No specific description provided

This product is a proton pump inhibitor of gastric parietal cells, which can specifically inhibit the secretory microtubules and H, K-ATPases on the tubular vesicles in the cytoplasm of the parietal cell apical membrane, thereby effectively inhibiting the secretion of gastric acid. It can not only non-competitively inhibit the gastric acid secretion caused by gastrin, histamine, choline, food, and stimulation of the vagus nerve, but also inhibit part of the basic gastric acid secretion that is not affected by choline or H2 receptor blockers. It also has a strong and lasting inhibitory effect on the gastric acid secretion caused by dibutyl cyclic adenosine monophosphate (DCAMP) stimulation that cannot be inhibited by H2 receptor antagonists. This product also has an inhibitory effect on the secretion of pepsin, has no obvious change in gastric mucosal blood flow, and does not affect body temperature, gastric cavity temperature, arterial blood pressure, venous hemoglobin, arterial oxygen partial pressure, carbon dioxide partial pressure and arterial blood pH.

This product is a proton pump inhibitor of gastric parietal cells, which can specifically inhibit the secretory microtubules and H, K-ATPases on the tubular vesicles in the cytoplasm of the parietal cell apical membrane, thereby effectively inhibiting the secretion of gastric acid. It can not only non-competitively inhibit the gastric acid secretion caused by gastrin, histamine, choline, food, and stimulation of the vagus nerve, but also inhibit part of the basic gastric acid secretion that is not affected by choline or H2 receptor blockers. It also has a strong and lasting inhibitory effect on the gastric acid secretion caused by dibutyl cyclic adenosine monophosphate (DCAMP) stimulation that cannot be inhibited by H2 receptor antagonists. In addition, this product also has an inhibitory effect on the secretion of pepsin, has no obvious change in gastric mucosal blood flow, and does not affect body temperature, gastric cavity temperature, arterial blood pressure, venous hemoglobin, arterial oxygen partial pressure, carbon dioxide partial pressure and arterial blood pH.

It is decomposed into diisopropylamine and dichloroacetic acid in the body. The former generates methionine, and the latter is metabolized to glycine. Under the action of glycine lyase, N5N10-CH2-FH4 (methyltetrahydrofolate) is generated, which provides energy at the same time. Both can provide methyl groups, promote choline synthesis, and choline reacts with liver fat to generate lecithin, promote liver fat decomposition; participate in lipoprotein formation, reduce fat accumulation in the liver; and reduce the concentration of related substances in arterial blood.

No specific pharmacological action is mentioned

It is broken down into diisopropylamine and dichloroacetic acid in the body, promoting the production and energy supply of methyltetrahydrofolate, providing methyl groups to promote choline synthesis, and thus consuming liver fat; at the same time, it participates in the production of lecithin and promotes the decomposition and transport of liver fat.

The specific pharmacological effects were not mentioned.