1、 Pharmacopoeia standard of Golden Snake
This product is the dried body of the young snake of Bungarus multicinctus Blyth, an animal of cobra family. .
. The back is black or grayish black, with 45-58 white ring patterns, alternating black and white. The white ring pattern is 1-2 rows of scales wide on the back, and gradually widens toward the ventral surface. The black ring pattern is 3-5 rows of scales wide, and a ridge ridge is obviously raised in the middle of the back. The ridge scale is expanded to be hexagonal, the back scale is fine and dense, with 15 rows of scales throughout the body and one row of scales under the tail. The smell is slightly fishy and the taste is slightly salty.
[extract] according to the hot leaching method under the alcohol soluble extract determination method (general rule 2201), using dilute ethanol as solvent, it shall not be less than 15.0%.
[nature, taste and meridian tropism] sweet, salty and warm; . .
[functions and indications] dispel wind, unblock collaterals, and stop spasm. It is used for rheumatism, numbness and contracture, middle vent, squint, hemiplegia, convulsion and spasm, tetanus, leprosy and scabies.
[usage and dosage] 2 ～ 5g. Swallow 1 ～ 1.5g of powdered flour.
[storage] put it in a dry place to prevent mold and moth.

2、 Chemical constituents of the white flower snake

The snake body contains 21 elements, including protein, fat, amino acids, calcium, phosphorus, magnesium, iron, aluminum, zinc, strontium, titanium, manganese, vanadium, copper, etc. The ash content of snake body is 19%, the drying loss is 11.63% - 12.45%, the water-soluble extract is 1.36% - 19.70%, the 95% ethanol extract is 0.54% - 5.40%, and the bile containsCholic acid。
Bungarus Bungarus venom contains α - Bungarus toxin with a relative molecular mass of about 28500, consisting of 180 amino acid residues and 20 cysteines. . However, β - bungarotoxin has a completely different configuration. It contains β 1-bungarotoxin with a relative molecular mass of about, 21000, and is treated with 2-mercaptoethanol. It is divided into two polypeptide chains. The a chain is composed of 120 amino acids, contains 13 cysteines, and has a relative molecular mass of about 1300. The N-terminus isL-asparagine， The C-terminus is glutamine; The B-chain is composed of 60 basic acid residues, containing 7 cysteines, with a relative molecular mass of 7000 and an N-terminal ofL-arginine， C-terminal isL-Proline ， A. . The snake venom also contains K2 bungarotoxin and K3 bungarotoxin. In addition, it also contains guanosine and phospholipase A2.

3、 Pharmacological action of white flower snake

1. neuromuscular blocking effect. It is generally believed that Bungarus venom has peripheral curare like effect. α - bungatotoxin or α - bungatotoxin acetate (1 × 10 (-5) g) contained in the venom completely blocked the isolated rat septal muscles in vitro. Alpha bungarotoxin can also effectively block the response of frog rectus abdominis muscle to choline acetate (ACh). The neuromuscular blocking effects of alpha bungarotoxin on rat septal muscle, chicken neck digastric muscle and frog sciatic nerve sartorius muscle were irreversible.

In the study of the neuromuscular blocking effect of 13 Bungarus venom components, it was found that three components had no effect, four components had strong postsynaptic blocking effect, three components had strong postsynaptic blocking effect, and five components had presynaptic blocking effect. It was also reported that 11 lethal protein components were isolated from the venom of Bungarus multicinctus, 9 of which were called α - Bungarus toxin, β - Bungarus toxin and toxins 7, 8, 9a, respectively. 11-14; .

The mechanism of neuromuscular blockade was thought to inhibit the release of ACh from nerve terminals in the early stage. Later, it was found that the β - neurotoxin in the venom of Bungarus multicinctus, which can block the presynaptic transmission of rat septal muscles, could reduce its ability to store norepinephrine (NE), γ - aminobutyric acid (GABA), 5-HT and choline when incubated with rat brain synaptosomes at 55 μ g/ml, while promoting the release of accumulated NE and Gana, indicating that this toxin mainly affects the storage of neurotransmitters. It was also reported that five synaptotagmites (β 1, β 2, β 3, β 4 and β -ceruleotoxin) in the venom of Bungarus multicinctus could cause a rapid decrease in the endplate potential, followed by a temporary increase and subsequent decrease until the transmitter release was completely eliminated. This effect was related to the phospholipase A activity of the toxin. All presynaptic neurotoxins have Ca2 + - dependent phospholipase A (phosphohpasea) activity, which plays an important role in the neuromuscular blockade of this toxin.

