CN116671633A - Application of hydrogen storage oyster calcium in special medical food, health care product and medicine for preventing and treating type I diabetes - Google Patents
Application of hydrogen storage oyster calcium in special medical food, health care product and medicine for preventing and treating type I diabetes Download PDFInfo
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- CN116671633A CN116671633A CN202310662640.8A CN202310662640A CN116671633A CN 116671633 A CN116671633 A CN 116671633A CN 202310662640 A CN202310662640 A CN 202310662640A CN 116671633 A CN116671633 A CN 116671633A
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- Prior art keywords
- hydrogen
- calcium
- hop
- oyster
- stz
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Classifications
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- General Health & Medical Sciences (AREA)
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Abstract
The invention discloses application of hydrogen-storing oyster calcium in special medical food, health-care product and medicine for preventing and treating type I diabetes, relates to the technical field of biology and medicine, and has obvious effect on preventing and treating type I diabetes by using the hydrogen-storing oyster calcium as a solid hydrogen carrier, being capable of reacting with water to generate hydrogen and sustainably releasing high-concentration hydrogen.
Description
Technical Field
The invention relates to the technical field of biology and medicine, in particular to application of calcium oyster hydrogen storage in foods, health products and medicines with special medical purposes for preventing and treating type I diabetes.
Background
Type i diabetes (Type I Diabetes Mellitus, T1 DM) is a chronic autoimmune disease characterized by insulin deficiency and resultant hyperglycemia. The disease is often due to autoimmune destruction, resulting in hyperglycemia and ketosis, and symptoms also include diuresis, frequent thirst, and weight loss. The rapid increase in research into type i diabetes has led to a wide understanding of many aspects of the disease over the past 25 years, including its genetics, epidemiology, immune and beta cell phenotypes, and disease burden. Currently, there are insulin or insulin analogue management and non-insulin drug therapies clinically, including metformin, glucagon-like peptide 1 receptor agonists, dipeptidyl peptidase 4 inhibitors and sodium-glucose co-transporter-2 (sglt 2) inhibitors to lower blood sugar, and in addition, islet function can be improved by pancreas or islet transplantation, gene therapy and stem cell therapy to improve islet beta cell function, ultimately achieving treatment and improvement of T1DM, but there is still a great gap for standardized clinical care of T1DM and reduction of the burden of disease-related complications. Although clinical treatment results in significant improvement in patient survival and health, healing of T1DM remains a significant challenge. Furthermore, despite technological advances, glycemic control is not optimized in most T1DM patients, making patients unsuited to modern therapies due to the high cost of basic care. Thus, there is a need for an economical and effective therapeutic regimen for alleviating and treating T1 DM.
The prior treatment technology has the defects that: insulin therapy requires daily injection therapy, consumes a great deal of money, cannot radically cure T1DM, and brings great challenges to life and economy of people. The non-insulin drug treatment can only partially relieve and not completely cure the T1DM, and the T1DM patient can also generate corresponding complications, so that the drug treatment is difficult to relieve and completely cure the development of the complications. The gene therapy, islet transplantation and stem cell transplantation therapy are huge in cost and cannot be applied to all T1DM patients, and the price of the medicine is high and cannot be borne by ordinary families, so that the need for an economical and practical treatment scheme capable of relieving the complications caused by T1DM and T1DM is urgent. Researchers have proposed novel treatment schemes, hydrogen treats T1DM, but hydrogen is unstable in water and cannot be stored for a long time, hydrogen-rich water adopts high pressure to inject hydrogen into water, once hydrogen in the pressure-free water can be quickly dissipated, the hydrogen cannot act in a living body for a long time, and the hydrogen cannot effectively act in the living body for a long time. The oyster calcium hydrogen storage is used as a solid hydrogen carrier, can react with water to continuously and efficiently release hydrogen, has sustainability and can maintain high-concentration hydrogen release for a long time, and the oyster calcium hydrogen storage can be used for treating type I diabetes.
