Composition for reducing emission of odor pollutants in pig breeding process from feed source, application of composition and pig feed

Abstract

The invention belongs to the field of feed, and discloses an additive composition which comprises myristic acid, ferulic acid, magnolol, phytosterol and gamma-aminobutyric acid, and the addition amount of each substance in the feed is as follows: 500-1500mg / kg of myristic acid; the content of ferulic acid is 500 to 1,500 mg / kg; the content of magnolol is 300 to 500 mg / kg; the content of phytosterol is 100 to 300 mg / kg; and 100 to 300 mg / kg of gamma-aminobutyric acid. According to the present invention, myristic acid, ferulic acid, magnolol, phytosterol and gamma-aminobutyric acid are adopted as active components, such that the growth performance of pigs can be improved, the content of total SCFA, acetic acid, propionic acid and butyric acid in manure can be increased, the immunity can be improved, the microbial diversity index can be significantly improved, and finally the emission reduction purpose can be achieved through the multi-aspect improvement. Meanwhile, the invention further provides application of the additive composition and pig feed.

Description

Technical Field

[0001] The present invention relates to the field of feed, and in particular to a composition for reducing the emission of odor pollutants in a pig breeding process from the feed source, an application thereof, and pig feed. Background Art

[0002] The applicant has conducted long-term research on pig emission reduction, such as:

[0003] Publication number CN111657394A, the subject of the patent application is a biological preparation composition for adsorbing toxins in pigs and regulating the reduction of intestinal odor substances and its preparation method;

[0004] The patent application with publication number CN113317230B is titled "Biological Composite Litter Cake Device for Poultry Farming and Method for Treating and Reducing Odor and Malodor Emissions";

[0005] Publication number CN117461725B, the subject of the patent application is a composition, feed, and use for reducing odorous substances in poultry;

[0006] After long-term research, we believe that the main direction to achieve emission reduction is to improve intestinal health, increase the content of intestinal probiotics, enhance animal immunity and other aspects. This is a comprehensive research direction.

[0007] The technical problem to be solved in this case is: how to develop a new feed additive with emission reduction function. Summary of the Invention

[0008] One of the objectives of the present invention is to provide a composition for reducing the emission of odor pollutants in the pig breeding process from the feed source. The additive uses myristic acid, ferulic acid, magnolol, phytosterols, and γ-aminobutyric acid as active ingredients, which can improve the growth performance of pigs, increase the content of total SCFA, acetic acid, propionic acid and butyric acid in feces, enhance immunity, and significantly improve the microbial diversity index. Ultimately, through multi-faceted improvements, the goal of emission reduction is achieved.

[0009] At the same time, the invention also provides application of the additive composition and pig feed.

[0010] To achieve the above object, the present invention provides a composition for reducing the emission of odor pollutants in the pig breeding process from the feed source, comprising myristic acid, ferulic acid, magnolol, phytosterol and γ-aminobutyric acid, and the amount of each substance added to the feed is:

[0011] Myristic acid 500-1500 mg / kg;

[0012] Ferulic acid 500-1500 mg / kg;

[0013] Magnolia officinalis 300-500 mg / kg;

[0014] Phytosterols 100-300 mg / kg;

[0015] γ-aminobutyric acid 100-300 mg / kg.

[0016] The individual effects of the above substances are:

