CN111700906A - Application of hydrogen molecule and construction method of mouse model for relieving inflammatory bowel disease - Google Patents

Application of hydrogen molecule and construction method of mouse model for relieving inflammatory bowel disease Download PDF

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CN111700906A
CN111700906A CN202010430080.XA CN202010430080A CN111700906A CN 111700906 A CN111700906 A CN 111700906A CN 202010430080 A CN202010430080 A CN 202010430080A CN 111700906 A CN111700906 A CN 111700906A
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hydrogen
normal saline
intestinal
bowel disease
inflammatory bowel
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葛丽
亓杰
阮真真
孙雪强
刘淑曼
李鹏飞
陈浩
王诗阳
徐新荣
邵波
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Shandong First Medical University and Shandong Academy of Medical Sciences
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    • A61P1/04—Drugs for disorders of the alimentary tract or the digestive system for ulcers, gastritis or reflux esophagitis, e.g. antacids, inhibitors of acid secretion, mucosal protectants

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Abstract

The present invention relates to exogenous hydrogen molecules (H)2) The field of hydrogen medical research intervening in improving the intestinal flora and the metabolism thereof to promote the steady recovery of the intestinal mucosa. Specifically, the invention provides an application of hydrogen molecules in preparing a medicine for promoting intestinal tract short-chain fatty acid generation and a construction method of a mouse model for relieving inflammatory bowel disease by using the hydrogen molecules, wherein the construction method comprises the following steps: exogenous H is given in a whole-course gastric lavage and intraperitoneal injection hydrogen-rich normal saline mode22.5% dextran sodium salt water for 7 days until mice acute UC, H2The intervention group increased HRS pretreatment of healthy animals for 10 days before modeling, HRS treatment for 17 days in total, and modeling was completed. The invention is used for treating healthy animals by increasingHRS preprocessing, finding H2Effectively exerting a time window for relieving UC symptoms; and found H2Targeting intestinal microbiota, and maintaining the biological effect of intestinal mucosal immune homeostasis by promoting intestinal SCFAs production, to alleviate acute ulcerative colitis. The establishment of the model system can provide theoretical and experimental basis for the clinical research of hydrogen medicine and the development of new UC treatment strategies in the future.