Disclosure of Invention
The invention aims to provide application of calcium oyster hydrogen storage in foods, health products and medicines with special medical purposes for preventing and treating type I diabetes, so as to solve the problems in the background technology.
In order to achieve the above purpose, the present invention provides the following technical solutions: the method comprises the step of using the hydrogen storage oyster calcium as a solid hydrogen carrier, so that the hydrogen can be generated by reacting with water, and high-concentration hydrogen can be continuously released.
Furthermore, the oyster calcium hydrogen storage can reduce the oxidative stress of key metabolic tissues and improve the antioxidation function.
Further, the application of the hydrogen storage oyster calcium in treating and promoting the beta oxidation of fatty acid in brown adipose tissue, inhibiting the synthesis of lipid in liver and muscle tissue and improving the lipid metabolism of T1DM disease is provided.
Furthermore, the application of the hydrogen storage oyster calcium treatment to reducing STZ-induced type I diabetes kidney inflammatory response and the expression of inflammatory factors in serum in the aspect of improving T1DM disease inflammatory response is provided.
Compared with the prior art, the invention has the beneficial effects that:
1. the application of the calcium hydrogen storage oyster in treating and reducing STZ-induced oxidative stress of key metabolic tissues and improving the antioxidation function.
2. The application of the calcium hydrogen storage oyster in improving lipid metabolism of T1DM diseases by promoting STZ-induced brown adipose tissue fatty acid beta oxidation and inhibiting lipid synthesis of liver and muscle tissues.
3. The application of the calcium hydrogen storage oyster in treating and reducing the expression of inflammatory factors in the kidney and serum of STZ induced type I diabetes mellitus in improving the inflammatory response of T1DM diseases.
Drawings
FIG. 1 shows the in vitro sustained release of hydrogen from oyster calcium hydrogen storage (HOP);
FIG. 2 is a graph showing that calcium-stored-oyster-Hydrogen (HOP) treatment reduces fasting blood glucose and blood lipid and restores insulin levels in serum in STZ-induced T1DM mice;
FIG. 3 shows recovery of STZ-induced T1DM liver, perirenal fat and epididymal fat with weight specific gravity for calcium hydrogen storage (HOP) treatment, improving liver function;
FIG. 4 shows that calcium hydrogen storage oyster (HOP) treatment reduces active oxygen and oxidative stress in key metabolic tissues of STZ-induced T1DM mice;
FIG. 5 is a graph showing that calcium hydrogen storage oyster (HOP) treatment promotes STZ-induced fatty acid beta oxidation in brown adipose tissue of T1DM mice and inhibits lipid synthesis in liver and muscle tissue;
FIG. 6 is a graph showing that calcium-stored-oyster-Hydrogen (HOP) treatment reduces STZ-induced expression of type I diabetic kidney inflammatory factor and serum creatinine levels;
FIG. 7 shows that calcium-stored-oyster-Hydrogen (HOP) treatment reduces STZ-induced serum inflammatory factor mRNA expression levels of type I diabetes.
Detailed Description
The following description of the embodiments of the present invention will be made clearly and completely with reference to the accompanying drawings, in which it is apparent that the embodiments described are only some embodiments of the present invention, but not all embodiments. All other embodiments, which can be made by those skilled in the art based on the embodiments of the invention without making any inventive effort, are intended to be within the scope of the invention.
Referring to fig. 1 to 7, in the embodiment of the present invention, the method for detecting the in vitro release of hydrogen by HOP comprises:
accurately weighing different doses of calcium hydrogen storage oyster powder, respectively preparing 5ml of calcium hydrogen storage oyster water solution with the concentration of 30mg/ml,100mg/ml and 300mg/ml by using water, placing the calcium hydrogen storage oyster water solution into a small baked cake with the concentration of 20ml, slightly stirring and uniformly mixing, sealing a cup mouth, opening the beaker when detecting, and detecting the concentration of hydrogen in the water solution by using a hydrogen electrode. The concentrations of hydrogen released from the hydrogen-storing oyster calcium were measured for 1h,4h,8h,24h,48h,72h,96h,120h,144h,168h,192h, respectively, while the pH of the solutions was measured.
