17 research outputs found

    Inadequate fat diet

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    Aim. To determine the main factors of inadequate fat diet (IAFD) and indicate the ways of their change.Methods. Analysis and generalization of existing scientific literature data and the results of our own research.Results. The following factors of IAFD have been identified:1) excess fat in the diet;2) an excess of palmitic acid in dietary fats;3) an excess of linoleic acid in dietary fats;4) consumption of thermoperoxide fats;5) deficiency of Ο‰-3 polyunsaturated fatty acids (PUFA).Conclusion. IAFD is a cause of metabolic and neuropsychiatric disorders underlying non-communicable diseases

    Effect of an antidisbiotic agent on the biosynthesis of fatty acids of liver lipids of rats which received palm oil on the background of dysbiosis

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    Background. To determine the effect of antidysbiotic agent on the biosynthesis of fatty acids of lipids in the liver of rats fed a high-fat diet (HFD) with palm oil against the background of dysbiosis. Methods. The HFD contained 15% palm oil. In a biological experiment, white rats were used, divided into 4 groups: the 1st group received a fat-free diet (FFD), the 2nd, 3rd, and 4th received HFD. In rats of the 3rd and 4th groups, dysbiosis was reproduced using lincomycin. Rats of the 4th group from the first day of the experiment received an antidysbiotic agent (inulin + quercetin, ADA) with food. The duration of feeding is 39 days. Liver lipids were divided into 3 fractions: neutral lipids (NL), phospholipids (PL), and free fatty acids (FFA). The fatty acid composition of the fractions was determined by gas chromatography. The β€œactivities” of fatty acid synthase, palmitic acid elongase, and stearylCoA- desaturase (SCD18 and SCD16) were determined. Results. The presence of all classes of fatty acids (FA) in the liver lipids of rats treated with FFD was established. Consumption of HFD with palm oil increased the content of NL in the liver by 6 times (gr. 2), and in group 3 by 8 times. The introduction of ADA reduces the content of NL almost to the level of the 1st group. The content of Ο‰-3 polyunsaturated fatty acids (PUFA) decreases in the PL fraction in rats of the 3rd group and is restored in rats of the 4th group. In rats treated with HFD, the "activity" of synthase, SCD18 and very strongly SCD16 are reduced. Conclusion: The negative effect of palm oil on the background of dysbiosis on the biosynthesis of fatty acids in the liver, leading to hepatic steatosis and deficiency of Ο‰-3 PUFA, can be prevented by the use of an antidysbiotic agent

    Effect of dietary fats on endogenous oleic acid biosynthesis in rat liver

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    Aim: Determine the effect of dietary fats with different fatty acid composition on the biosynthesis of oleic acid and its metabolic precursors in the liver . Methods: High linoleic sunflower oil (HLSO), high oleic sunflower oil (HOSO) and palm oil (PO) were used. Rats were fed a semi-synthetic fat-free diet (FFD) and fat diets containing 5 % of the above oils (instead of starch) for 30 days. Liver lipids were divided into 3 fractions: neutral lipids (NL), phospholipids (PL) and free fatty acids (FFA). The fatty acid composition of the fractions was determined by gas chromatography. The β€œactivity” of fatty acid synthase was determined from the total content of the products of this reaction (C16:0 and C16:1). The β€œactivity” of palmitic acid elongase was determined by the ratio Π‘18:0/Π‘16:0, as well as by the formula (Π‘18:0+Π‘18:1)/(Π‘16:0–Б16:1). The β€œactivity” of stearic acid desaturase (SCD1) was determined by the ratio C16:1/C16:0 (SCD16) and by the ratio C18:1/C18:0 (SCD18). Results: In rats treated with fat diets, the content of palmitic and oleic acids is reduced only in the NL fraction, and to the greatest extent when consuming the diet with HLSO. The β€œactivity” of palmitic acid elongase increases significantly with the consumption of a diet with HLSO. SCD16 desaturase β€œactivity” decreases with fat diet, while SCD18 desaturase β€œactivity” increases. The level of SCD18 is significantly higher than the level of SCD16. Consumption of HLSO reduces the content of Ο‰-3 PUFA in rat liver lipids, while the intake of HOSO increases it. Conclusions: HLSO diet reduces the endogenous biosynthesis of oleic and palmitic acids, as determined by the analysis of the rat liver NL fraction. A fat diet reduces SCD16 β€œactivity” but increases SCD18 β€œactivity”, especially when fed a diet with HOSO. The diet with HLSO reduces the content of Ο‰-3 PUFA in liver lipids

    Influence of consumption of high oleic sunflower oil on the biosynthesis of fatty acids in the liver of rats