Description

Application of hydrogen molecule and construction method of mouse model for relieving inflammatory bowel disease
Technical Field
The present invention relates to exogenous hydrogen molecules (H)2) The field of hydrogen medical research intervening in improving the intestinal flora and the metabolism thereof to promote the steady recovery of the intestinal mucosa. In particular to application of hydrogen molecules and a construction method of a mouse model for relieving inflammatory bowel disease.
Background
Inflammatory Bowel Disease (IBD) is a chronic recurrent inflammatory Disease of intestinal tract with ulcer of intestinal mucosa as the main pathological feature, mainly including Crohn's Disease (CD) and Ulcerative Colitis (UC), which are abnormal immune response and chronic intestinal inflammation caused by complex interaction of genetic factors, environmental factors, intestinal flora and host immune system, but the exact pathogenesis is not fully elucidated, and the treatment is difficult, and the physical and mental health and life quality of patients are seriously affected. At present, the increasing trend of IBD patients in Asian countries is obvious by the integration of civil economic development and western diet, and clinical and basic research of IBD has become a research hotspot of Asian digestive pathologist. The research on the pathogenesis and novel clinical auxiliary therapeutic agents of the traditional Chinese medicine composition can help to improve the life quality of patients.
It has been reported in the literature that IBD mice/rats intestinal mucosal lesions can be relieved by drinking Hydrogen Rich Water (HRW) or injecting hydrogen rich normal saline (HRS) intraperitoneally, but H is caused2The research system of animal models which play a significant role is not complete, and the action mechanism of the animal models for relieving IBD is not clear. For one, the above literature reports are all performed during or after modeling2Treatment, the above document considers H2The UC inflammatory injury is relieved through the antioxidant and anti-inflammatory properties of the UC, but whether the specific action mechanism is just the same or not is not reported, and no deeper research is carried out.
Disclosure of Invention
In order to solve the technical problems, the invention provides application of hydrogen molecules and a method for constructing a mouse model for relieving inflammatory bowel disease. By adding the pretreatment of HRS (high resolution S) of healthy animals, H is found2Effectively exert the time window for relieving UC symptoms and develop H2The new strategy of clinical adjuvant therapy provides experimental basis; the second purpose of the invention is to research the intestinal characteristics of the mouse under the model based on the model and construct H2System for research of medical effects, finding H2The new mechanism of action, i.e. H2Can promote the production of Short Chain Fatty Acids (SCFAs) in intestinal tract.
The technical scheme adopted by the invention is as follows: an application of hydrogen molecules, in particular to an application of hydrogen molecules in preparing medicines for promoting the generation of intestinal tract short-chain fatty acids.
Further, the hydrogen molecular carrier is in the form of nano bubble hydrogen-rich normal saline.
Further, the preparation method of the hydrogen-rich normal saline is to use a multifunctional hydrogen molecule generator to convert pure H2Dissolving in normal saline for 20min to obtain H2Saturated hydrogen-rich normal saline.
Further, the hydrogen-rich normal saline is H2The concentration is not less than 3.0 ppm.
A method for constructing a mouse model for relieving inflammatory bowel disease by hydrogen molecules comprises the following steps:
(1) preparing nano bubble hydrogen-rich normal saline;
(2) a male C57BL/6J mouse which is 6-8 weeks old and 20-22g in weight is adopted to be treated as follows, normal drinking water is changed to drinking 2.5% sodium dextran sulfate (DSS) from the 11 th day after the injection and the intragastric administration of hydrogen-rich normal saline for 1-17 days, and the drinking is carried out for 7 days, so that the mouse model of the hydrogen molecule relieving inflammatory bowel disease is obtained.
Furthermore, the nano-bubble hydrogen-rich normal saline is freshly prepared every time, so that H can be guaranteed2The concentration was 3.0 ppm.
Furthermore, the administration mode of the hydrogen-rich normal saline is intraperitoneal injection combined intragastric administration, the dosage and the time of the intraperitoneal injection are 5mL/kg, AM9:00 is 1 time/day; the gavage dose and time were 10mL/kg, AM9:00 and PM15:00, 2 times/day.
Earlier stage research of the application finds that H before UC modeling is increased2Preprocessing, and performing H after modeling2The treatment group can inhibit weight loss and relieve inflammatory injury to a greater extent. In addition, exogenous H is generated under the 'mouse model system for relieving inflammatory bowel disease by hydrogen molecules' constructed by the application2The generation of SCFAs can be promoted by up-regulating the abundance of SCFAs-producing bacteria specially in the intestinal tract, the metabolism reprogramming of the colonic epithelial cells is regulated and controlled in time and space, the recovery of the anaerobic environment of the intestinal cavity and the immune steady maintenance of the intestinal mucosa are promoted, and the inflammatory injury of a UC mouse is relieved finally by improving the microbial hydrogen metabolism in the intestinal tract. The model system uncovers H2Acting microorganism and immunological mechanism, displaying exogenous H2The interference can improve the unique research view of the UC intestinal tract 'microbial hydrogen metabolism'. Thus, look for H2Effectively exerting the time window for relieving UC symptom and establishing a stable and effective novel H2Intervention model system, development of novel H2Clinical adjuvant treatment strategies are of great significance.
Drawings
FIG. 1 is a schematic view showing the various embodiments of the present invention.
Fig. 2 is a graph of the change in body weight of mice during the modeling.
FIG. 3 is a statistical chart of colon length measurements.
FIG. 4 is a statistical chart of the expression level changes of the serum proinflammatory cytokines TNF-alpha and IL-6.
FIG. 5 is a stained light image of a paraffin section HE of distal colon tissue.
FIGS. 6a and 6b show that 16s rDNA sequencing analysis of HS treatment inhibited the decrease of species diversity of UC mouse intestinal flora.
FIG. 7 is a 16s rDNA sequencing analysis of the regulatory effect of HS treatment on the species abundance of UC mouse intestinal flora Phylum taxonomic level (Phylum) and Order taxonomic level (Order).
FIGS. 8a, 8b, and 8c are graphs showing the control effect of 16s rDNA sequencing analysis HS treatment on the enrichment of UC mouse intestinal flora classification level (Family) species.
FIGS. 9a and 9b are graphs showing the effect of 16s rDNA sequencing analysis of HS treatment on the control of UC mouse intestinal flora classification level (Genus) species abundance.
FIGS. 10a, 10b, and 10c are graphs of the control effect of 16s rDNA and metagenomic sequencing analysis HS treatment on the Species abundance at the UC mouse intestinal flora classification level (specifices).
FIGS. 11a, 11b, 11c are graphs of gas chromatography combined with mass spectrometry (GC-MS) for determining the content of SCFAs in intestinal tract.
FIG. 12 is a graph showing the expression level of the colonic epithelial metabolic marker signaling molecules iNOS and PPAR- γ.
FIG. 13 is a light image of Pimonidazole (PMDZ) immunofluorescent stained colonic epithelium.
Fig. 14 is a scanned electrical mirror image of the mucosal mucus layer of the colon.
FIG. 15 is a graph showing the measurement of the expression levels of claudin-1 and occludin between intestinal epithelial cells.
FIG. 16 is a diagram of the detection of the barrier function of the intestinal epithelium in the fluorescein isothiocyanate (FITC-dextran) intestinal epithelium permeability experiment.
Detailed Description
The embodiments of the present invention will be described in further detail with reference to the drawings and examples.
(1) Construction of a mouse model for relieving inflammatory bowel disease by hydrogen molecules.
Preparing nano bubble hydrogen-rich normal saline: by usingMultifunctional Hydrogen molecule Generator (NB-B81, Nanobab technologies, Shanghai) purified H2Dissolving in Normal Saline (NS) for 20min to obtain H2Saturated Hydrogen Rich Saline (HRS). HRS was freshly prepared just before use in each experiment to ensure H2The concentration was 3.0 ppm.
B. Animal models and H2A medical effect research system is constructed by adopting male C57BL/6J mice with the weight of 20-22g and the age of 6-8 weeks, an animal group, namely ① healthy Control group (Control), which is not treated and is fed and drunk normally in the whole process, ② sham operation Control group (Vehicle), wherein mice are injected with NS (i.p. 5mL/kg, AM9:00, 1 time/day) and are filled with NS (10mL/kg, AM9:00 and PM15:00, 2 times/day) in the abdominal cavity for 17 days, and are fed and drunk normally in the normal mode for 17 days, ③ DSS induces an enteritis group (DSS), which is used for drinking DSS water from 11 days and drinking DSS water for 7 days, induces and establishes a mouse acute UC model, and the normal drinking water is changed to drinking 2.5% (wt/vol) DSS (36-50kDa, MP Biomedicals, DSS, USA) water in 11-17 days, and other treatments are similar to that of Vehicle H + ④1The group comprises injection and gastric perfusion NS on days 1-10, HRS on days 11-17, and other operations are the same as DSS group ⑤ DSS + H2Group i.e. the hydrogen molecule-relieved inflammatory bowel disease mouse model: increasing 10 days of pretreatment of HRS before modeling DSS, namely injecting and intragastrically HRS in 1-17 days, and performing other operations in the same DSS group. At the end of 17 days, each group of animals was sacrificed. The specific scheme design is shown in figure 1.
(2) H2Determination of alleviating inflammation injury of UC mice:
① measurement of body weight of mice during modeling and colon length after modeling, HRS treatment was able to alleviate weight loss and colon shortening, and DSS + H2Group ratio DSS + H1The group relief effect is better.
Secondly, after the model construction is finished, taking blood at the canthus in the eyes of the mouse, centrifuging and taking supernatant, and carrying out expression detection on TNF-alpha and IL-6 of the serum of the mouse of different treatment groups according to the steps of an ELISA kit specification, wherein HRS treatment obviously inhibits the expression of proinflammatory cytokines TNF-alpha and IL-6 as shown in figure 4.