2. ganglion blocking effect two α - toxins (bgt3.1 and 3.3) in Bungarus Bungarus venom can reduce the sensitivity of ciliary ganglion nerve cells to a in cell culture. When the Neurogen was incubated with one of the two toxins at a concentration of 10 (-7) mol/l at 37 ℃ for 1h, the reactivity of nerve cells to ACh was inhibited by more than 90%. When the toxin is washed away for 1-2h, the receptivity can be partially restored. The venom component Ⅱ of Bungarus multicinctus can be divided into Ⅱ - S2 (α - bungarotoxin) with a relative molecular mass of 9000 and Ⅱ - S2 with a relative molecular mass of 15000. At 1 μ g / ml, it can block neuromuscular conduction, but can not block the nicotinic reaction of sympathetic ganglia in rats; Ⅱ -s1 could block ganglion transmission, but could not block neuromuscular transmission at 1 μ g/ml. K-bungarotoxin in the venom of Bungarus multicinctus is a strong inhibitor of nicotinic transmission in the chick ciliary ganglion. At 75nmol/l, it can produce a reversible and comprehensive ganglion blocking effect lasting for several hours, and its blocking site is the same as that of α - bungarotoxin. K2 and K3 bungarotoxin isolated from the venom of Bungarus multicinctus are two novel nicotinic receptor blockers for chick ciliary ganglion neurons. The weaker K3 bungarotoxin can completely block nicotinic transmission for 60min at 250nmol/l. It was also reported that β - bungarotoxin could not block the synaptic transmission of chick ciliary ganglion at 50 μ g/ml, while another neurotoxin (toxin f) could block this ganglion at 1-3 μ g /ml, and could block the depolarization of ganglion caused by choline chloride (carbacho). Experiments have proved that the ganglion blocking effect of toxin f belongs to the postsynaptic mechanism. Toxin f can also block the nicotinic synaptic shock of cultured sympathetic neurons in the superior cervical ganglion of neonatal rats, and the concentration required to block most of the nicotinic potential is 40nmol/l. Dihydrovdo- β -erythroidin can resist the ganglionic blocking effect of toxin.

3. respiratory enzyme inhibition the venom component of Bungarus multicinctus with high phospholipase A activity is a very strong inhibitor of Xiaopai acid oxidase and racquet acid cytochrome c reductase in mouse heart homogenate, while hyaluronic acid dehydrogenase and cytochrome oxidase are less sensitive to these venoms

4. other effects Silver Ring snake venom can also inhibit the respiratory center and cause gastrointestinal paralysis and myocardial damage. At the concentration of 10 μ g/ml, the cardiotoxin like protein contained in the venom of Bungarus multicinctus can cause skeletal muscle contraction in chickens and mice, depolarize mouse septal muscles, inhibit spontaneous atrial contraction and electrical conduction of ventricular muscle strips in rats, and directly hemolyze guinea pig red blood cells. These effects are similar to the cardiotoxicity of eye snake venom. Phospholipase A2 contained in the venom of Bungarus multicinctus can significantly inhibit the binding of rat meninges to substance P with an IC50 of 10 (-8) mol/l.

5. toxic Bungarus multicinctus venom is a severe neurotoxin. When bitten by Bungarus multicinctus, there is only numbness in the local area. Once neurological symptoms occur, severe cases will cause respiratory paralysis, and death will often occur if the rescue is not proper. The typical neurotoxic symptoms are that the bite site is not painful, itchy, or red and swollen. A few hours later, when the disease occurs, it will become delirious, paralyzed, and dyspnea. Finally, the patient will die of respiratory paralysis. The LD50 of β - neurexin, which has the effect of presynaptic neuromuscular blockade of rat septal muscles, to mice is 0.1mg/kg. The LD50 of cardiotoxin like protein in Bungarus multicinctus venom injected intraperitoneally into mice was 2.5 (1.9-3.2) mg/kg.