Animal model:
(1) Establishment of STZ-induced type i diabetes model:
32C 57/BL6J mice of 5-week-old size were selected and, after acclimatization, the mice were randomly divided into two groups:
A.C57 8
B.C57+STZ(65mg/kg) 24
2.1g of citric acid is weighed and added into 100mL of double distilled water to prepare solution A, then 2.94g of sodium citrate is added into 100mL of double distilled water to prepare solution B, A, B solutions are mixed according to a certain proportion (14:11), the pH value is measured, and the pH value is regulated to 4.4, thus obtaining the citric acid buffer solution for preparing STZ. Weighing a certain amount of STZ powder, dissolving in a citric acid buffer solution, continuously injecting the C57 mice into the abdominal cavity according to the dosage of 65mg/kg, injecting the citric acid buffer solution with the same dosage into the mice in the group A of the control group when injecting the STZ, starving the mice overnight, continuously injecting for five days once a day, measuring the random blood sugar of the mice after the injection is finished, and determining that the random blood sugar of the mice is more than or equal to 16.7mmol/L, wherein the success of molding is indicated.
(2) Animal experiment protocol group:
after successful mouse modelling, the above STZ-induced T1DM mice were randomly grouped, and then STZ-induced T1DM mice were given low dose (L-HOP) and high dose of oyster calcium hydrogen storage (H-HOP) respectively:
A.C57 8
B.STZ(65mg/kg) 8
STZ (65 mg/kg, after model success) +Low dose oyster CaUtility model (L-HOP, 30 mg/kg) 8
STZ (65 mg/kg, after model success) +high dose of calcium oyster hydrogen storage (H-HOP, 300 mg/kg) 8
After the animals were acclimatized, the weight and feeding of the mice were then recorded 2 times per week, the duration of the experiment was 2 months, the blood glucose was randomized, the blood glucose was fasting, after a remarkable effect, the mice were sacrificed after overnight fast, and various metabolic tissues (brain, heart, liver, muscle, fat (brown fat, epididymal fat and perirenal fat), kidney), pancreas, serum were collected.
Experimental method
1) Reactive Oxygen Species (ROS) level determination
(1) Preparing H2DCF-DA stock solution: the H2DCF-DA reagent is prepared into 10mmol/L storage solution, care is needed in the preparation process, the prepared storage solution is split into small parts, and the small parts are placed at the temperature of minus 20 ℃ and stored in a dark place.
(2) Determination of reactive oxygen species in tissue: weighing 20mg of tissue, shearing with scissors, cleaning with preset PBS (phosphate buffer solution) once, adding 200 mu L of precooled PBS again, grinding with a tissue grinder, homogenizing, centrifuging at 4 ℃ for 10min at 1000g, taking the supernatant, centrifuging again, collecting the supernatant to a centrifuge tube with 1.5mL of heart, adding 10 mu L of the supernatant into a 96-well plate, diluting an H2DCF-DA reagent with PBS for 1000 times, adding 100 mu L of the reagent into each hole, incubating the 96-well plate at 37 ℃ for 30min in a dark place, and performing fluorescence detection with an enzyme-labeled instrument, wherein excitation light and emission light are set to 485nm and 538nm; simultaneously quantifying BCA protein from the supernatant sample; the ROS content in a tissue is the ratio of the fluorescent OD value to the corresponding protein content.
2) Western blot
Total proteins were extracted from cell lysates, protein separated in SDS-PAGE gels, and printed onto PVDF membranes. After 1 hour of blocking with 1% bovine serum albumin, incubation with the specific primary antibody was carried out overnight at 4 ℃. The following day, after incubation with horseradish peroxidase-crosslinked secondary antibody for 1 hour at room temperature, the strips were developed on a booster chemiluminescent instrument (Bio-Rad Laboratories, hercules, calif., USA).
