CN111773207A - Application of selenomethionine in preventing and treating rabbit liver injury caused by T-2 toxin - Google Patents
Application of selenomethionine in preventing and treating rabbit liver injury caused by T-2 toxin Download PDFInfo
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- CN111773207A CN111773207A CN202010652291.8A CN202010652291A CN111773207A CN 111773207 A CN111773207 A CN 111773207A CN 202010652291 A CN202010652291 A CN 202010652291A CN 111773207 A CN111773207 A CN 111773207A
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- toxin
- semet
- selenomethionine
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- feed
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Images
Classifications
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- A—HUMAN NECESSITIES
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- A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
- A61K31/00—Medicinal preparations containing organic active ingredients
- A61K31/185—Acids; Anhydrides, halides or salts thereof, e.g. sulfur acids, imidic, hydrazonic or hydroximic acids
- A61K31/19—Carboxylic acids, e.g. valproic acid
- A61K31/195—Carboxylic acids, e.g. valproic acid having an amino group
- A61K31/197—Carboxylic acids, e.g. valproic acid having an amino group the amino and the carboxyl groups being attached to the same acyclic carbon chain, e.g. gamma-aminobutyric acid [GABA], beta-alanine, epsilon-aminocaproic acid, pantothenic acid
- A61K31/198—Alpha-aminoacids, e.g. alanine, edetic acids [EDTA]
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- A—HUMAN NECESSITIES
- A23—FOODS OR FOODSTUFFS; TREATMENT THEREOF, NOT COVERED BY OTHER CLASSES
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- A23K10/30—Animal feeding-stuffs from material of plant origin, e.g. roots, seeds or hay; from material of fungal origin, e.g. mushrooms
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- A—HUMAN NECESSITIES
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- A—HUMAN NECESSITIES
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Abstract
The invention relates to the technical field of feed additives, in particular to application of selenomethionine in preventing and treating rabbit liver injury caused by T-2 toxin. The application is obtained by adding selenomethionine into feed, wherein 0.1-0.8 mg of selenomethionine is added into each kilogram of feed. The invention also provides a feed for rabbits, which uses selenomethionine as an additive and comprises the following components: 15% of corn, 11% of bean cake, 20% of wheat bran, 50% of grass meal, 1.5% of salt and the balance of trace elements. The selenomethionine provided by the invention can be used as a feed additive for rabbits, can effectively prevent and treat the liver injury of the rabbits induced by T-2 toxin, and can inhibit the liver cell apoptosis.
Description
Technical Field
The invention relates to the technical field of feed additives, in particular to application of selenomethionine in preventing and treating rabbit liver injury caused by T-2 toxin.
Background
The T-2 toxin is a secondary fungal metabolite generated by fusarium in a proper environment, is a trichothecene A-type toxin with the strongest toxicity, is widely distributed in nature, easily pollutes grain crops such as corn, oat, wheat and the like and animal feeds, is known as an inevitable fungal toxin in nature, and seriously harms human and animal health. The T-2 toxin has strong toxicity, and animals can cause chronic poisoning effects after being ingested with low-dose T-2 toxin-contaminated grains or feeds for a long time, such as inappetence, growth and development retardation, obvious weight reduction, obvious reduction of the return rate of animal feeds and huge economic loss for animal husbandry production. The rabbit is a common economic animal, is an important component of livestock husbandry in China, and is very sensitive to mycotoxin. T-2 toxin has strong toxic effects after being exposed through various ways such as oral administration, skin, respiration and the like, and can be generally classified into immunotoxicity, reproductive and developmental toxicity, blood and skin toxicity, liver toxicity and the like.
Prevention of contamination with T-2 toxin is accomplished by first grasping the source of the toxin, keeping it as dry as possible during harvesting and storage as described above, choosing the appropriate harvest time, and storing it in a correct stack. When the feed is processed, attention should be paid to the processing procedure and the control of temperature and humidity, and a proper amount of preservative is added for storage if necessary. In addition, the management of field crops should be enhanced for the inevitable factors, and the anti-fungal line crops are selected as much as possible, so that the generation of T-2 toxin is restrained from the source. For already contaminated cereals or feeds, the methods currently used for detoxification are mainly physical, chemical and biological.