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    Background. To determine the effect of consumption of high-oleic sunflower oil on the content and biosynthesis of energy and polyunsaturated (PUFA) fatty acids in rat liver lipids. Methods. Rats received a semi-synthetic fat-free diet in which 5 % or 15 % starch was replaced with high oleic sunflower oil. One group of rats received a diet with 5 % regular (high linoleic) sunflower oil. The duration of feeding was 30 days. Liver lipids were divided into three fractions: neutral lipids, phospholipids and free fatty acids, in which the fatty acid composition was determined by gas chromatography. The "activity" of fatty acid synthase, palmitic acid elongase, and stearyl-CoA desaturase (SCD18) was determined by the ratio of fatty acid content. Results. It was found that the largest amount (60-80 %) of fatty acids in liver lipids are energy (C16:0 + C16:1 + C18:0 + C18:1). PUFA account for 10-30% of all fatty acids, and they are also found in the liver lipids of rats fed a free-fat diet (FFD). Fatty diets reduce the "activity" of synthase, but increase the "activity" of elongase and desaturase. A diet with high linoleic sunflower oil reduces the content of Ο‰-3 PUFA in lipids, while a diet with high oleic sunflower oil increases it dose-dependently. Fatty diets containing high oleic sunflower oil dose-dependently reduce the "activity" of palmitic acid desaturase (SCD16). Consumption of high linoleic sunflower oil sharply increases the ratio of Ο‰-6/Ο‰-3 PUFA in liver lipids, while diets with high oleic oil reduce it dose-dependently

    Influence of fat-free, fat and sucrose diets on the indicators of lipid metabolism in rats

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    The aim. To determine the effect on lipid metabolism in the serum of rats of diets: fat-free, fat and sucrose. Materials and methods. Feeding experiments were carried out on rats divided into 3 groups: the first received a fat-free diet (FFD), the second received a diet with 5 % sunflower oil and the third received a diet with 50 % sucrose. The condition of lipid metabolism was assessed according to the following indicators of blood serum: the content of triglycerides (TG), cholesterol, MDA, fatty acid composition of neutral lipids (TG + cholesterol esters) and phospholipids. The duration of feeding was 30 days. Results. An increase in TG levels in rats fed with oil or sucrose and a decrease in MDA levels in rats fed a sucrose diet was found. The greatest gain in live weight was found in rats fed a fat diet. The presence of all essential fatty acids in the blood serum lipids of rats receiving FFD and a sucrose diet was found, and the content of Ο‰-3 PUFAs was the highest in rats treated with FFD. Conclusions. Rats have endogenous sources of PUFA, including the Ο‰-3 series. Consumption of sunflower oil inhibits the formation of Ο‰-3 PUFAs and increases the Ο‰-6/Ο‰-3 PUFA ratio by 2.5-4 times. Consumption of sucrose increases the formation of oleic acid and decreases lipid peroxidation

    Reduction of mineralizing activity of periodontal bone tissue in rats with consumption of ordinary sunflower oil

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    More than 20 % of people over the age of 50 suffer from osteoporosis. Lipids play an important role in the pathogenesis of osteoporosis. Background. To investigate the effect of ordinary (high-linoleic) sunflower oil (OSO) on the state of periodontal bone tissue. Methods. In 5 series of experiments, determine the mineralization activity of the alveolar appendix of the mandible rats that were obtained with feed 5 or 15 percent of OSO for from 22 to 75 days. Mineralizing activity was determined by the ratio of activity of alkaline and acid phosphatase. In liver lipids (fractions of phospholipids and free fatty acids) were determined by the content of long-chain polyunsaturated fatty acids (LCPUFA) by the gas chromatographic method. Results. A decrease in mineralizing activity in OSO consumption, especially when using a feed with 15 % of OSO against a dysbiosis or metabolic syndrome. A significant (almost 10 times) is shown to reduce the content of Ο‰-3 PUFA in fraction of phospholipids of the liver of rats receiving a diet with a content of OSO. Conclusion. Sunflower oil reduces the mineralizing activity of periodontal bone tissue by reducing the endogenous biosynthesis of Ο‰-3 PUFA

    Therapeutic and prophylactic efficiency of polyfunctional anti-disbiotic drugs under conditions of experimental lipid intoxication

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    Aim: to compare the therapeutic and prophylactic efficiency (TPE) of four polyfunctional antidisbiotic drugs (PFAD) in experimental lipid intoxication. Methods: TPE was assessed by the nature of changes in blood serum levels of biochemical markers of inflammation (elastase, MDA), bacteremia (urease), nonspecific immunity (lysozyme). The following PFAD were used: Kvertulin (quercetin + inulin + calcium citrate), Lekvin (lecithin + quercetin + inulin + calcium citrate), Lekasil (lecithin + milk thistle meal + calcium citrate) and Lysozyme-forte (lysozyme + quercetin + inulin + gelatin + calcium citrate). Lipid intoxication was carried out on rats by introducing thermal peroxide sunflower oil (TPSO) with food at a dose of 4 g/kg for 75 days. PFAD was administered from day 31 at a dose of 300 mg/kg for 45 days. Results: there was a significant increase in the level of elastase, MDA, urease and a significant decrease in the activity of lysozyme in the blood serum of rats treated with TPSO. After the introduction of all drugs, a significant decrease in the level of elastase, MDA, urease and a significant increase in the activity of lysozyme were observed. Conclusion: with lipid intoxication, a dysbiotic syndrome develops, manifested by bacteremia, a decrease in the level of nonspecific immunity and manifestations of systemic inflammation. Taking polyfunctional antidisbiotic drugs reduces bacteremia, enhances nonspecific immunity and prevents the development of systemic inflammation. The most effective remedy turned out to be "LysozymeForte"