Anti-TFAM (D5C 8, # 8076S) antibodies, anti-beta-action (8H 10D10, # 3700S) antibodies and Anti-GAPDH (14C 10, # 2118S) antibodies, PPARgamma (2435S) antibodies, FAS (3189S) antibodies, alpha-Tubulin (3873S) antibodies, anti-P-ACC (# 3661S) antibodies, anti-ACC (3676S) antibodies were purchased from Cell Signaling Technology (Danvers, mass.). Anti-NDUFS3 (Complex I, # 459130) antibody, anti-SDHB (Complex II, # 459230) antibody, anti-UQCRC1 (Complex III, # 45914) antibody, anti-MTCO1 (Complex IV, # 459600) antibody, anti-ATP Synthase Subunit Alpha (Complex V, # 459240) antibody were purchased from Invitrogen (media, USA). AntiDRP 1%
611113 Antibodies and Anti-OPA1 (612607) antibodies were purchased from BD Biosciences (Mexico, US). Anti-MFN1 (D-10, sc-166644) antibody, anti-MFN2 (F-5, sc-515647) antibody, anti-NQO1 (H-9, sc-376023) antibody, anti-SOD1 (24, sc-101523) antibody, anti-SOD2 (E-10, sc-137254) antibody and Anti-cataase (F-17, sc-34285) antibody, PPARα (Sc-9000) antibody, SREBP1 (Sc 13551) antibody, purchased from Santa Cruz Biotechnology (Dallas, TX). The Anti-KEAP1 (# 60027-1-Ig) antibody and the Anti-NRF2 (# 66504-1-Ig) antibody were purchased from Proteintech (Rosemont, IL). CPT1A (A5307) antibody, UCP1 (A5857) antibody, UCP3 (A16996) antibody were purchased from ABclonal (Wuhan, china).
3) Real-time quantitative PCR
Total RNA was extracted from cells using TriPure Isolation Reagent (Roche, basel, switzerland) and then reverse transcribed into cDNA using the kit (BioRad, hercules, calif., USA). PCR reactions were performed using iQ SYBR Green Supermix (BioRad) and data analysis was performed using CFX Connect real-time PCR detection system (BioRad). After designing and synthesizing the primer of the target gene, the primer is dissolved into 100 mu M stock solution by sterilized ultrapure water and stored at-20 ℃. The upstream primer and the downstream primer are mixed before use, and the mixture is diluted by 10 times to obtain the application liquid with the final concentration of 10 mu M for standby.
Determination of TG and TC levels
According to the operation instructions in the purchased detection kit of Nanjing established company, the TG and TC levels in serum and liver tissues are detected, and specific operation steps are operated according to the instructions.
Fasting blood glucose test (Fasting blood glucose)
Fasting glucose test (Glucose tolerance tests, GTT) test. Mice were fasted overnight (12 hours) and tail vein was bled and blood glucose levels were measured using a glucometer and experimental data recorded.
Statistical analysis
Statistical analysis was performed using Graphpad Prism8 software. The normal distribution of the samples was first checked using a Shapiro-Wilk normal test. If the normal distribution is met, the variance alignment is further checked. If the data also passes the variance alignment test, the p-value is calculated using a two-tailed Student t-text or One-way ANOVA (Tukey post test); otherwise, the p-value was calculated using the Welch t-test or the Kruskal-Wallis test. For samples that do not fit the normal distribution, mann-Whitney or Kruskal-Wallis non-parametric test was used. Data are expressed as mean ± SEM. Significant statistical significance is p <0.05, p <0.01, p <0.001.
Description of the drawings:
FIG. 1 shows the in vitro sustained release of hydrogen from HOPs. A is the condition that the concentration of hydrogen is continuously released in 192h by a hydrogen storage oyster calcium water solution with the concentration of 30mg/mL,100mg/mL and 300 mg/mL. B is the PH monitoring of the aqueous solution of calcium in hydrogen storage oyster at a concentration of 30mg/mL,100mg/mL,300mg/mL released with hydrogen over 192h (n=3, ×p < 0.001).