③ mouse distal colon tissue, paraffin sectionHE staining, and observing intestinal mucosa injury, as shown in FIG. 5, the mucosa of Control and Vehicle groups is intact, the intestinal glands are abundant, the DSS group has epithelial exfoliation and necrosis, the intestinal glands are decreased, and DSS + H2The damage of the intestinal mucosa is obviously relieved.
(3) H2Determination of intestinal flora of targeted UC mice:
before sacrifice, fresh fecal tissue was subjected to 16s rDNA and metagenomic sequencing to analyze the species abundance and diversity change of intestinal flora as shown in FIGS. 6a and 6b, and the diversity analysis of α and β showed that HRS treatment inhibited the decrease in species diversity of UC mouse intestinal flora after DSS actionProteobacteria) Increased abundance promotes Bacteroides (A) and (B)Bacteroidetes) And the phylum of firmicutes (Firmicutes) Recovery of abundance (see fig. 7); at the eye level, HRS treatment promoted obligate anaerobes, clostridiales: (Clostridiales) Increase in abundance (see fig. 7); at the family level, HRS treatment promoted butyric acid producing bacteria, Spirochaceae: (Lachnospiraceae) Beneficial bacteria in intestinal tract (Rikenellaceae) AndS24_7an increase in abundance. Furthermore, HRS treatment inhibited DSS-induced enterobacteriaceae (a) as a potentially pathogenic bacteriumEnterobacteriaceae) And Bacteroides family (Bacteroidaceae) Increase in abundance (see fig. 8a, 8b, 8 c); on the genus level, HRS treatment promoted butyric acid producing bacteria, Proteus (A)Prevotella) Increase in abundance and inhibition of potentially pathogenic Escherichia bacterium (A), (B)Escherichia) Increase in abundance (see fig. 9a, 9 b); at the seed level, HRS treatment inhibited mucolytic bacteriaAkkermansia muciniphila(A.muciniphila) AndRuminococcus gnavus(R.gnavus) And opportunistic pathogenic E.coli: (E.coli) Increase of abundance and promote butyric acid producing bacteriaEubacterium ventriosum(E.ventriosum)，Roseburia hominis(R.hominis) AndRoseburia faecis(R.hominis) Increase in abundance (see FIGS. 10a, 10b, 10 c).
(4) H2Measurement of regulation and control effects on generation of UC mouse intestinal short-chain fatty acids (SCFAs):
before sacrifice, fresh fecal tissue is taken and assayed for SCFAs content, including acetate (acetate), propionate (propionate), butyrate (n-butyrate), isobutyrate (iso-butyrate), pivalate (n-valete) and isovalerate (iso-valete) using gas chromatography coupled mass spectrometry (GC-MS).
As shown in FIGS. 11a, 11b and 11c, exogenous HRS treatment can up-regulate the production of acetate (acetate) and butyrate (n-butyrate) in UC mice intestinal tract, the content of SCFAs in other species, and the enteritis group (DSS) and HRS treatment group (DSS + H)2) There was no significant difference. Therefore, it is considered that bacterial metabolites of fecal samples are highly sensitive to the inflammatory state of mice, and the measurement of SCFAs content thereof can sufficiently show the effect of HRS.
(5) H2Measurement of intestinal epithelial metabolism of reshaped UC mice:
① Nuclear proteins were extracted from colon tissue with Nuclear protein extraction reagent and analyzed by iNOS, PPAR- γ protein expression by western blot As shown in FIG. 12, HRS treatment was able to down-regulate pro-inflammatory Signal iNOS expression, relieving inhibition of inflammatory injury on PPAR- γ, indicating that in metabolic reprogramming for colonic epithelial cell injury repair, H is2The generation of butyrate can be promoted by increasing the abundance of the intestinal butyric acid producing bacteria, PPAR-gamma signals are activated, and the colon epithelial cell metabolism is induced to develop towards β -oxidation, so that the recovery of the anaerobic environment of the intestinal cavity is promoted.
② Paraffin section is prepared from distal colon tissue, immunofluorescence is used to detect colonic epithelial hypoxia degree, Pimonidazole (PMDZ) probe (red) shows hypoxia level, as shown in FIG. 13, the stronger red fluorescence intensity indicates higher hypoxia degree of cell, DSS + H2Compared with the DSS group, the red fluorescence signal of the colon epithelium is obviously enhanced, and the epithelial hypoxia state is obviously improved, which shows that the HRS treatment promotes the recovery of the intestinal cavity anaerobic environment.
(6) H2Measurement for enhancing intestinal barrier of UC mice:
firstly, the mucosal surface of the intestine is scanned for electrical mirror image to observe the change of the thickness of the mucus layer, and as shown in fig. 14, the HRS treatment relieves DSS-induced mucus reduction on the mucosal surface of the colon, thereby enhancing the intestinal barrier function.
Secondly, total protein is extracted from colon tissues by RAPA lysate, expression conditions of intestinal epithelial intercellular tight junction protein claudin-1 and occludin are detected by western blot, as shown in figure 15, reduction of expression quantity of the intestinal epithelial intercellular tight junction protein claudin-1 and occludin induced by DSS is inhibited by HRS treatment, and thus the intestinal barrier function is enhanced.
③ fluorescein isothiocyanate (FITC-dextran) intestinal epithelial permeability test to detect the intestinal epithelial barrier function. Peripheral blood FITC-dextran signal (excitation wavelength 488nm, emission wavelength 520nm) was detected after 4h by intragastric 4kDa fluorescein isothiocyanate (FITC-dextran). As shown in FIG. 16, the FITC-dextran signal was significantly reduced in the DSS + H2 group compared to the DSS group. It was shown that HRS treatment enhanced the intestinal epithelial barrier function in UC mice.