    Influence of high-fat nutrition with different fat-acid composition of fats on lipid peroxidation processes in rat's organs and tissues

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    The aim. To determine the effect of high-fat diet (HFD) using fats of different fatty acid composition on the content of malondialdehyde (MDA) in the organs and tissues of rats and on catalase activity. Materials and methods. The following edible fats were used: regular (high linoleic) sunflower oil, high oleic sunflower oil, palm, butter and coconut oils at a concentration of 15 % by weight of the diet. The rats were fed for 64 days. Before euthanasia, rats were bled from v. porta and v. cava inferior. The MDA content and catalase activity were determined in blood serum, in liver homogenates, intestinal mucous membranes, in skeletal muscles, heart and brain. The antioxidant-prooxidant index of API was calculated from the ratio of catalase activity and MDA content. Results. found that the content of the MDA in v. cava is significantly higher than v. porta. High-fat diet (HFD) increases the MDA content in all tissues except the brain, and most of all in the liver and after the consumption of high-palmitic fats (palm and butter), as well as high-linoleic sunflower oil. The exception is high oleic sunflower oil, the consumption of which does not increase the MDA content. Catalase activity reacts little to HFD. Conclusions. the liver secrete MDA into the blood. HFD increases the level of MDA in organs and tissues, except for the brain, without significantly reducing the activity of catalase. The antioxidant effect of HFD using high oleic sunflower oil can be explained by the antioxidant properties of oleic acid

    Therapeutic and preventive effectiveness of oral application of phitogels β€œKvertulin”, β€œBiotrit” and β€œDubovy” in inflammatory complications in the digestive system of rats treated with thermoperoxide sunflower oil

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    Aim. It has been established that the consumption of thermoperoxide fats causes the development of pathological processes in the tissues of the mouth, stomach, intestines and liver. The purpose of this work is to determine the possibility of their normalization using oral applications of phytogels. Methods. Thermoperoxide oil (TPSO) was obtained by heating sunflower oil in the presence of H2O2 at a temperature of +180 Β°C for 60 minutes. Oral TPSO applications were made on the oral mucosa at a dose of 2.25 g/kg daily for 5 days. Used mucose-adhesive phytogels "Kvertulin" (quercetin + inulin), "Biotrit" (juice from wheat sprout) and "Dubovy" (extract of polyphenolic compounds from oak wood) in the form of oral applications at a dose of 2.25 g/kg for half an hour before TPSO applications daily for 5 days. Elastase and urease activity and malonic dialdehyde (MDA) content were determined in homogenates of the mucous membranes of the cheek, stomach, small and large intestines, as well as in the liver. Results. Oral applications of TPSO increased the levels of MDA, elastase and urease in the tissues of the digestive system. Applications of phytogels significantly normalized these parameters. Conclusions. Oral applications of TPSO cause the development of inflammation in the digestive system, especially in the liver. Oral applications of phytogels have a protective effect, especially "Kvertulin"

    ВлияниС потрСблСния высокоолСинового подсолнСчного ΠΆΠΌΡ‹Ρ…Π° Π½Π° биохимичСскиС ΠΏΠΎΠΊΠ°Π·Π°Ρ‚Π΅Π»ΠΈ Π²ΠΎΡΠΏΠ°Π»ΠΈΡ‚Π΅Π»ΡŒΠ½Ρ‹Ρ… ΠΈ Π·Π°Ρ‰ΠΈΡ‚Π½Ρ‹Ρ… процСссов Π² сывороткС ΠΊΡ€ΠΎΠ²ΠΈ крыс с ΡΠΊΡΠΏΠ΅Ρ€ΠΈΠΌΠ΅Π½Ρ‚Π°Π»ΡŒΠ½Ρ‹ΠΌ дисбиозом

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    ΠœΠ΅Ρ‚Π° Ρ€ΠΎΠ±ΠΎΡ‚ΠΈ: Π²ΠΈΠ·Π½Π°Ρ‡ΠΈΡ‚ΠΈ Π»Ρ–ΠΊΡƒΠ²Π°Π»ΡŒΠ½ΠΎ-ΠΏΡ€ΠΎΡ„Ρ–Π»Π°ΠