Research Progress of HSP70 and Chronic Atrophic Gastritis

Chronic atrophic gastritis is still one of the main diseases threatening human health, and CAG patients have an increased risk of gastric cancer. Heat shock protein 70 protects the gastric mucosa by inhibiting the activation of protein kinase JNK and NF-kB inflammatory pathways in chronic atrophic gastritis. At present, HSP70 has been clinically used in the treatment and prevention of chronic atrophic gastritis. This article reviews the research on the relationship between HSP70 and chronic atrophic gastritis in recent years.


Introduction
Chronic atrophic gastritis (CAG) means that the epithelial cells of the gastric mucosa are repeatedly and long-term invaded, which firstly causes local inflammation of the gastric mucosa, which in turn affects the blood circulation of the gastric mucosa and destroys the gastric mucosal barrier. The proper glands began to shrink, the mucosa became thinner and even accompanied by metaplasia and dysplasia of the intestinal epithelium. CAG is the result of multiple factors, and helicobacter pylori infection is the main pathogenic factor. Studies have shown that the gastric mucosa activates a variety of defense systems when stimulated by food, smoking, alcohol, helicobacter pylori and other factors. The heat shock response system is one of the defense functions in the acute phase, and the most important type of heat shock protein Heat shock proteins (HSP) is a family of HSP70 with a molecular weight of about 70kD.
It reduces stress by assisting in protein repair, inhibiting oxidative damage, and regulating gastric mucosal blood flow.

HSP70 Classification and Molecular Structure
The HSP70 family is the most conserved, most important and abundant class of heat shock proteins, which consists of 21 proteins.
HSP70 is mainly expressed in the cytoplasm of lamina propria glandular epithelial cells and mucosal epithelial cells, which can be subdivided into 4 types: Terminate the transcription of HSP70 gene [3].

Anti-Apoptosis
Apoptosis means that when cells are subjected to certain

Improve Cell Tolerance
HSP70 inhibits the activity of nuclear factor kappa B (NF-kB) promoters, so that the inflammatory factors tumor necrosis factor-α, interleukin (IL)-6 and IL-1β downstream of the signaling pathway the product is reduced and the cell inflammatory reaction process is reduced.

Anti-Oxidant Stress
Under stress conditions, the body produces a large number of oxygen free radicals, which act on cells, mitochondria, lysosomes and other biofilms, and reduce the ability to regulate Ca2+ in and out of cells, causing cytotoxicity. HSP70 inhibits the key enzyme that produces oxygen free radicals, namely nicotinamide adenine dinucleotide phosphate oxidase, inhibits the production of oxygen free radicals, and can also increase the level of endogenous

The Effect of HSP70 on Chronic Atrophic Gastritis
HSP70 exists in the gastric mucosa. The increased expression of HSP can cause the up-regulation of the expression of reduction oxidase 1 and oxidative synthetase, and reduction oxidase 1 increases the production of prostaglandin E2, which has a protective effect on the mucosa, while the catalytic product of oxidative synthetase is oxidized. Nitrogen can increase the blood flow of the gastric mucosa and is also a protective effect on the gastric mucosa.

Studies have shown that HSP70 can inhibit mucosal inflammation
and promote the healing of ulcers. At the same time, HSP70 can resist the effects of Helicobacter pylori-induced gastric mucosal cell apoptosis, weakened epithelial cell migration, reduced local blood flow, and inhibition of neovascularization. Wu Yong Mei et al. [4] showed that HSP70 is expressed in superficial gastritis, CAG, and gastric cancer tissues. HSP70 functions as a molecular chaperone,

HSP70 and CAG Treatment Physiotherapy
All objects (temperature higher than -273°C) can radiate infrared rays. The main thermal effect produced on the body is a series of biological effects produced through direct action and nerve reflex. In the study of Dai Jie et al. [5], the expression of HSP70 in the gastric mucosa of HSP70 and CAG rats after infrared irradiation was significantly different, and the expression rate reached 100%, and the expression level was also significantly increased. It can be seen that infrared radiation can treat CAG by promoting the expression of HSP70.

Chemotherapy
Polaprezinc is often used clinically to treat CAG. Polaprezinc is a chelate of L-carnosine and zinc, which induces the production of HSPs, thereby playing an anti-ulcer effect. As a heavy metal element, zinc can activate the metal response elements present in the HSP70 promoter region [6]. Therefore, zinc is believed to induce HSP synthesis by activating HSPs gene transcription.

TCM Treatment
According to the clinical manifestations of CAG, such as poor appetite and lack of food, delayed transport and chemistry, gastric pain, gradual weight loss, etc., it belongs to the category of "fullness" and "stomach pimple" in Chinese medicine. The diseased part Moxibustion is an important part of acupuncture and moxibustion therapy. Modern research has also shown that moxibustion has the effects of analgesia, improving blood gastric mucosal cell apoptosis index, which is significantly different from the model group and the control group. It indicates that moxibustion at Zusanli and Liangmen has a protective effect on the gastric mucosa of stress gastric ulcer. The mechanism may be that it promotes the synthesis of TGF-α, stimulates the proliferation of gastric mucosal cells, and inhibits cell apoptosis. This process may be similar to moxibustion. It is related to the induction of HSP70 expression [12].
In a word, HSP70 is a kind of molecular chaperone. The study of HSP70 in different degrees of chronic atrophic gastritis, overexpression and intracellular distribution in gastric cancer will further explore its molecular mechanism for the treatment of chronic atrophic gastritis and the prevention of gastric cancer.
Biological therapy provides theoretical basis. In addition, the heat shock protein peptide complex can also be used for the treatment of precancerous lesions of the digestive tract, tumor prevention and gene therapy, which is expected to improve patient survival rate, reduce trauma, greatly reduce medical expenses, and improve the quality of life.