[0017] Myristic acid, a multifunctional fatty acid, exhibits important biological functions in various areas, including protein modification, signal transduction, and immunomodulation. Myristic acid modifies proteins through N-myristoylation, a modification typically occurring at the N-terminal glycine residue. This modification facilitates protein binding to cell membranes, thereby affecting their localization and function. Although myristic acid does not directly affect the enzymatic activity of the catalytic subunit of cAMP-dependent protein kinase, it participates in its interactions with other proteins. Myristic acid-treated hepatocytes increases the formation and secretion of VLDL (very low-density lipoprotein) transport vesicles, suggesting a regulatory role in lipid metabolism and transport. Furthermore, myristic acid activates phospholipase D (PLD), affecting the production of phosphatidic acid (PA), thereby regulating cell proliferation and differentiation. Myristic acid-modified lipid A analogs can induce the release of tumor necrosis factor α (TNF-α), interleukin 1 (IL-1), and interleukin 6 (IL-6) from monocytes, demonstrating potential immunomodulatory effects. Myristic acid exhibits excellent antibacterial activity against bacteria such as Staphylococcus aureus and Streptococcus suis. Its antibacterial mechanism primarily operates by interfering with the structure and function of bacterial cell membranes. Myristic acid interacts with phospholipids in bacterial cell membranes, disrupting their integrity and causing leakage of cellular contents, thereby inhibiting bacterial growth and reproduction. Furthermore, myristic acid exerts its antibacterial effects by inhibiting the secretion of toxic proteins by bacteria. For example, studies on Streptococcus suis have shown that myristic acid significantly inhibits the oligomerization and pore-forming activity of cytolysin, thereby alleviating its toxic effects on host cells. This mechanism of action significantly mitigates S. suis-induced cytotoxicity without exhibiting antibacterial activity, providing a potential application for the development of new antibacterial drugs. The antibacterial activity of myristic acid is also closely related to its chemical structure. Studies have shown that functional groups such as the carboxyl (-COOH) group of myristic acid can penetrate microbial cell walls, thereby interfering with intracellular physiological processes. Furthermore, the antibacterial activity of myristic acid exhibits a concentration-dependent nature, with higher concentrations more effectively inhibiting bacterial growth. Myristic acid derivatives have also been found to possess selective bactericidal effects, achieved by targeting specific glycerophospholipids in bacterial biofilms. Glycosphingolipids containing 2-hydroxymyristic acid can significantly stimulate polymorphonuclear leukocyte (PMN) phagocytosis and phagosome-lysosome fusion, thereby enhancing immune responses.

[0018] Ferulic acid is a phenolic acid compound widely found in plants and exhibits multiple biological functions, including antioxidant and anti-inflammatory effects. Ferulic acid exhibits significant antioxidant capacity, scavenging free radicals and mitigating cellular damage caused by oxidative stress. Its antioxidant mechanisms include direct scavenging of reactive oxygen species (ROS) and enhancing the activity of endogenous antioxidant enzymes. Furthermore, ferulic acid exerts anti-inflammatory effects by inhibiting the release of inflammatory mediators (such as the NF-κB signaling pathway), thereby alleviating inflammatory responses. Furthermore, ferulic acid and its metabolites can promote intestinal mucus secretion and enhance the physical barrier function of the intestinal mucosa. Furthermore, ferulic acid has a significant regulatory effect on the intestinal microbiota. Studies have found that ferulic acid can increase the number of beneficial bacteria such as Bifidobacterium and Lactobacillus while inhibiting the overgrowth of harmful bacteria. In a mouse model of antibiotic stress, ferulic acid has been shown to improve the intestinal microbiota structure by upregulating the ratio of Firmicutes to Proteobacteria, promoting the proliferation of beneficial bacteria such as Clostridium, and preventing the overgrowth of opportunistic pathogens such as Enterococcus. Furthermore, the protective effect of ferulic acid on intestinal barrier function has also garnered attention. In a mouse model of sepsis, ferulic acid significantly improved intestinal mucosal barrier function, reduced intestinal bacterial translocation, and lowered serum endotoxin levels. Furthermore, ferulic acid can also maintain the integrity of intestinal epithelial cells by increasing the expression of tight junction proteins (such as occludin and ZO-1), thereby strengthening the intestinal mechanical barrier.