The prevention and treatment methods are measures taken under the condition that polluted grains or feeds are not eaten by animals, however, in most cases, whether the stored grains or feeds are polluted or not is difficult to identify, and the animals can only know the poisoning symptoms after eating the grains or feeds, so that timely measures are particularly important for preventing the animals.
Disclosure of Invention
One of the purposes of the invention is to provide the application of selenomethionine in preparing products for preventing and treating rabbit liver injury caused by T-2 toxin.
Furthermore, in the application, the selenomethionine is dissolved by water and is added into the feed for rabbits, and each kilogram of the feed is added with 0.1-0.8 mg of the selenomethionine.
Further, the feed comprises the following components in percentage by mass: 15% of corn, 11% of bean cake, 20% of wheat bran, 50% of grass meal, 1.5% of salt and the balance of trace elements; 0.1-0.8 mg of selenomethionine is added into each kilogram of feed.
Further, the trace element componentThe following were used: each kilogram of feed is added with Cu 8mg, Zn 75mg, Fe80mg, Mn 100mg and vitamin A125000IU, vitamin D32500IU, vitamin E18mg, vitamin K32.8 mg, vitamin B12mg of vitamin B26mg of vitamin B120.025mg, biotin 0.0325mg, folic acid 1.25mg, pantothenic acid 12mg, nicotinic acid 50 mg.
Compared with the prior art, the invention has the following beneficial effects:
1. the low dose of selenomethionine (hereinafter also referred to as SeMet) is effective in preventing T-2 toxin-induced liver function impairment and histopathological changes.
2. SeMet at low doses is effective in preventing T-2 toxin-induced oxidative stress of the liver.
3. SeMet at low doses can be effective in preventing T-2 toxin-induced apoptosis of hepatocytes.
Drawings
FIG. 1 shows the effect of SeMet on serum biochemical indicators of T-2 toxin-induced liver injury in rabbits, wherein AST is shown in FIG. 1, ALT is shown in FIG. 2, ALP is shown in FIG. 3, TP is shown in FIG. 4, A. a control group, B.T-2 toxin group, C. low-dose SeMet + T-2 toxin group, D. medium-dose SeMet + T-2 toxin group, E. high-dose SeMet + T-2 toxin group, # shows a significant difference from the control group, and P is less than 0.05; indicates significant difference compared to the T-2 toxin group, P < 0.05. # indicates very significant difference compared to control, P < 0.01; indicates a very significant difference compared to the T-2 toxin group, P < 0.01.
FIG. 2 shows the effect of SeMet on liver glycogen content in T-2 toxin-induced liver injury in rabbits, in which A. a control group, B.T-2 toxin group, C. low-dose SeMet + T-2 toxin group, D. medium-dose SeMet + T-2 toxin group, and E. high-dose SeMet + T-2 toxin group, the magnification of the first row of pictures was 100X, and the scale bar was 200. mu.m. The second row is a close-up of the first row of pictures, at 400 x magnification, on a scale of 50 μm.
FIG. 3 is a graph showing the effect of SeMet on T-2 toxin-induced morphological changes in rabbit liver tissue. In the figure, A. the control group, B.T-2 toxin group, C. the low dose SeMet + T-2 toxin group, D. the medium dose SeMet + T-2 toxin group, E. the high dose SeMet + T-2 toxin group, the magnification of the first row of pictures was 200X, and the scale bar was 100. mu.m. The second row is a partial enlargement of the first row of pictures at 400 x magnification on a scale of 50 μm
FIG. 4 is a graph of the effect of SeMet on T-2 toxin-induced rabbit ROS content. In the figure, fluorescence intensity of A. control group, B.T-2 toxin group, C. low dose, SeMet + T-2 toxin group, D. middle dose SeMet + T-2 toxin group, E. high dose SeMet + T-2 toxin group, F. DHE staining was quantitatively analyzed. # indicates a significant difference compared to the control group, P < 0.05; indicates significant difference compared to the T-2 toxin group, P < 0.05.
# indicates very significant difference compared to control, P < 0.01; indicates a very significant difference compared to the T-2 toxin group, P < 0.01. The magnification of the picture is 200 x and the scale bar is 100 μm.
FIG. 5 shows the effect of SeMet on T-2 toxin-induced oxidative stress-related markers in rabbit liver. FIG. 1 is T-AOC, FIG. 2 is SOD, FIG. 3 is GSH-PX, FIG. 4 is MDA, in which A. a control group, B.T-2 toxin group, C. low dose SeMet + T-2 toxin group, D. medium dose SeMet + T-2 toxin group, E. high dose SeMet + T-2 toxin group, # indicates a significant difference from the control group, P < 0.05; indicates significant difference compared to the T-2 toxin group, P < 0.05. # indicates very significant difference compared to control, P < 0.01; indicates a very significant difference compared to the T-2 toxin group, P < 0.01.
FIG. 6 is a graph showing the effect of SeMet on T-2 toxin-induced apoptosis in rabbit hepatocytes. A. A control group of B.T-2 toxin, a c. low dose set of SeMet + T-2 toxin, a d. medium dose set of SeMet + T-2 toxin, and an e. high dose set of SeMet + T-2 toxin, at a magnification of 250 x, at a scale bar of 100 μm.
FIG. 7 shows the effect of SeMet on expression of T-2 toxin-induced apoptosis-related index genes and proteins in rabbit liver. FIG. 1 shows the expression level of Bcl-2mRNA, FIG. 2 shows the expression level of Bax mRNA, FIG. 3 shows the expression level of Caspase-3mRNA, FIG. 4 shows the expression level of Caspase-9mRNA, FIG. 5 shows the expression level of Bcl-2protein, FIG. 6 shows the expression level of Bax protein, FIG. 7 shows the expression level of Caspase-3protein, FIG. 8 shows the expression level of Caspase-9protein, in the graphs, A. control group, B.T-2 toxin group, C. low dose SeMet + T-2 toxin group, D. medium dose SeMet + T-2 toxin group, E. high dose SeMet + T-2 toxin group, # shows a significant difference from the control group, P < 0.05; indicates significant difference compared to the T-2 toxin group, P < 0.05. # indicates very significant difference compared to control, P < 0.01; indicates a very significant difference compared to the T-2 toxin group, P < 0.01.
Detailed Description
The invention is described in detail below with reference to the figures and the specific embodiments, but the invention should not be construed as being limited thereto. The technical means used in the following examples are conventional means well known to those skilled in the art, and materials, reagents and the like used in the following examples can be commercially available unless otherwise specified.
Example 1
Preparation method of feed for preventing and treating rabbit liver injury caused by T-2 toxin
The feed ingredients shown in table 1 were pulverized and mixed to obtain a specific amount of added SeMet of 0.5mg/kg, 1mg/kg, and 1.5mg/kg of ration, based on the amount of selenium added and the selenium content of SeMet (40%). Each of the low, medium and high three-dose SeMet treatment groups weighed 4kg of the daily ration, and then dissolved with 100ml of distilled water to obtain 2mg, 4mg and 6mg of SeMet, and uniformly sprayed on the daily ration, and put into a 37 ℃ oven to be dried for later use.
TABLE 1 feed formulation and nutritional levels
In the feed formula, the specific components of the trace elements are as follows: each kilogram of feed is added with Cu 8mg, Zn 75mg, Fe80mg, Mn 100mg and vitamin A125000IU, vitamin D32500IU, vitamin E18mg, vitamin K32.8 mg, vitamin B12mg of vitamin B26mg of vitamin B120.025mg, biotin 0.0325mg, folic acid 1.25mg, pantothenic acid 12mg, nicotinic acid 50 mg.