FIG. 2 is a graph showing that HOP treatment reduces fasting blood glucose and blood lipid and restores insulin levels in serum in STZ-induced T1DM mice. A is random blood glucose levels after STZ induction for 2 weeks. B is random blood glucose levels 4 weeks after HOP treatment for T1DM disease. C is fasting blood glucose levels 7 weeks and 8 weeks after HOP treatment of T1 DM. D is TG and TC levels and FFA levels 7 weeks and 8 weeks after HOP treatment of T1DM disease. E is the level of insulin in serum after HOP treatment is completed. (C57, n=8, stz, n=8, stz+lhop, n=8, stz+h-HOP, n=7; p < 0.01; p < 0.001).
FIG. 3 shows how HOP treatment restores STZ-induced T1DM liver, perirenal fat and epididymal fat specific gravity with body weight, improving liver function. A is the measurement of body weight during HOP treatment. B is the detection of food intake during HOP treatment. C is the detection of water intake during HOP treatment. D is liver weight and body weight specific gravity after HOP treatment is completed. E is the weight of perirenal fat and weight specific gravity after HOP treatment is completed. F is epididymal fat weight and body weight specific gravity after HOP treatment. G is the ALT/AST ratio in serum after HOP treatment is completed, n=3. (c57, n=8, stz, n=8, stz+lhop, n=8, stz+h-HOP, n=7; p <0.05, <0.01, < p < 0.001).
FIG. 4HOP treatment reduces STZ-induced T1DM mice key metabolic tissue reactive oxygen species and oxidative stress. A is ROS level in liver tissue after HOP treatment is completed, n=4. B is ROS level in brain tissue after HOP treatment is over, n=4. C is ROS level in heart tissue after HOP treatment is over, n=4. D is ROS level in muscle tissue after HOP treatment is over, n=4. E is the expression level of antioxidant protein in liver tissue after the end of HOP treatment, n=3. F is the expression level of antioxidant protein in muscle tissue after the end of HOP treatment, n=3. P <0.05, p <0.01, p < 0.001).
FIG. 5 is a graph showing that HOP treatment promotes STZ-induced T1DM mice brown adipose tissue fatty acid beta oxidation and inhibits lipid synthesis in liver and muscle tissue. A is expression of genes related to lipid metabolism and fatty acid beta oxidation in brown adipose tissue, n=3. B is the expression level of a protein related to lipid metabolism and fatty acid beta oxidation in liver tissue, n=3. C is the expression level of a protein associated with lipid metabolism and fatty acid β oxidation in muscle tissue, n=3. P <0.05, p <0.01, p < 0.001).
FIG. 6 shows that HOP treatment reduces STZ-induced expression of type I diabetic kidney inflammatory factors and serum creatinine levels. A is the expression level of inflammatory factors in kidney tissue, n=6. Serum B creatinine level, n=3. P <0.01, p < 0.001).
FIG. 7 shows that HOP treatment reduces STZ-induced serum inflammatory factor mRNA expression levels for type I diabetes. The expression levels of inflammatory factors tnfα, IL6, IL1 β in serum, n=3. P <0.05, < p < 0.01).
The relevant results of the experiments of the present invention are given below.
And (one) the process of continuously and efficiently releasing hydrogen in vitro by HOP.