[0019] Magnolia officinalis, a biphenolic compound isolated from the stem bark of Magnolia officinalis, a traditional Chinese medicine, exhibits anti-inflammatory, antioxidant, and lipid metabolism-enhancing properties. In mice with ulcerative colitis, magnolia officinalis reduces the activity of tumor necrosis factor α (TNFα), interleukin-1β (IL-1β), and interleukin-12 (IL-12) induced by dextran sulfate sodium by downregulating nuclear factor κB (NF-κB) and upregulating peroxisome proliferator-activated receptor γ (PPARγ) mRNA. Furthermore, magnolia officinalis significantly increases the mRNA expression of ZO-1 and occludin in mice with dextran sulfate-induced ulcerative colitis. In a model of renal ischemia-reperfusion injury, magnolol was found to reduce the levels of TNFα, IL-1β, interleukin-6 (IL-6), and Bax, while inhibiting the phosphorylation of pro-apoptotic mitogen-activated protein kinase (MAPK) and enhancing the mRNA expression levels of interleukin-10 (IL-10) and Bcl-2, thereby inhibiting apoptosis from both intrinsic and extrinsic pathways. Previous studies have shown that magnolol inhibits Porphyromonas gingivalis lipopolysaccharide-induced macrophage inflammation by activating the MAPK and Nrf-2 / HO-1 signaling pathways. The same study found that magnolol can effectively eliminate free radicals in animals, enhance the activity of antioxidant enzymes, improve the growth performance and antioxidant capacity of yellow-feathered broilers, and improve meat quality and intestinal microbiota. Magnolol, when used in combination with chemotherapy drugs, can improve skeletal muscle atrophy and inhibit weight loss in patients with bladder cancer. This may be related to magnolol's ability to inhibit carnosine and activin A formation, increase the activity of phosphorylated protein kinase B (p-Akt) and phosphorylated FOXO3 (p-FOXO3), enhance the mRNA expression of insulin-like growth factor 1 (IGF-1) and phosphorylated mammalian target of rapamycin (p-mTOR), and reduce the activity of proinflammatory cytokines. Acrolein, a neurotoxin, can induce oxidative stress and activate MEK / ERK signaling and mitochondrial caspases, leading to apoptosis in neuroblasts and thus inducing neurodegeneration. Pretreatment of cells with magnolol reduces ROS production and inhibits JNK / mitochondrial caspase, PI3K / MEK / ERK, and PI3K / Akt / FOXO1 signaling pathways, thereby protecting the brain from oxidative damage. During pressure-mediated venous remodeling, magnolol interferes with venous proliferation, ERK1 / 2 activity, and gelatinase activity in mice, while not affecting endothelial capillary formation. Choi et al. showed that magnolol exerted its protective effect by reducing phospholipid peroxidation in antimycin A-treated osteoblasts MC3T3-E1.

[0020] In addition to their cholesterol-lowering effects, phytosterols also possess antioxidant and anti-inflammatory properties. Their antioxidant effects primarily protect cell membrane lipids from oxidative damage by capturing free radicals and interrupting free radical chain reactions. Regarding anti-inflammatory properties, phytosterols may achieve cholesterol-lowering effects by reducing the oxidation of low-density lipoproteins, inhibiting the accumulation of inflammatory cells in the arterial intima, and controlling the production of inflammatory cytokines. Phytosterols can exert immunomodulatory effects by intercalating into cell membrane structures, affecting leukocytes and complement production. Phytosterols regulate the phosphorylation of NF-κBp65 protein within the cell nucleus, controlling the nuclear translocation of NF-κB. Phytosterols promote an innate immune response in cells and tissues by influencing the binding of ligands to nuclear receptors such as liver X receptors.

[0021] γ-Aminobutyric acid (GABA) binds to GABA receptors on neurons, generating inhibitory postsynaptic potentials and thereby reducing neuronal excitability. This inhibitory effect helps maintain the stability and homeostasis of the nervous system. GABA plays a crucial role in the central nervous system and possesses important biological functions, including improving intestinal function, enhancing immunity, increasing antioxidant capacity, and alleviating environmental stress. GABA, through central neurotransmitters, mediates the release of somatostatin in the gastrointestinal tract, increases immunoglobulin levels, inhibits the production of inflammatory factors, activates B lymphocytes, and suppresses T lymphocyte cytotoxicity, playing a crucial role in enhancing nonspecific immunity. GABA significantly reduces H2O2-induced ROS formation and inhibits H2O2-induced activation of NF-κB and caspase 3 signaling. Furthermore, under H2O2 stress, GABA can regulate the Keleh-like epichlorohydrin-associated protein 1 (Keap1)-nuclear factor E2-related factor 2 (Nrf2) and Notch1 signaling pathways to maintain redox homeostasis. GABA works by regulating corticotropin-releasing hormone (CRH) neurons in the HPA axis of animals, thereby alleviating the animal's stress response.

[0022] In the present invention, the purpose of odor reduction can be achieved by combining various components; the effect of odor reduction comes from the antibacterial and antioxidant effects of individual substances, inhibition of inflammatory factors, regulation of intestinal flora, etc.

[0023] In the above composition, the amount of each substance added to the feed is:

[0024] Myristic acid 800-1300 mg / kg;

[0025] Ferulic acid 800-1300 mg / kg;

[0026] Magnolia officinalis 350-450 mg / kg;

[0027] Phytosterols 150-250 mg / kg;

[0028] γ-aminobutyric acid 150-250 mg / kg.

[0029] At the same time, the present invention also discloses the use of the composition as described above to prepare feed for improving the growth performance of pigs or achieving the purpose of reducing pig odor emissions.

[0030] In addition, the present invention also discloses a pig feed containing the following substances:

[0031] Myristic acid 500-1500 mg / kg;

[0032] Ferulic acid 500-1500 mg / kg;

[0033] Magnolia officinalis 300-500 mg / kg;

[0034] Phytosterols 100-300 mg / kg;

[0035] γ-aminobutyric acid 100-300 mg / kg.

[0036] The above-mentioned pig feed contains the following substances:

[0037] Myristic acid 800-1300 mg / kg;

[0038] Ferulic acid 800-1300 mg / kg;

[0039] Magnolia officinalis 350-450 mg / kg;

[0040] Phytosterols 150-250 mg / kg;

[0041] γ-aminobutyric acid 150~250mg / k.

[0042] Beneficial effects

[0043] 1. The composition of the present invention has a positive effect on the growth performance of piglets and can reduce the feed-to-weight ratio;

[0044] 2. The composition of the present invention can significantly reduce the rate of diarrhea;

[0045] 3. The composition of the present invention can reduce the emission of odor components and greenhouse gases;

[0046] 4. The combination of the present invention can increase the content of short-chain fatty acids in feces, improve the immune function of piglets, and increase the abundance of specific microorganisms in feces. BRIEF DESCRIPTION OF THE DRAWINGS

[0047] Figure 1It is a comparison chart of the short-chain fatty acid content in feces of the control group and experimental group 1;

[0048] Figure 2 This is a comparison chart of the immune function of piglets in the control group and experimental group 1;

[0049] Figure 3 This is a comparison chart of the abundance of specific fecal microorganisms in the control group and experimental group 1. DETAILED DESCRIPTION

[0050] The present invention will be further described below in conjunction with the embodiments, but this does not constitute any limitation to the present invention. Any limited modifications made within the scope of the claims of the present invention are still within the scope of the claims of the present invention.

[0051] 1. Breeding Experiment

[0052] This study employed a single-factor design and involved 36 weaned barrow piglets, each of which had a similar initial weight. The piglets were divided into six treatments: a control group and experimental groups 1 through 5. The control group was fed a standard basal diet (see Table 2), while the experimental groups were fed a basal diet supplemented with a supplement (see Table 1). Both groups were housed under the same feeding regimen, with the principle of feeding sparingly and supplementing frequently. Feeding was ad libitum, with no restrictions, for a total of 15 days.

[0053] The following additive compositions were added to each group:

[0054] Table 1 Additive composition

[0055]

[0056]

[0057] Table 2 Basic diet composition (%, feeding basis)

[0058] project Basic diet corn 55.9 Dehulled soybean meal 15.0 Extruded full-fat soybeans 5.0 Soy protein concentrate 4.0 fishmeal 5.0 whey powder 8.0 sucrose 2.0 soybean oil 1.4 Calcium hydrogen phosphate 1.2 Stone powder 0.75 salt 0.2 Lysine 0.45 Methionine 0.2 Threonine 0.1 Tryptophan 0.1 Valine 0.2 Premix 0.5 total 100

[0059] Performance testing method:

[0060] Growth performance

[0061] At the start of the trial, all weaned piglets were weighed, and their initial weights were recorded before the start of the trial. At the end of the trial, they were weighed and their feed consumption was calculated. Average daily gain (ADG), average daily feed intake (ADFI), and feed-to-gain ratio (FCR) were calculated during the trial period. Environmental monitoring data and mortality were also recorded.

[0062] Short-chain fatty acids

[0063] One gram of sample was placed in a 10-mL centrifuge tube, 2 mL of 0.1% hydrochloric acid (v / v) was added, and the mixture was placed on ice for 25 min. After mixing, the mixture was centrifuged at 15,000 rpm for 15 min. The supernatant was collected and filtered through a 0.22-μm filter membrane (Millipore, Bedford, OH, USA) and injected into a gas chromatograph (Agilent HP 6890 series, Santa Clara, CA, USA) to detect the content of volatile fatty acids in the fecal sample.

