궤제여조절위비소상관.
Buzhong Yiqi decoction(BYD) is a classic recipe for replenishing qi and invigorating spleen. Gastrin stimulates the secretion of the gastric acid, promotes the production of the cells in gastric mucosa membrane, and maintains the integrality of the mucous membrane. It has been proved that gastrin is closely related to spleen-deficiency, and the content of gastrin is in disorder during the course of spleen-deficiency. Our laboratory has already successfully established the method of isolating the gastric parietal cells and measuring the gastrin receptor binding capacity in rats, and found the binding capacity of gastrin receptor in isolated gastric parietal cells more markedly decreased in spleen-deficiency rats than in the normal rats. After treated with huangqi, a kind of herb attributed to invigorating spleen and replenishing qi, huangqi, the decreased binding capacity is improved. In the study the subjects observed further are: the changes of the binding capacity and affinity of the gastrin receptor in isolated gastric parietal cells in spleen-deficiency rats; the effect of the serum containing BYD on gastrin receptor in isolated gastric parietal cells in vivo in rats; the influence of BYD on the amount of nitric oxide(NO) in gastric mucosa in spleen-deficiency rats; whether BYD can regulate the sensitivity of the gastric acid secretion stimulated by gastrin through celiac injection in spleen-deficiency rats, and with which the changes of gastrin receptor are associated. In all, the study is about the effect of BYD on gastrin receptor in gastric parietal cells and its associated invigorating spleen mechanisms in spleen-deficiency rats. Meanwhile the essence of the syndrome of spleen deficiency from the level of gastrin receptor and molecular signal transduction in the isolated parietal cells is also explored.