In order to clearly determine the condition that the hydrogen is released by the hydrogen-storing oyster calcium in vitro, 5ml of the hydrogen-storing oyster calcium water solution with the concentration of 30mg/ml,100mg/ml and 300mg/ml is respectively prepared by water, and is placed in a small baked cake with the concentration of 20ml, after being gently stirred and uniformly mixed, the mouth of a beaker is sealed, the beaker is opened when the hydrogen is detected, and the concentration of the hydrogen in the water solution is detected by a hydrogen electrode. The concentrations of hydrogen released from the hydrogen-storing oyster calcium were measured for 1h,4h,8h,24h,48h,72h,96h,120h,144h,168h,192h, respectively, while the pH of the solutions was measured, and the measurement results were shown in FIG. 1, and in FIG. 1 (A), we found that the concentrations of hydrogen in the aqueous hydrogen-storing oyster calcium solutions of 30mg/ml,100mg/ml,300mg/ml increased and then decreased with time, and that the concentrations of hydrogen in the aqueous hydrogen-storing oyster calcium solutions of 30mg/ml,100mg/ml,300mg/ml reached peak at 8h (peak concentrations of hydrogen were 520ppb,600ppb,740ppb, respectively), the concentration of the released hydrogen is increased along with the increase of the concentration of the hydrogen-storing oyster calcium, the concentration of the hydrogen released by the 300mg/ml hydrogen-storing oyster calcium aqueous solution is obviously higher than 30mg/ml and 100mg/ml, the hydrogen release gradually decreases along with the extension of time, the hydrogen release of the 30mg/ml hydrogen-storing oyster calcium aqueous solution is 0 after 96 hours, the hydrogen release of the 100mg/ml hydrogen-storing oyster calcium aqueous solution is 0 after 120 hours, and the hydrogen release of the 300mg/ml hydrogen-storing oyster calcium aqueous solution is 0 after 192 hours; as shown in FIG. 1 (B), the pH detection results show that the aqueous solution of hydrogen storage oyster calcium is alkaline (pH > 8), the pH of the aqueous solution of hydrogen storage oyster calcium is obviously increased along with the increase of the concentration, the pH of the aqueous solution of hydrogen storage oyster calcium with high dosage of 300mg/ml is higher than 13 and can be maintained for 96 hours, then the aqueous solution of hydrogen storage oyster calcium with high dosage starts to be reduced, the pH of the aqueous solution of hydrogen storage oyster calcium with high dosage of 100mg/ml is higher than 12 and is maintained for 24 hours, then the aqueous solution of hydrogen storage oyster calcium with high dosage starts to be gradually reduced, and the pH of the aqueous solution of hydrogen storage oyster calcium with high dosage of 30mg/ml is higher than 12 and is maintained for 8 hours.
(II) HOP treatment reduced fasting blood glucose and blood lipid and restored serum insulin levels in STZ-induced T1DM mice.
To investigate the therapeutic effect of HOP treatment on STZ-induced T1DM, we first induced T1DM with STZ, found that type i diabetic mice had random blood glucose greater than 16.7mmol/L after two weeks of STZ induction (fig. 2A), and that mice appeared to be polyphagic, diuretic, indicating that the STZ-induced T1DM model was successful. We then began administration of 30mg/mL HOP (L-HOP), 300mg/mL HOP (H-HOP) treatment to diabetic mice, and the C57 control and STZ model groups were administered with equal volumes of physiological saline, and H-HOP treatment was found to reduce fasting blood glucose in T1DM mice during the second week of administration (FIG. 2B), and L-HOP, H-HOP treatment was found to significantly reduce fasting blood glucose in T1DM mice for 12 hours during both the fifth and sixth weeks of administration (FIG. 2C). Furthermore, we found that administration of H-HOP treatment at week five could reduce the levels of Triglyceride (TG) and cholesterol (TC) in serum of T1DM mice starved for 12H (fig. 2D), and that both L-HOP and H-HOP treatments could significantly reduce the levels of TG and Free Fatty Acid (FFA) in serum of T1DM mice at week six of administration (fig. 2D). More importantly, in STZ-induced T1DM mice, reduced levels of insulin were found in the serum, and administration of H-HOP treatment significantly restored the levels of insulin in the serum (FIG. 2E). Overall, L-HOP and H-HOP can significantly improve the fasting blood glucose and blood lipid levels in STZ-induced T1DM mice.
And (III) the HOP treatment recovers liver, perirenal fat and epididymal fat and weight proportion of STZ induced T1DM mice, and improves liver function.
