What Is Thiosinaminum?

Vitamin B1 (Vitamin B1, VB1), also known as thiamine, is the first water-soluble vitamin purified by people. The chemical name is 3-[(4-amino-2-methyl-5-pyrimidinyl) -methyl ] -5-2-Hydroxyethyl) -4-methylthiazolium hydrochloride, which has the function of maintaining normal glucose metabolism. It is often used clinically to prevent and treat beriberi caused by lack of VB1. Adjuvant treatment of ill embolism. ^[1]

Thiamine often appears in the form of its hydrochloride salt ^[2]

Vitamin B1 used clinically is a chemically synthesized product. In the cell ^[5]

Alcohol-related vitamin B1 deficiency is one of the most common clinical causes of vitamin B1 deficiency, known as Wernicke-Korsakoff's Syndrome (WKS). In addition to patients with significant cognitive loss and memory loss In addition, the intracerebral lesion is selective neuron death, and KKGHC activity is significantly reduced, accompanied by neurofibrillary tangles similar to those in patients with Alzheimer's disease. Pathological changes in mouse brain caused by TD first appeared in the subthalamic thalamic nucleus (SmTN) of the thalamic midline, showing selective neuron death, hypertrophy and proliferation of microglia, and expression of oxidative stress Heme oxyge-nase-1 (HO-1), vascular endothelial cells express intercellular adhesion molecule-1 (ICAM-1), and astrocytes appear later Hyperplasia with hemorrhagic foci and amyloid accumulation in the diseased brain area. When vitamin B1 is deficient, the tricarboxylic acid cycle is impaired, pyruvate and lactic acid accumulate, and ATP production is hindered. First, it affects nerve tissues that rely mainly on sugar metabolism to provide energy. TD can cause oxidative stress in vivo and in vitro, and is a classic model for studying selective neuronal death caused by brain metabolic disorders. Further research has shown that mitochondrial dysfunction, endoplasmic reticulum stress, inflammation and immune factors are all involved in the neuronal death process caused by TD. ^[4]

The amyloid hypothesis is the core doctrine of Alzheimer's disease (AD). -amyloid polypeptide is a natural product of physiological metabolism and is formed by amyloid precursor protein (APP) catalyzed by different endoproteinases. There are three main proteases in the cleavage process of APP, which are called -secretase, -secretase and -secretase according to the order in which they are found. The shearing process of APP can be divided into amyloid pathway and non-amyloid pathway. In the amyloid pathway, -secretase first cleaves APP into two fragments: the free-form N-terminal protein fragment (sAPP) and the C-terminus (C99) of -amyloid peptide-containing peptide remaining on the membrane. The -secretase complex further cleaves the C-terminus to produce A and APP intracellular domain fragments (AICD). The non-amyloid pathway is mainly that APP is cleaved by -secretase to produce the free form N-terminal sAPP and C-terminal fragment C83. Because the site of -secretase is located inside the A domain, A cannot be produced. . C83 is further cleaved by the -secretase complex to generate P3 and AICD. Most full-length A is composed of 40 amino acids (A40), and a small part (about 10%) is composed of 42 amino acids (A42). A42 is easier to aggregate due to the addition of two hydrophobic amino acid residues, and is also the main component of amyloid plaque. A itself can aggregate spontaneously to form multiple coexistent forms. It can form oligomers from 2 to 6 peptides and further fuse to form intermediate aggregates. It can also form fibers and arrange them as -sheets to further form insoluble fibers , Which eventually leads to the formation of amyloid plaques. Soluble oligomers and amyloid intermediate aggregates are the two main forms of toxic A, and the amyloid plaques formed by their aggregation are the main reasons affecting the normal function of neurons. ^[4]

Early research has shown that high doses of thiamine help restore memory and cognitive function in patients with early Alzheimer's dementia. Subsequently, studies by other researchers have also shown that vitamin B1 supplementation can improve the condition of patients with Alzheimer's dementia. However, some studies have found that vitamin B1 supplementation does not improve the condition of Alzheimer's disease. The reason may be that the bioavailability of vitamin B1 is not high, which prevents it from functioning well. ^[4]

There are several main sources of VB1. First, grains, beans, hard fruit and dried yeast are rich in content, so brown rice and bran flour are higher in VB1 content than polished white rice. Second, the animal's internal organs such as liver, Kidney, lean meat and egg yolk contain VB1; third, some vegetables such as celery and laver have different levels of VB1. ^[6]

Vitamin B1 is formed by combining a pyrimidine ring and thiazole ring through a methylene group. The synthetic routes reported in the literature can be divided into two categories: convergent and straight

VB1 Vitamin b1, VB1 and sour are not afraid of alkali and should not be fried at high temperature

Commonly used thiamine hydrochloride is a white crystalline powder, which can cause deterioration in alkaline drugs such as phenobarbital sodium, sodium hydrogen sulfate, and potassium citrate, and is more stable in acidic solutions. But also remind everyone that because VB1 is easily decomposed in neutral or alkaline, when the pH value is greater than 7, or heated, most or even all of VB1 decomposes. As a result, vitamin B1 in foods that are fried, baked, or smoked at high temperatures can lose a lot. ^[6]

VB1 Vitamin B1 heavy drinking can easily reduce VB1

Vitamin B1 is indispensable for breaking down alcohol in the body. However, if you drink alcohol for several days, the absorption capacity of vitamin B1 will be reduced, people will easily lose understanding and judgment, easily get bored, forget about things, can not stand the temptation, and then develop into alcoholic psychosis. It can even tremble with fingers, produce hallucinations and delusions, and eventually develop into severe memory loss and even lethargy and seizures. So remind people to add enough VB1 when drinking. If you do not ingest vitamin VB1 in large quantities when drinking alcohol, brain nerves will become impaired. Some people suggest that catfish is the best because of its rich VB1 to prevent drunkenness. ^[6]

Vitamin b1 vitamins and anti-vitamins

There are countless opposing things in nature, such as adding and subtracting positive and negative numbers, assimilation and alienation in the human body. The same is true for vitamins, as there are opposite substances. Anti-vitamins are often similar to the structure of the corresponding vitamins, they interfere with the metabolism of vitamins in the body, making vitamins unable to function properly. For example, there is a vitamin B1 enzyme in raw fish, which can break down vitamin B1 and make it ineffective. Only anti-vitamin B1 substances can not break down vitamin B1 after cooking fish. Although anti-vitamins are the opposite of vitamins, they are not all bad for humans. The key is how to use them properly. For example, drugs that destroy microorganisms are all anti-vitamins. People use them to inhibit bacteria or other microorganisms to achieve therapeutic effects. The presence of anti-vitamins reveals that when taking certain anti-vitamin drugs, we should add corresponding vitamins or take other measures to prevent vitamin deficiency. ^[6]