[0064] Microbial diversity

[0065] Fresh pig fecal samples were collected and genomic DNA was extracted. Total bacterial DNA in the samples was extracted using a DNA kit (Omega Bio-tek, Norcross, GA, USA), and DNA concentration and purity were determined using NanoDrop2000. The bacterial universal primers 515F (5′-GTGCCAGCMGCCGCGG-3′) and 907R

[0066] The bacterial 16S rRNA gene V4-V5 variable region was amplified by PCR using the primer (5′-CCGTCAATTCMTTTRAGTTT-3′). The PCR amplification product was recovered and purified using the Axyprep DNA Gel Extraction Kit (Axygen Biosciences, CA, USA), eluted with Tris-HCl, and detected by 2% agarose gel electrophoresis. A library was constructed from the purified amplified fragments and sequenced using the Illumina Miseq platform. The raw sequence was quality-controlled using Trimmomatic (version 3.29) software and assembled using FLASH software. Sequences were then clustered into operational taxonomic units (OTUs) at 97% similarity using UPARSE software. Chimeras were removed using UCHIME software. Each sequence was annotated with species classification using RDP classifier and compared with the Silva database (SSU123). The alignment threshold was set at 90% and the 16S rRNA microbial gene sequence was analyzed using PICRUSt (Phylogenetic Investigation of Communities by Reconstruction of Unobserved States) software. The resulting OTUs table was used to predict the metabolic function of the microbial community by referencing the Kyoto Encyclopedia of Genes and Genome (KEGG) database.

[0067] immune factors

[0068] Serum immunoglobulin A (IgA), IgG, IgM, IL1β, IL-6, and IL-10 were detected according to the instructions of the enzyme-linked immunosorbent assay.

[0069] Quantitative analysis of fecal microorganisms

[0070] Specific primers were used to amplify specific fragments. The sequences of the specific primers are shown in Table 3. Standard plasmids were constructed using pMD 19-T Vector (Takara, Dalian, China) and introduced into competent cells. Single white colonies were selected on LB-agar plates containing X-Gal, IPTG, and ampicillin and expanded in LB medium. Plasmids were extracted using an Omega D6943 (Guangzhou, China), and the target fragments were amplified. Agarose gel electrophoresis was performed, and fragments of appropriate sizes were recovered and sequenced to verify the target fragment's incorporation. Qualified plasmids were serially diluted in multiples of 10. A linear relationship between the lg (copy number) (abscissa) and the quantification cycle number (ordinate) was constructed to calculate the absolute copy number of specific microorganisms per gram of feces. The quantitative reaction system was as follows: SYBR Green Supermix 5.0 μL; fecal bacterial / plasmid DNA 2 μL; upstream primer 0.4 μL; downstream primer 0.4 μL; and ddH2O 2.2 μL.

[0071] Table 3 Microbial primer sequences

[0072]

[0073] Fecal polyphenols and indole compounds

[0074] The phenolic and indole substances in feces were determined by HPLC, mainly detecting the contents of cresol, phenol, and skatole. The specific operation steps were referred to the literature (Jensen, MT, Cox, RP, & Jensen, BB (1995). 3-Methylindole (skatole) and indole production by mixed populations of pig fecalbacteria. Applied and environmental microbiology, 61(8), 3180–3184.)

[0075] Biogenic amine determination

[0076] The contents of methylamine, tryptamine, tyramine, putrescine, cadaverine, spermine, and spermidine in piglet feces were determined by high-performance liquid chromatography, and the total biogenic amine content was calculated. The specific operation steps were referred to the previously published literature (Yang YX, Mu CL, Zhang JF, et al. Determination of biogenic amines in digesta by high-performance liquid chromatography with precolumn dansylation [J]. Analytical Letters, 2014, 47(8): 1290-1298.).

[0077] Greenhouse gas detection

[0078] A 100 mL representative gas sample was collected using a gas bag, and 1 mL of the gas sample was injected into a gas chromatograph (Agilent 8890, USA) to determine the CH4, CO2, and N2O contents in the gas sample.