To investigate the effect of HOP treatment on STZ-induced T1DM body weight, food intake, water intake and metabolic tissue weight, we measured the body weight, food intake and water intake of mice every two days. Our study found that STZ-induced type i diabetic mice found a significant decrease in body weight on day 17, a significant increase in water intake on day 19, and a significant increase in food intake on day 27, but treatment with L-HOP and H-HOP did not significantly improve body weight, water intake, and food intake (fig. 3A-3C). Interestingly, we found that STZ-induced T1DM mice had significantly elevated liver to body weight specific gravity compared to control (C57), whereas administration of L-HOP and H-HOP treatments significantly reduced liver to body weight specific gravity of STZ-induced T1DM mice (fig. 3D); compared to the control group (C57), STZ induced a significant decrease in the specific gravity of perirenal fat and epididymal fat to body weight in T1DM mice, whereas administration of L-HOP and H-HOP treatments significantly restored these metrics (fig. 3E and 3F); in addition, L-HOP and H-HOP treatment restored STZ-induced levels of ALT/AST in liver tissue of T1DM mice (FIG. 3G). These data indicate that HOP treatment restores STZ-induced T1DM mice liver, perirenal fat and epididymal fat to body weight specific gravity, improves liver ALT/AST levels, and restores liver function.
(IV) HOP treatment reduces STZ-induced active oxygen levels and oxidative stress in key metabolic tissues of T1DM mice.
To explore the effect of HOP treatment on oxidative stress in key metabolic tissues of STZ-induced T1DM mice, we analyzed the levels of reactive oxygen species in liver, brain, heart and muscle tissues. STZ-induced T1DM mice had significantly elevated levels of ROS in liver, brain, heart and muscle tissue (FIGS. 4A-4D), and treatment with HOP reduced ROS levels in liver, brain, heart and muscle tissue (FIGS. 4A-4D) compared to control mice.
More importantly, HOP treatment can enhance liver tissue NQO1 levels and muscle tissue NRF2, NQO1, catase and SOD1 protein expression levels (fig. 3E-F).
(V) HOP treatment promotes STZ-induced fatty acid beta oxidation in brown adipose tissue of T1DM mice and inhibits lipid synthesis in liver and muscle tissues.
To explore the effect of HOP treatment on lipid metabolism in STZ-induced T1DM mice key metabolic tissues, we analyzed the level of lipid metabolism in liver, muscle and brown adipose tissue (brown adipose tissue, BAT). HOP treatment promoted STZ-induced expression of T1DM mice brown adipose tissue fatty acid beta oxidation-related gene CPT1A (fig. 5A), and inhibited expression of P-ACC, ACC and FAS lipid synthesis genes in liver and muscle tissues (fig. 5B and 5C) compared to control mice. In addition, HOP treatment promoted the expression of UCP1 protein in liver tissue, promoting thermogenesis (fig. 5B).
Sixth, HOP treatment improves the index of renal inflammation and renal function in STZ-induced type i diabetic mice.
To explore the effect of HOP treatment on the kidney function of STZ-induced type i diabetic mice, we evaluated glomerular filtration using quantitative polymerase chain reaction to detect the expression level of inflammatory factors in kidney tissue and creatinine levels in serum. Tumor necrosis factor α (tumor necrosis factor α, tnfα) in kidney tissue of STZ-induced type i diabetic mice, interleukin-1 β (interleukin 1beta, il1β), interleukin 6 (interleukin 6, il6), interleukin 10 (interleukin 10, il10) and chemokine ligand 2 (chemokine) ligand 2, MCP 1) were significantly elevated compared to control mice, and administration of L-HOP and H-HOP treatments significantly reduced the mRNA levels of il1β, IL6, IL10 inflammatory factors in kidney tissue of type i diabetic mice, L-HOP and H-HOP treatments reduced the mRNA levels of tnfα, and H-HOP could reduce the mRNA levels of MCP1 (fig. 6A). Meanwhile, to evaluate the glomerular filtration function, we examined the levels of creatinine (Scr) in Serum, and found that STZ-induced type i diabetic mice had significantly elevated levels of Scr in Serum compared to the normal control group, and administration of H-HOP treatment reduced significantly lower levels of Scr (fig. 6B). The results show that HOP treatment can reduce the transcription level of inflammatory factors and serum creatinine level in kidney tissues and can significantly improve kidney functions.
