CN111265510A - Application of iron death inhibitor in preparation of medicine for treating acute liver injury - Google Patents
Application of iron death inhibitor in preparation of medicine for treating acute liver injury Download PDFInfo
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Abstract
The invention discloses an application of an iron death inhibitor in preparing a medicament for treating acute liver injury, wherein the iron death inhibitor is pretreated to obviously reduce the levels of alanine Aminotransferase (ALT) and aspartate Aminotransferase (AST) in serum after the acute liver injury induced by sodium Thiosulfate (TAA); reducing MDA content in liver tissue after TAA-induced acute liver injury, and increasing reducing glutathione GSH and glutathione peroxidase GSH-PX content in liver tissue; reducing inflammatory cell infiltration into the liver in TAA-induced acute liver injury; the protective effect of the iron death inhibitor on TAA-induced acute liver injury is related to inhibition of hepatocyte iron death, which shows that the iron death inhibitor can obviously increase the expression of iron death marker genes of glutamic acid/cystine antiporter xCT and Gpx4 glutathione peroxidase 4 in a TAA-induced acute liver injury model.
Description
Technical Field
The invention relates to the technical field of biological pharmacy, in particular to application of an iron death inhibitor in preparing a medicine for treating acute liver injury.
Background
Liver disease is a huge global public health problem that threatens the health of billions of people. More seriously, the incidence of many liver diseases is increasing. The increasing number of immigrants, frequent trips and economic globalization have led to widespread spread of viruses. Acute liver injury refers to acute and severe hepatic insufficiency that occurs in people without liver disease due to massive death or loss of hepatocytes. The structure and function of the liver are complex, and the liver is used as an important organ for protein synthesis and storage, and provides various substances for the body to operate and regulate the stability of other tissues and organs. Moreover, the liver is the main storage place for iron in the body, and is the main organ for maintaining and regulating iron metabolism in the body. These factors all suggest that treatment of liver disease is very complex and fraught with difficulties.
TAA is commonly used for making models of acute liver injury, hepatic fibrosis and hepatic encephalopathy. TAA stimulation resulted in mouse hepatocyte necrosis and apoptosis, with elevated serum glutamic-pyruvic transaminase (ALT) and glutamic-oxalacetic transaminase (AST) levels, and massive inflammatory cell infiltration into the liver. The TAA-induced liver injury model process is relatively simple and easy to implement, has good response to liver cell injury, has the advantages of good feasibility, repeatability, approaching of hepatic fibrosis tissues to human, high preparation success rate and the like, and is commonly used for preparing hepatic fibrosis and acute liver failure models.
Acute liver injury refers to an abnormality of liver function caused by various causes, and liver injury is the basis of acute liver failure, which ultimately results from severe or persistent liver injury. Acute liver injury is caused by many reasons, including virus infection, improper medication, food additives, excessive ethanol intake and contact, toxic food intake, radiation injury and the like.
The invention discovers that the iron death inhibitor Fer-1 can be used for preparing the medicine for treating acute liver injury. In the case of iron chelators, studies over the past decades have assumed that iron is involved only in the pathophysiological processes of apoptosis or necrosis. With the development of cell biology technology, more and more novel forms of cell death are gradually discovered, including iron death. Iron death (Ferroptosis) is an iron-dependent cell death pathway, different from other death pathways such as apoptosis, necrosis, autophagy, and the like. Iron death is manifested by an increased level of cellular lipid peroxidation, which can be specifically inhibited by iron ion chelators. Fer-1 is a currently accepted iron death inhibitor, and as an N-cyclohexyl-containing compound, the Fer-1 has high affinity with a cell membrane phospholipid bilayer and can effectively eliminate cell membrane lipid peroxidation, but the content of iron is not changed, so that a plurality of clinical side effects caused by an iron chelator can be avoided. To date, there has been no report of the effects of iron death and its inhibitors on acute liver injury.
Disclosure of Invention
In order to solve the problems and the defects of the prior art, the invention provides the application of the iron death inhibitor in preparing the medicine for treating acute liver injury.
The invention adopts the following technical scheme: application of iron death inhibitor in preparing medicine for treating acute liver injury is provided.
As a preferred technical scheme of the invention: the iron death inhibitor is Ferrostatin-1, which is called Fer-1 for short.
As a preferred technical scheme of the invention: the application is to reduce alanine aminotransferase ALT and/or aspartate aminotransferase AST in serum after acute liver injury induced by sodium thiosulfate TAA.
As a preferred technical scheme of the invention: the application is to inhibit the MDA level of the malondialdehyde in liver tissues during acute liver injury.
