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. 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.

Methylcobalamin is an endogenous coenzyme B12. It plays an important role as a coenzyme of methionine synthase in the transmethylation reaction of homocysteine to methionine. It is easily transferred to the organelles of nerve cells and promotes the synthesis of nucleic acids and proteins. It is easier to transfer into the organelles of rat nerve cells than cyanocobalamin. In experiments on brain cells and spinal cord nerve cells of mice, it participates in the process of synthesizing thymidine from deoxyuridine, promotes the utilization of folic acid and the metabolism of nucleic acids. It can promote the synthesis of nucleic acids and proteins in rats better than cobalamin. It promotes axonal transport and axonal regeneration. It can normalize the transport of axonal structural proteins in the sciatic nerve cells of diabetic rats caused by streptozotocin. It has a positive effect on the drug-induced neuropathy and axonal degeneration mouse models caused by doxorubicin, acrylamide, and vincristine, and the naturally occurring diabetic rats. It can inhibit the occurrence of degenerated nerves in the neuropathology and electrophysiology of rats with neurological disorders; promote the formation of myelin sheath (phospholipid synthesis), and can promote the synthesis of phosphatidylcholine, the main structure of myelin sheath, more than adenosylcobalamin, thereby improving the formation of myelin sheath; restore the transmission delay of synapses and the reduction of neurotransmitters. In the experiment of scraped sciatic nerve, it can restore the induction of terminal potential by increasing the excitation of nerve fibers, and can also normalize the low amount of acetylcholine in the brain of rats fed with choline-deficient bait; promote the maturation and division of erythrocytes, and improve the anemic blood picture. Vitamin B12 deficiency may lead to megaloblastic anemia. This drug promotes the synthesis of nucleic acids and the maturation and division of erythrocytes in the bone marrow, increases the production of red blood cells, and can quickly restore the red blood cell count, hemoglobin, and hematocrit values of rats that are reduced due to B12 deficiency.

This product is a semi-synthetic ergot alkaloid derivative. It has alpha-receptor blocking and vasodilation effects. It can enhance the metabolism of brain cell energy and increase the utilization of oxygen and glucose. It promotes the conversion of neurotransmitter dopamine to increase nerve conduction, strengthens the synthesis of brain protein, and improves brain function.

This product is a semi-synthetic ergot alkaloid derivative. It has alpha-receptor blocking and vasodilation effects. It can enhance the metabolism of brain cell energy and increase the utilization of oxygen and glucose. It promotes the conversion of neurotransmitter dopamine to increase nerve conduction, strengthens the synthesis of brain protein, and improves brain function.