Example 2
Effect of SeMet on T-2 toxin-induced liver function and histomorphometric changes in rabbits
Experimental methods
1.1 Breeding management
50 male New Zealand white rabbits are separately raised in animal rooms with the temperature of 21-25 ℃ and the relative humidity of 50-70% and are freely eaten for one week. Then randomly divided into a control group, a T-2 toxin group, a low-dose SeMet + T-2 toxin group, a medium-dose SeMet + T-2 toxin group and a high-dose SeMet + T-2 toxin group which are 5 groups, wherein each group contains 10 toxins. Wherein the control group and the T-2 toxin group are fed with normal feed for 21 d. Low, medium, and high doses of SeMet + T-2 toxin fractions were fed to feeds containing 0.2mg/kg, 0.4mg/kg, and 0.6mg/kg selenium, respectively (SeMet was dissolved in water, sprayed evenly on the feeds with a spray can, and then dried for later use) for 21 d. At 17d of feeding, the rabbits of the control group start to be intragastrically filled with 1ml of olive oil every day for 5d continuously; rabbits in the T-2 toxin group and the low, medium, and high dose SeMet + T-2 toxin groups began gavage with 0.4mg/kgT-2 toxin (T-2 toxin dissolved in 1ml olive oil) for 5 consecutive days. Rabbits were sacrificed 24h after the last gavage and livers were immediately removed. Uniformly cutting and taking the liver of the left lobe, putting the liver of the left lobe into 4% paraformaldehyde for fixation to prepare a paraffin section, taking the liver of the right lobe by using an RNase-free instrument, immediately putting the liver of the right lobe into an RNase-free tube for qRT-PCR detection, and putting the liver of the right lobe and the liver of the rest into a refrigerator at the temperature of 80 ℃ below zero for storage.
1.2 test items
Collecting 10ml blood from rabbit heart, standing, coagulating, centrifuging at 3000r/min for 10min, and storing in refrigerator at-80 deg.C.
(1) And (3) detecting the activity of AST and ALT enzyme by using an AST and ALT detection kit.
(2) ALP enzyme activity was detected using an ALP detection kit.
(3) And detecting the content of TP by using a TP detection kit.
(4) Paraffin sections of liver were made and PAS stained.
(5) Paraffin sections of liver were made and HE stained.
1.3 results
As shown in figure 1, the activities of AST, ALT and ALP in the rabbit serum and the TP content are respectively and remarkably improved by 78.28 percent, 2.5 times and 1.93 times (P is less than 0.01) compared with the rabbit serum of a control group after the rabbit is perfused with T-2 toxin for 5 days, and simultaneously, the TP content of the T-2 toxin group is also remarkably reduced by 30.89 percent (P is less than 0.01) compared with the rabbit serum of the control group, which indicates that the rabbit is seriously damaged by liver function. After SeMet pretreatment, the results show that compared with the T-2 toxin group, the activities of AST, ALT and ALP in the serum of the rabbits of the low-dose SeMet + T-2 toxin group are respectively reduced by 39.04%, 69.07% and 52.83% (P <0.01) remarkably, and the TP content is improved by 29.3% (P <0.05) remarkably. However, with the increase of the SeMet dose, the activities of AST, ALT and ALP in the serum of the rabbits in the middle-dose SeMet + T-2 toxin group are respectively and obviously reduced by 19.3 percent, 50.62 percent and 16.06 percent, and the TP content is obviously increased by 19.09 percent, and the reduction and increase amplitude of the activity are obviously lower than those of the low-dose SeMet + T-2 toxin group. And the high-dose SeMet + T-2 toxin group has no significant difference from the T-2 toxin group. The above results suggest that low doses of SeMet are effective in ameliorating T-2 toxin-induced liver function impairment in rabbits.
PAS staining was performed to investigate the change in hepatic glycogen synthesizing ability of rabbits of different groups, and the results are shown in FIG. 2, wherein the purple red color represents synthesized hepatic glycogen, the liver function of the control group normally synthesizes a large amount of hepatic glycogen, and the hepatic glycogen content of the rabbit liver of the T-2 toxin group is significantly reduced after the rabbit liver is perfused with T-2 toxin for 5 days. Liver glycogen was significantly increased compared to the T-2 toxin group after pretreatment with low doses of SeMet. However, we found that the liver glycogen content did not increase further but rather decreased gradually with increasing SeMet dose. These results indicate that low doses of SeMet can significantly improve the synthesis capacity of hepatic glycogen, contributing to the maintenance of normal liver function.
HE staining was used to analyze changes in liver tissue morphology of rabbits between groups. As shown in FIG. 3, the liver cells and liver sinuses of the control rabbit were radially arranged around the central vein, and the nuclei were large and round, with intact structure. After the T-2 toxin is perfused for 5 days, the liver cells are found to be unclear in contour, disordered in arrangement, severe vacuolation of cytoplasm and fragmentation and dissolution of cell nucleus. The liver tissue morphology after low-dose SeMet pretreatment is obviously improved and tends to be normal, however, with the continuous increase of the SeMet dose, the liver sinuses in the tissue are found to be obviously enlarged and are accompanied with massive hemorrhage. These results indicate that low doses of SeMet can significantly improve T-2 toxin-induced pathological changes in rabbit liver tissue.