As a preferred technical scheme of the invention: the application is that the content of the reduced glutathione GSH and/or glutathione peroxidase GSH-PX in the liver tissue is increased when the liver is injured urgently.
As a preferred technical scheme of the invention: the application is to increase the expression of an iron death marker gene glutamic acid/cystine antiporter xCT and/or Gpx4 glutathione peroxidase 4 in a TAA-induced acute liver injury model.
As a preferred technical scheme of the invention: the application is to inhibit iron death in liver caused by acute liver injury.
As a preferred technical scheme of the invention: the application is to reduce inflammatory cell infiltration into liver in TAA-induced acute liver injury.
As a preferred technical scheme of the invention: the application is liver protection.
Has the advantages that:
compared with the prior art, the application of the iron death inhibitor in preparing the medicine for treating acute liver injury has the following technical effects:
1. the Fer-1 pretreatment provided by the invention can obviously reduce ALT and AST levels in serum during TAA-induced acute liver injury, reduce MDA level in liver tissues, increase GSH and GSH-Px levels in liver tissues, inhibit inflammatory cells from infiltrating into liver tissues and promote xCT and Gpx4 expression in livers;
2. the protective effect of Fer-1 on TAA-induced acute liver injury is related to inhibition of hepatocyte iron death. Therefore, the invention provides a new possible direction and specific measures for the treatment of clinical liver diseases.
Drawings
FIG. 1 is a graph showing the results of measurement of serum ALT and AST levels in mice after TAA stimulation in the acute liver injury protection experiment of example 1 of the present application.
FIG. 2 is a graph showing the results of measuring the levels of MDA, GSH, and GSH-Px in liver tissues of mice after TAA stimulation in the acute liver injury protection experiment of example 1 of the present application.
FIG. 3 is a graph showing the results of HE staining of liver tissue in mice after administration of TAA stimulation in the acute liver injury protection experiment of example 1 of the present application.
FIG. 4 is a graph showing the expression of xCT and Gpx4 in the liver tissues of mice after TAA stimulation in the acute liver injury protection experiment of example 1.
Detailed Description
The experimental procedures used in the following examples are all conventional procedures unless otherwise specified.
Materials, reagents and the like used in the following examples are commercially available unless otherwise specified.
The experimental data in the following examples are expressed as mean-earth standard errors (x ± s.e.m), multiple sets of measured data were compared by analysis of variance or Kruskal-Wallis H test, and two sets of data were compared by LSD test. All data were statistically analyzed using graphpad7.0 software, with P <0.05 being statistically significant for differences.
Male ICR inbred mice (6-8 weeks, 18-22g) were purchased from the university of Nantong laboratory animals center. The general feed was purchased from the laboratory animal center of southeast university.
Compound monomer Fer-1 was purchased from Selleck.
Sodium Thiosulfate (TAA) was purchased from Sigma, USA.
ALT, AST, MDA, GSH-PX detection kit is purchased from Nanjing institute of bioengineering, Inc.
Other chemical reagents were purchased from the national pharmaceutical group.
PI dyes, hematoxylin, eosin, immunohistochemical reagents were purchased from Biyuntian Biotech Ltd.
Preparing a PI dye solution: 129.6 ml of normal saline, PI10mg, RNase2mg, 1.0 percent by volume of TritonX-1000.5 ml and 200mg of sodium citrate, adding distilled water to a constant volume of 200ml, adjusting the pH to 7.2-7.6, and storing in a refrigerator at 4 ℃ in a dark place for later use.
Preparing hematoxylin: dissolving 0.2 g hematoxylin in 25ml absolute ethyl alcohol, dissolving 1 g aluminum sulfate in 75 ml deionized water, mixing the two solutions, heating and boiling for 2min, and adding 0.05g sodium iodate and 0.1 g citric acid.
And (3) eosin configuration: 2g of eosin was dissolved in 100ml of 95% ethanol.
The physiological saline in the following examples is sterile physiological saline.
In the examples TAA-induced liver injury is acute liver injury.
Example 1:
application of Fer-1 in acute liver injury induced by TAA.
Experimental grouping:
24 male ICR inbred mice (6-8 weeks, 18-22g) were randomized by body weight into 3 groups, i.e., normal control, TAA model, TAA + Fer-1, 8 mice per group.
(II) experimental treatment:
3 days before the intraperitoneal injection of the TAA injection (250 mg/kg/day, the volume of 0.25ml and continuous 3 days) is carried out on each group of mice (except normal control group mice), 0.25ml of physiological saline is respectively injected into the intraperitoneal injection of the TAA model group of mice, and the Fer-1 injection (1 mg/kg/day, the volume of 0.25ml and continuous 3 days) is respectively injected into the intraperitoneal injection of the TAA + Fer-1 group of mice.