(seventh) HOP treatment reduced serum inflammatory factor levels in STZ-induced type I diabetic mice.
To explore the effect of HOP treatment on STZ-induced inflammatory levels in type i diabetic mice, we examined the serum for the inflammatory factor tumor necrosis factor α (tumor necrosis factor α, tnfα), interleukin-1 β (interleukin 1beta, IL1 β), and interleukin 6 (interleukin 6, IL 6) levels in STZ-induced type i diabetic mice serum significantly increased compared to control mice, and administration of H-HOP treatment significantly reduced the levels of tnfα inflammatory factor in type i diabetic mice serum, and L-HOP treatment significantly reduced IL6 levels in type i diabetic mice serum (fig. 7). The above results indicate that HOP treatment can significantly reduce inflammatory factor levels in serum.
It will be evident to those skilled in the art that the invention is not limited to the details of the foregoing illustrative embodiments, and that the present invention may be embodied in other specific forms without departing from the spirit or essential characteristics thereof. The present embodiments are therefore to be considered in all respects as illustrative and not restrictive, the scope of the invention being indicated by the appended claims rather than by the foregoing description, and all changes which come within the meaning and range of equivalency of the claims are therefore intended to be embraced therein.
Furthermore, it should be understood that although the present disclosure describes embodiments, not every embodiment is provided with a separate embodiment, and that this description is provided for clarity only, and that the disclosure is not limited to the embodiments described in detail below, and that the embodiments described in the examples may be combined as appropriate to form other embodiments that will be apparent to those skilled in the art.
Claims (4)
1. The application of the hydrogen-storing oyster calcium in foods, health products and medicines for preventing and treating type I diabetes is characterized in that the hydrogen-storing oyster calcium is used as a solid hydrogen carrier, can react with water to generate hydrogen, and can continuously release high-concentration hydrogen.
2. Use according to claim 1, characterized in that its calcium in hydrogen storage oyster can reduce the oxidative stress of critical metabolic tissues and improve the antioxidant function.
3. Use according to claim 1, characterized in that its use for the treatment of calcium in hydrogen storage oyster promotes the oxidation of fatty acid beta in brown adipose tissue and inhibits the lipid synthesis in liver and muscle tissue, improving the lipid metabolism of T1DM disease.
4. Use according to claim 1, characterized in that its calcium-stored crassostrea treatment reduces STZ-induced renal inflammatory response of type i diabetes and the expression of inflammatory factors in the serum, for improving inflammatory response of T1DM disease.
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| CN102524785A (en) * | 2012-02-08 | 2012-07-04 | 姚鼎山 | Negative hydrogen ion powder and preparation method thereof |
| CN113105221A (en) * | 2021-02-03 | 2021-07-13 | 日照生命谷生物科技发展股份公司 | Negative hydrogen ion water activating material and its producing method |
| CN115708838A (en) * | 2022-11-14 | 2023-02-24 | 日照生命谷生物科技发展股份公司 | Oyster negative hydrogen tablet and preparation method thereof |
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2023
- 2023-06-06 CN CN202310662640.8A patent/CN116671633A/en active Pending
Patent Citations (3)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN102524785A (en) * | 2012-02-08 | 2012-07-04 | 姚鼎山 | Negative hydrogen ion powder and preparation method thereof |
| CN113105221A (en) * | 2021-02-03 | 2021-07-13 | 日照生命谷生物科技发展股份公司 | Negative hydrogen ion water activating material and its producing method |
| CN115708838A (en) * | 2022-11-14 | 2023-02-24 | 日照生命谷生物科技发展股份公司 | Oyster negative hydrogen tablet and preparation method thereof |
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