Example 3
Effect of SeMet on T-2 toxin-induced oxidative stress in rabbit liver
Experimental methods
1.1 breeding management: same as example 2
1.2 test items
(1) Liver cryosections were made and stained for DHE, and the fluorescence intensity of DHE staining was quantified using ImageJ.
(2) Preparing liver tissue homogenate for detecting indexes of T-AOC, GSH-Px, MDA and SOD.
1.3 results
ROS are byproducts of the body's metabolism, and excessive ROS production by the body is a major cause of oxidative stress. We assessed ROS content in the livers of groups of rabbits by DHE staining, where red fluorescence intensity represents ROS levels in the livers. As shown in FIG. 4, the ROS content in the liver of the rabbit in T-2 toxin group was increased 1.2 times (P <0.01) significantly compared with the control group. After SeMet pretreatment, the ROS level in the livers of the rabbits of the low-dose SeMet + T-2 toxin group is reduced by 40.38 percent compared with that of the T-2 toxin group, however, with the increase of the addition dose of the SeMet, the lower dose of the SeMet + T-2 toxin group is reduced by 23.82 percent compared with that of the T-2 toxin group, the reduction range is obviously reduced, and the high-dose SeMet + T-2 toxin group has no significant difference compared with that of the T-2 toxin group. The results indicate that the low-dose SeMet can effectively inhibit the increase of ROS content in the livers of the rabbits induced by the T-2 toxin.
The enzyme activities of SOD and GSH-Px and the levels of T-AOC and MDA in the livers of the rabbits of each group are shown in figure 5, compared with a control group, the enzyme activities of SOD and GSH-Px and the levels of T-AOC in the livers of the rabbits of the T-2 toxin group are respectively and remarkably reduced by 34.16 percent, 51.71 percent and 46.39 percent (P <0.01), and the content of MDA is remarkably increased by 46.5 percent (P < 0.01). After SeMet pretreatment, compared with a T-2 toxin group, the enzyme activity of SOD, GSH-Px and T-AOC level of the rabbit liver of a low-dose SeMet + T-2 toxin group are obviously improved by 41.02%, 82.59% and 77.05%, and the MDA content is obviously reduced by 27.56%. However, with the increase of SeMet dosage, we found that the enzymatic activities of SOD, GSH-Px and T-AOC levels in the livers of rabbits with medium-dosage SeMet + T-2 toxin group are only increased by 16.62%, 22.73% and 56.39% compared with the T-2 toxin group, and the MDA content between the two groups has no significant difference. The enzyme activities of SOD and GSH-Px in the livers of the rabbits with the high-dose SeMet + T-2 toxin group are only increased by 13.71%, 21.59% and 18.91%, and the MDA contents between the two groups have no significant difference. Compared with the low-dose SeMet + T-2 toxin group, the change amplitude of the medium-dose and high-dose SeMet + T-2 toxin groups is obviously reduced. The above results show that low doses of SeMet can effectively maintain the body's own defense system, and inhibit abnormal changes of indexes related to liver oxidation induced by T-2 toxin.
Example 4
Effect of SeMet on T-2 toxin-induced apoptosis of liver cells in rabbits
Experimental methods
1.1 Breeding management, same as example 2
1.2 test items
(1) Liver cryosections were made and TUNEL stained, visualized under a fluorescent microscope and photographed.
(2) qRT-PCR detection of apoptosis-related gene expression in liver
The method comprises the following specific steps:
a. extraction of liver RNA: total RNA was extracted from each group of livers according to the Cwbio Trizol reagent protocol.
b. Primers were designed and the primer information is shown in Table 2.
TABLE 2 primer information
c. The reverse transcription system is shown in table 3, the reaction reagents are sequentially added and mixed, then metal bath is carried out at 72 ℃ for 5min, ice water bath is carried out for rapid cooling for 3min, then the reagents are sequentially added according to table 4, then reaction is carried out at 42 ℃ for 120min, inactivation is carried out at 80 ℃ for 10min, and storage is carried out at-20 ℃ for standby.
