Youcare Pharmaceutical Group Co., Ltd.

It can promote the binding of insulin to receptors and improve the sensitivity of diabetic patients to insulin, increase the anaerobic glycolysis of sugar in peripheral tissues and promote the utilization of sugar, inhibit fat decomposition, reduce plasma free fatty acid levels, weaken insulin resistance and improve the utilization of glucose, thereby playing a role in lowering blood sugar, lowering blood lipids and inhibiting arteriosclerosis.

It can promote the binding of insulin to receptors and improve the sensitivity of diabetic patients to insulin, increase the anaerobic glycolysis of sugar in peripheral tissues and promote the utilization of sugar, inhibit fat decomposition, reduce plasma free fatty acid levels, weaken insulin resistance and improve the utilization of glucose, thereby playing a role in lowering blood sugar, lowering blood lipids and inhibiting arteriosclerosis.

This product is a proton pump inhibitor of gastric parietal cells. It can specifically inhibit the secretory microtubules and tubular vesicles in the cytoplasm of the parietal cell apical membrane, thereby effectively inhibiting the secretion of gastric acid. Since H, K-ATPase is the last process of acid secretion of parietal cells, this product has a strong acid inhibition ability. It can not only non-competitively inhibit 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 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 pepsin secretion, 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.

This product is a proton pump inhibitor of gastric parietal cells. It can specifically inhibit the secretory microtubules and tubular vesicles in the cytoplasm of the parietal cell apical membrane, thereby effectively inhibiting the secretion of gastric acid. Since H, K-ATPase is the last process of acid secretion of parietal cells, this product has a strong acid inhibition ability. It can not only non-competitively inhibit 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 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 pepsin secretion, 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.