[0079] Test results

[0080] The growth performance test results can be seen in Table 4;

[0081] Table 4 Growth performance test results

[0082] Project (n=6) control group Experimental group 1 Experimental Group 2 Experimental Group 3 Experimental Group 4 Experimental Group 5 Initial weight, kg 9.80 9.80 9.87 9.83 9.83 9.87 Weight at the end of the test, kg 16.26 16.80 16.47 16.73 16.67 16.50 Daily weight gain, g 431 467 440 460 456 442 Daily feed intake, g 756 763 758 774 790 756 Material-to-weight ratio 1.76 1.64 1.72 1.68 1.74 1.71 Diarrhea rate, % 6.32 3.26 3.98 3.35 3.63 3.38

[0083] The test results of indole, skatole, total biogenic amines, and greenhouse gas emissions in feces are shown in Table 5;

[0084] Table 5 Emission statistics of indole, skatole, total biogenic amines and greenhouse gases in feces

[0085] project control group Experimental group 1 Experimental Group 2 Experimental Group 3 Experimental Group 4 Experimental Group 5 Methane, ppm / kg feces 63.53 54.16 61.00 58.00 63.00 60.00 Carbon dioxide, ppm / kg feces 1592.47 1163.96 1476.18 1334.67 1388.88 1566.85 Nitrous oxide, ppm / kg feces 2.47 2.30 2.42 2.34 2.46 2.43 Indole, μg / g 24.00 13.70 22.97 14.30 22.00 14.10 Skatole, μg / g 45.00 28.00 42.33 31.67 38.77 29.33 Total biogenic amines, μg / g 308.00 226.00 287.00 257.00 274.00 260.00

[0086] In addition, the present invention also tested the content of fecal short-chain fatty acids, microbial diversity index, immune function and inflammatory factors, and the abundance of specific fecal microorganisms in the control group and the experimental group 1. The test results are as follows: Figure 1 、 Figure 2 、 Figure 3 and Table 6;

[0087] Table 6 Statistical results of microbial diversity index

[0088] project control group Experimental group 1 Ace 348.53 343.59 Chao1 365.66 350.44 Sobs 333.02 331.76 Shannon 3.56 4.28 Simpson 0.09 0.05

[0089] Result analysis:

[0090] 1. As can be seen from Table 3, experimental group 1 has the best growth effect, followed by experimental group 3, indicating that ferulic acid has a slightly smaller effect on growth performance than myristic acid; based on the data of experimental groups 2, 3, 4, 5 and the control group, it can be basically concluded that magnolol and myristic acid have a more important effect on improving growth performance.

[0091] 2. In terms of improving diarrhea rates, magnolol, myristic acid, and ferulic acid are almost equally important;

[0092] 3. From the perspective of reducing greenhouse gas emissions, myristic acid plays a crucial role. In the presence of magnolol, myristic acid and ferulic acid show significant synergy;

[0093] 4. In terms of odor emission, the performance of myristic acid is almost similar to that of the experimental group composed of myristic acid and ferulic acid, indicating that myristic acid is also important in reducing odor emission.

[0094] 5. The results of the detection of fecal short-chain fatty acid content, microbial diversity index, immune function and inflammatory factors, and fecal specific microbial abundance in the control group and the experimental group can prove that the formula of the present invention achieves the optimization of the above-mentioned performance based on multiple angles such as immune function, biodiversity, anti-inflammatory and antioxidant properties, and intestinal microbial balance.

Claims

1. A composition for reducing the emission of odor pollutants from the feed source in the pig breeding process, characterized in that: Including myristic acid, ferulic acid, magnolol, phytosterol and γ-aminobutyric acid, the amount of each substance added to the feed is: Myristic acid 500-1500 mg / kg; Ferulic acid 500-1500 mg / kg; Magnolia officinalis 300-500 mg / kg; Phytosterols 100-300 mg / kg; γ-aminobutyric acid 100-300 mg / kg.

2. The composition according to claim 1, characterized in that The amount of each substance added to the feed is: Myristic acid 800-1300 mg / kg; Ferulic acid 800-1300 mg / kg; Magnolia officinalis 350-450 mg / kg; Phytosterols 150-250 mg / kg; γ-aminobutyric acid 150-250 mg / kg.

3. Use of the composition according to claim 1 or 2 in preparing feed for improving the growth performance of pigs or reducing pig odor emissions.

4. A pig feed, characterized in that: Contains the following substances: Myristic acid 500-1500 mg / kg; Ferulic acid 500-1500 mg / kg; Magnolia officinalis 300-500 mg / kg; Phytosterols 100-300 mg / kg; γ-aminobutyric acid 100-300 mg / kg.

5. The pig feed according to claim 4, characterized in that Contains the following substances: Myristic acid 800-1300 mg / kg; Ferulic acid 800-1300 mg / kg; Magnolia officinalis 350-450 mg / kg; Phytosterols 150-250 mg / kg; γ-aminobutyric acid 150-250 mg / kg.

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