TABLE 3 reverse transcription System 1
TABLE 4 reverse transcription System 2
PCR reaction
The system was 10. mu.l, and each well was filled with each reagent according to Table 5. After pre-denaturation at 95 ℃ for 3-8 min, performing 45 cycles according to the conditions of (95 ℃ for 15s, 60 ℃ for 15s and 72 ℃ for 15s), and drawing a dissolution curve at 55-95 ℃. The mRNA transcription level of each gene was measured by a relative quantitative method.
TABLE 5 PCR reaction System
(3) Enzyme linked immunosorbent assay for detecting expression of apoptosis-related protein
a. Weighing 300mg of liver tissue, adding 2.7ml of PBS solution according to the mass ratio of 1:9, grinding by using a tissue grinder, and centrifuging for 10min at 4 ℃ under 3000r/min to prepare 10% homogenate to be tested.
b. And (3) setting a standard sample hole and a sample hole to be detected, setting a blank hole (the blank hole is not added with an enzyme standard reagent and a sample, and other steps are the same), adding 40 mu l of each concentration gradient standard sample into the standard sample hole, and repeating each hole for 2 times for constructing a standard curve.
c. Adding 40 mul of sample diluent into a sample hole to be detected on an enzyme-labeled coated plate, and then adding 10% of liver tissue homogenate.
d. The microplate was blocked with a blocking membrane and incubated at 37 ℃ for 30 min.
e. Carefully uncovering the sealing plate membrane, discarding liquid, spin-drying water in the holes, adding 300 mu l of washing liquid into each hole, soaking for 1min, then patting dry on absorbent paper, and repeating for 5 times.
f. 50. mu.l of enzyme-labeled reagent was added to each well, and no enzyme-labeled reagent was added to the blank wells.
j. Sealing the ELISA plate with a sealing plate membrane, and incubating at 37 deg.C for 30 min.
h. Removing the sealing plate film, discarding liquid, spin-drying water in the holes, adding 300 μ l of washing solution into each hole, standing for 1min, patting dry on absorbent paper, and repeating for 3 times.
i. Color developing solution A50 μ l and color developing solution B50 μ l are added into each hole, and mixed uniformly by a horizontal oscillator. The reaction was carried out at 37 ℃ for 15min in the absence of light.
g. Mu.l of stop solution was added to each well, and the reaction was terminated for 15min and then measured.
k. And (4) adjusting zero by using a blank hole, detecting a light absorption value at 450nm by using an enzyme-labeling instrument, and calculating the protein content according to the constructed standard curve.
1.3 results
Apoptotic cells were stained with TUNEL staining to label the apoptotic cells to explore the change in hepatocyte apoptosis among the groups, with green fluorescence representing apoptotic cells. The results are shown in FIG. 6, where the hepatocytes of the control group were normal and essentially free of apoptotic cells. After the T-2 toxin is perfused for 5 days, the number of apoptotic cells in the livers of the rabbits in the T-2 toxin group is obviously increased. After SeMet pretreatment, we found that the number of apoptotic cells in the low-dose SeMet + T-2 toxin group was significantly reduced compared to the T-2 toxin group, whereas the number of apoptotic cells in the medium-dose and high-dose SeMet + T-2 toxin groups gradually increased with the increase in the amount of SeMet addition. These results indicate that low doses of SeMet can significantly inhibit T-2 toxin-induced apoptosis in hepatocytes.