Mice in the normal control group were given an intraperitoneal injection of 0.25ml of physiological saline twice, and for the purpose of excluding the influence of time, the time for injecting the physiological saline twice was the same as that in each of the other groups described above.
After 3 consecutive days of TAA injection, each group of mice was sacrificed and blood and liver tissue of each group of mice were collected for subsequent index determination.
And (III) measuring the serum glutamic-pyruvic transaminase (ALT) and glutamic-oxaloacetic transaminase (AST) levels of the mice.
Serum glutamic-pyruvic transaminase (ALT) and glutamic-oxaloacetic transaminase (AST) levels are measures of liver function
Anaesthetizing the mouse after continuously giving TAA stimulation for 3 days, removing the eyeball of the mouse to take blood, placing the blood in a sterile EP tube without anticoagulant, placing the EP tube at the normal temperature for 1 h, and centrifuging at 4 ℃ and 3000 g for 15 min; the supernatant serum was carefully pipetted into another sterile EP tube and the pellet discarded. The separated serum was diluted 4-fold with sterile physiological saline and used for the assay.
ALT and AST serum detection kits provided by Nanjing institute of bioengineering are used to respectively determine ALT and AST content in serum.
After 3 days of TAA stimulation, serum was collected and the results of ALT, AST and MDA content measurement are shown in FIGS. 1A and 1B.
In fig. 1A-1B, P <0.05 and P < 0.001.
FIGS. 1A-1B show that serum ALT and AST levels were significantly higher in mice of the TAA model group than in the normal control group (P < 0.001); compared with the mice in the TAA model group, the mice in the TAA + Fer-1 group can obviously reduce the difference of the levels of ALT and AST (P is less than 0.05) in serum under the condition of Fer-1 pretreatment, and the statistical significance is realized.
(IV) measuring the contents of MDA, GSH and GSH-Px in liver tissues:
after 3 consecutive days of TAA stimulation, the mice were sacrificed and the livers were removed by laparotomy, and after weighing and recording, a small liver tissue of about 0.2 g of the same portion of the liver lobe was removed, hematocele was removed with ice physiological saline, the surface was blotted with filter paper and weighed, and placed in a 10 ml EP tube, and an appropriate amount of ice physiological saline was added to prepare a 10% liver homogenate, which was centrifuged at 4000 r/min for 15min, and the supernatant was taken for measurement.
Respectively measuring the contents of MDA, GSH and GSH-PX in the liver tissue by using MDA, GSH and GSH-Px tissue detection kits provided by Nanjing institute of established bioengineering; MDA, GSH-Px water average are indexes for measuring lipid peroxidation level.
The results of taking liver tissue after 3 days TAA stimulation and measuring MDA, GSH and GSH-PX contents are shown in FIG. 2A, FIG. 2B and FIG. 2C.
In fig. 2A-2C, P <0.05, P < 0.01, and P < 0.001.
FIG. 2A shows that the liver MDA level of mice in TAA model group is significantly higher than that of normal control group (P < 0.001); compared with the TAA model group mice, the difference that the TAA + Fer-1 group mice can obviously reduce the MDA level (P < 0.001) in the liver tissue under the condition of Fer-1 pretreatment has statistical significance.
FIGS. 2B-2C show that the levels of GSH and GSH-PX in liver tissues of TAA model mice were significantly lower than those of normal controls (P < 0.001); compared with mice in a TAA model group, the mice in the TAA + Fer-1 group can obviously increase the difference of GSH and GSH-Px levels (P < 0.05) in liver tissues under the condition of Fer-1 pretreatment, and has statistical significance.
And (V) paraffin embedding and HE staining of liver tissues:
after 3 days of continuous TAA stimulation, the mice were sacrificed, the abdominal cavity was rapidly opened, the liver was separated, and liver tissues with appropriate size at a specific position of the right lobe of the liver were excised and fixed in a paraformaldehyde solution with a volume percentage of 4% for 24 hours. After fixation, paraffin embedding was carried out, and 5 μm serial sections were each carried out, followed by HE staining according to the following procedure:
xylene dewaxing, gradient alcohol dehydration, tap water washing for 1 min, hematoxylin staining for 5min, tap water washing for 3min, hydrochloric acid aqueous solution with the volume percentage of 1% for 30 s, tap water washing for 3min, ammonia aqueous solution with the volume percentage of 1% for 30 s, tap water washing for 4 min, eosin staining for 1 min, alcohol gradient dehydration, xylene transparency and neutral gum sealing piece.