Claims (7)

1. Use of hydrogen molecules, characterized in that: application of hydrogen molecules in preparation of medicines for promoting generation of intestinal short-chain fatty acids.
2. Use of hydrogen molecules according to claim 1, characterized in that: the hydrogen molecular carrier is in the form of nano bubble hydrogen-rich normal saline.
3. Use of hydrogen molecules according to claim 2, characterized in that: the preparation method of the hydrogen-rich normal saline comprises the step of utilizing a multifunctional hydrogen molecule generator to convert pure H2Dissolving in normal saline for 20min to obtain H2Saturated hydrogen-rich normal saline.
4. Use of a hydrogen molecule according to claim 3, characterized in that: h in the hydrogen-rich normal saline2The concentration is not less than 3.0 ppm.
5. A method for constructing a mouse model for relieving inflammatory bowel disease by hydrogen molecules is characterized by comprising the following steps:
(1) preparing nano bubble hydrogen-rich normal saline;
(2) a male C57BL/6J mouse which is 6-8 weeks old and 20-22g in weight is adopted to be treated as follows, hydrogen-rich normal saline is injected and perfused for 1-17 days, 2.5 percent of sodium dextran sulfate is drunk from the 11 th day, and the drinking time is 7 days, so that the mouse model of the hydrogen molecule relieving inflammatory bowel disease is obtained.
6. The method for constructing a mouse model for relieving inflammatory bowel disease by hydrogen molecules according to claim 5, wherein the method comprises the following steps: the nano bubble hydrogen-rich normal saline is freshly prepared every time, and can ensure H2The concentration was 3.0 ppm.
7. The method for constructing a mouse model for relieving inflammatory bowel disease by hydrogen molecules according to claim 5, wherein the method comprises the following steps: the administration mode of the hydrogen-rich normal saline is intraperitoneal injection combined intragastric administration, the dosage and the time of the intraperitoneal injection are 5mL/kg, AM9:00 and 1 time/day; the gavage dose and time were 10mL/kg, AM9:00 and PM15:00, 2 times/day.
CN202010430080.XA 2020-05-20 2020-05-20 Application of hydrogen molecule and construction method of mouse model for relieving inflammatory bowel disease Withdrawn CN111700906A (en)

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Cited By (4)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
CN112870218A (en) * 2021-01-27 2021-06-01 山东中农普宁药业有限公司 Mixture for the treatment of Staphylococcus aureus mastitis
CN113331137A (en) * 2021-05-24 2021-09-03 山东省药学科学院 Colitis composite immunologic adjuvant and application method thereof
CN114391511A (en) * 2021-12-25 2022-04-26 遂宁市中心医院 Modeling method of DSS-induced inflammatory bowel disease susceptible animal model
CN115634235A (en) * 2022-07-06 2023-01-24 中国人民解放军海军军医大学 Application of molecular hydrogen in preparation of medicine for preventing or relieving jellyfish sting

Cited By (6)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
CN112870218A (en) * 2021-01-27 2021-06-01 山东中农普宁药业有限公司 Mixture for the treatment of Staphylococcus aureus mastitis
CN113331137A (en) * 2021-05-24 2021-09-03 山东省药学科学院 Colitis composite immunologic adjuvant and application method thereof
CN113331137B (en) * 2021-05-24 2023-02-03 山东省药学科学院 Colitis composite immunologic adjuvant and application method thereof
CN114391511A (en) * 2021-12-25 2022-04-26 遂宁市中心医院 Modeling method of DSS-induced inflammatory bowel disease susceptible animal model
CN114391511B (en) * 2021-12-25 2022-09-23 遂宁市中心医院 Modeling method of DSS-induced inflammatory bowel disease susceptible animal model
CN115634235A (en) * 2022-07-06 2023-01-24 中国人民解放军海军军医大学 Application of molecular hydrogen in preparation of medicine for preventing or relieving jellyfish sting

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