qRT-PCR and ELISA methods are adopted to detect the expression of genes and proteins of apoptosis related indexes Bax, Bcl-2, Caspase-3 and Caspase-9 in the liver. As shown in FIG. 7, the expression trends of genes and proteins of these markers were the same, and the levels of mRNA expression of Bax, Caspase-3 and Caspase-9 in the T-2 toxin group were significantly increased by 1.94 times, 75.9% and 1.37 times (P <0.01) and the levels of protein expression were significantly increased by 62.78%, 3.47 times and 45.98% (P <0.01) compared to the control group. The mRNA and protein expression levels of Bcl-2 were very significantly reduced by 54.56% and 62.7%, respectively (P < 0.01). After pretreatment of low-dose SeMet, the mRNA expression levels of Bax, Caspase-3 and Caspase-9 are greatly reduced by 49.7%, 38.61% and 42.09% (P <0.01), the protein expression levels are greatly reduced by 28.85%, 55.1% and 23.87%, and the mRNA and protein expression levels of Bcl-2 are also greatly increased by 94.45% and 1.57 times (P <0.01) compared with the T-2 toxin group. However, we found that with increasing SeMet dose, the expression levels of Bax, Caspase-3 and Caspase-9 increased gradually, and the expression level of Bcl-2 decreased gradually. And the SeMet + T-2 toxin group with high dose and the T-2 toxin group have no significant difference in mRNA and protein expression level. These results suggest that low doses of SeMet can effectively inhibit abnormal changes in gene and protein expression of T-2 toxin-induced apoptosis-related markers.
It should be noted that when the following claims refer to numerical ranges, it should be understood that both ends of each numerical range and any numerical value between the two ends can be selected, and the preferred embodiments of the present invention are described for the purpose of avoiding redundancy.
While preferred embodiments of the present invention have been described, additional variations and modifications in those embodiments may occur to those skilled in the art once they learn of the basic inventive concepts. Therefore, it is intended that the appended claims be interpreted as including preferred embodiments and all such alterations and modifications as fall within the scope of the invention.
It will be apparent to those skilled in the art that various changes and modifications may be made in the present invention without departing from the spirit and scope of the invention. Thus, if such modifications and variations of the present invention fall within the scope of the claims of the present invention and their equivalents, the present invention is also intended to include such modifications and variations.
Sequence listing
<110> university of Henan science and technology
<120> feed additive for preventing and treating rabbit liver injury caused by T-2 toxin and corresponding feed
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Claims (4)
1. Application of selenomethionine in preparing products for preventing and treating rabbit liver injury caused by T-2 toxin.
2. The use according to claim 1, wherein the selenomethionine is dissolved in water and added to the feed for rabbits, wherein 0.1-0.8 mg of selenomethionine is added to each kilogram of feed.
3. The use of claim 2, wherein the feed for rabbits comprises the following components in percentage by mass: 15% of corn, 11% of bean cake, 20% of wheat bran, 50% of grass meal, 1.5% of salt and the balance of trace elements; 0.1-0.8 mg of selenomethionine is added into each kilogram of feed.
4. Use according to claim 3, characterized in that the trace elements are as follows: each kilogram of feed is added with Cu 8mg, Zn 75mg, Fe80mg, Mn 100mg and vitamin A125000IU, WeiBiotin D32500IU, vitamin E18mg, vitamin K32.8 mg, vitamin B12mg of vitamin B26mg of vitamin B120.025mg, biotin 0.0325mg, folic acid 1.25mg, pantothenic acid 12mg, nicotinic acid 50 mg.
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Citations (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US20030083383A1 (en) * | 1999-08-16 | 2003-05-01 | Spallholz Julian E. | Method of using synthetic L-Se-methylselenocysteine as a nutriceutical and a method of its synthesis |
| CN110724662A (en) * | 2019-08-08 | 2020-01-24 | 湖南农业大学 | Method for applying L-selenomethionine in animal cell antioxidation and product thereof |
-
2020
- 2020-07-08 CN CN202010652291.8A patent/CN111773207A/en active Pending
Patent Citations (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| US20030083383A1 (en) * | 1999-08-16 | 2003-05-01 | Spallholz Julian E. | Method of using synthetic L-Se-methylselenocysteine as a nutriceutical and a method of its synthesis |
| CN110724662A (en) * | 2019-08-08 | 2020-01-24 | 湖南农业大学 | Method for applying L-selenomethionine in animal cell antioxidation and product thereof |
Non-Patent Citations (2)
| Title |
|---|
| LIU Y ET AL: "Protective effect of selenomethionine on T-2 toxin-induced liver injury in New Zealand rabbits", 《BMC VETERINARY RESEARCH》 * |
| 杨凌宸: "T-2/HT-2毒素对肉鸡毒性机理及其减控作用研究", 《中国优秀博硕士学位论文全文数据库(博士) 农业科技辑》 * |
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