Results of paraffin embedding and HE staining of liver tissue from mice after 3 consecutive days of TAA stimulation are shown in FIG. 3.
FIG. 3 shows that under microscope, the hepatic lobules in liver tissues of normal mice have clear structures and abundant and uniform cytoplasm, and hepatic cells are radially and orderly arranged around central veins and a sink region to form hepatic cords. The TAA model group mice have disordered lobular arrangement of liver tissues, loose and large amount of liver cells, balloon degeneration of more liver cells, focal necrosis, obvious inflammatory cell infiltration in a sink region and congestion of liver tissues. Compared with mice in a TAA model group, after the mice in the TAA + Fer-1 group are pretreated by Fer-1, the swelling degree of liver cells can be reduced, the cytoplasm loosening is weakened, the balloon deformation is obviously improved, and the necrosis around the central vein can be reduced. Indicating that the Fer-1 pretreatment can obviously improve the TAA-induced liver injury of mice.
(VI) immunohistochemical staining of liver tissue:
placing the cut tissue paraffin section in a 60 ℃ oven to be baked for 40-60min, and cooling to room temperature to carry out the following steps: dewaxing the slices in xylene solution for 3 times, 5min each time, adding anhydrous ethanol for transparent treatment for 3 times, 5min each time, treating the slices with 90% ethanol for 5min, treating the slices with 80% ethanol for 5min, treating the slices with 70% ethanol for 5min, and treating the slices with PBS for 5 min.
0.2% Triton X-100 was added for membrane permeation for 8min and washed 1 time with PBS. Antigen retrieval to remove endogenous peroxidase. Heating citric acid repairing solution (pH = 6.0) to 95 + -1 deg.C, placing into slices, heating for 15min, naturally cooling at room temperature, washing with PBS for 5min for 2 times, and soaking in methanol solution containing 3% H2O2 for 15 min. Wash 3 times with PBS for 5min each.
PBS around the section was carefully wiped dry with paper towel, a small circle was drawn around the tissue with crayon, goat serum was added dropwise after drying, and the wet box was closed for 30min at room temperature. The tissue was washed 3 times with PBS for 5 minutes each time, and the liquid surrounding the tissue was wiped dry with a paper towel, and diluted anti-Nrf2, anti-Gpx4 were added dropwise and incubated overnight at 4 ℃ in a wet box.
After removing the primary antibody the next day, wash with PBS 3 times for 5min each, add diluted HRP-labeled secondary antibody drop by drop, incubate in wet box at 37 ℃ for 30min, wash with PBS 3 times for 5min each. Adding prepared DAB color developing solution, developing for 5-10min, and flushing with running water for 5-10 min.
Re-dyeing with prepared hematoxylin dye solution for 1-2min, washing with running water for 5-10min, treating with 75% ethanol for 5min, treating with 95% ethanol for 5min, treating with anhydrous ethanol for 5min, treating with xylene for 3 times, and performing transparent treatment for 5min each time. And sealing the neutral gum into a piece, airing, and taking a picture under a microscope for storage.
FIG. 4 shows that Fer-1 pretreatment promoted xCT and Gpx4 expression in liver tissue compared to the TAA-induced acute liver injury model group.
Claims (9)
1. Application of iron death inhibitor in preparing medicine for treating acute liver injury is provided.
2. The use of an iron death inhibitor according to claim 1 in the preparation of a medicament for the treatment of acute liver injury, wherein: the iron death inhibitor is Ferrostatin-1, which is called Fer-1 for short.
3. The use of an iron death inhibitor according to claim 1 in the preparation of a medicament for the treatment of acute liver injury, wherein: the application is to reduce alanine aminotransferase ALT and/or aspartate aminotransferase AST in serum after acute liver injury induced by sodium thiosulfate TAA.
4. The use of an iron death inhibitor according to claim 1 in the manufacture of a medicament for the treatment of acute liver injury, wherein: the application is to inhibit the MDA level of the malondialdehyde in liver tissues during acute liver injury.
5. The use of an iron death inhibitor according to claim 1 in the manufacture of a medicament for the treatment of acute liver injury, wherein: the application is that the content of the reduced glutathione GSH and/or glutathione peroxidase GSH-PX in the liver tissue is increased when the liver is injured urgently.
6. The use of an iron death inhibitor according to claim 1 in the manufacture of a medicament for the treatment of acute liver injury, wherein: the application is to increase the expression of the iron death marker gene glutamate/cystine antiporter (xCT) and/or glutathione peroxidase 4 (Gpx 4) in a TAA-induced acute liver injury model.
7. The use of an iron death inhibitor according to claim 1 in the manufacture of a medicament for the treatment of acute liver injury, wherein: the application is to inhibit iron death in liver caused by acute liver injury.
8. The use of an iron death inhibitor according to claim 1 in the manufacture of a medicament for the treatment of acute liver injury, wherein: the application is to reduce inflammatory cell infiltration into liver in TAA-induced acute liver injury.
9. The use of an iron death inhibitor according to claim 1 in the manufacture of a medicament for the treatment of acute liver injury, wherein: the application is liver protection.
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Cited By (7)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN112920989A (en) * | 2021-02-09 | 2021-06-08 | 中国科学院广州生物医药与健康研究院 | Liver organoid model, establishment method and application thereof, and pharmaceutical composition for treating hepatocyte iron death |
| CN114533760A (en) * | 2022-03-01 | 2022-05-27 | 华中农业大学 | Manganese-based nanoenzyme as iron death inhibitor and application thereof in liver injury |
| CN115054696A (en) * | 2022-08-17 | 2022-09-16 | 南方医科大学 | Application of iron death inhibitor in preparation of medicine for preventing and treating hepatotoxic injury caused by aurantio-obtusin |
| CN115089573A (en) * | 2022-07-06 | 2022-09-23 | 复旦大学 | Application of entacapone in preparation of medicine for treating acute kidney injury and iron death inhibitor |
| CN115944620A (en) * | 2022-12-28 | 2023-04-11 | 中国农业大学 | Application of icaritin in protecting medicine property and liver injury disease based on iron death |
| CN116036087A (en) * | 2022-12-26 | 2023-05-02 | 中国人民解放军空军军医大学 | Use of iron death inhibitor in preparing medicine for repairing damaged liver |
| WO2023216280A1 (en) * | 2022-05-09 | 2023-11-16 | 重庆医科大学附属儿童医院 | Use of ferroptosis inhibitor in preparation of drug for treating gastritis |
Citations (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN110538172A (en) * | 2019-09-28 | 2019-12-06 | 郑州大学 | Application of iron death inhibitor in preparation of medicine for treating auranofin hepatotoxicity |
-
2020
- 2020-03-09 CN CN202010156582.8A patent/CN111265510A/en active Pending
Patent Citations (1)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN110538172A (en) * | 2019-09-28 | 2019-12-06 | 郑州大学 | Application of iron death inhibitor in preparation of medicine for treating auranofin hepatotoxicity |
Non-Patent Citations (1)
| Title |
|---|
| NAOYA YAMADA等: "Ferroptosis driven by radical oxidation of n-6 polyunsaturated fatty acids mediates acetaminophen-induced acute liver failure", 《CELL DEATH AND DISEASE》 * |
Cited By (9)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN112920989A (en) * | 2021-02-09 | 2021-06-08 | 中国科学院广州生物医药与健康研究院 | Liver organoid model, establishment method and application thereof, and pharmaceutical composition for treating hepatocyte iron death |
| CN114533760A (en) * | 2022-03-01 | 2022-05-27 | 华中农业大学 | Manganese-based nanoenzyme as iron death inhibitor and application thereof in liver injury |
| CN114533760B (en) * | 2022-03-01 | 2022-12-02 | 华中农业大学 | Manganese-based nanoenzyme as iron death inhibitor and application thereof in liver injury |
| WO2023216280A1 (en) * | 2022-05-09 | 2023-11-16 | 重庆医科大学附属儿童医院 | Use of ferroptosis inhibitor in preparation of drug for treating gastritis |
| CN115089573A (en) * | 2022-07-06 | 2022-09-23 | 复旦大学 | Application of entacapone in preparation of medicine for treating acute kidney injury and iron death inhibitor |
| CN115054696A (en) * | 2022-08-17 | 2022-09-16 | 南方医科大学 | Application of iron death inhibitor in preparation of medicine for preventing and treating hepatotoxic injury caused by aurantio-obtusin |
| CN116036087A (en) * | 2022-12-26 | 2023-05-02 | 中国人民解放军空军军医大学 | Use of iron death inhibitor in preparing medicine for repairing damaged liver |
| CN116036087B (en) * | 2022-12-26 | 2023-09-05 | 中国人民解放军空军军医大学 | Use of iron death inhibitor in preparing medicine for repairing damaged liver |
| CN115944620A (en) * | 2022-12-28 | 2023-04-11 | 中国农业大学 | Application of icaritin in protecting medicine property and liver injury disease based on iron death |
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Application publication date: 20200612 |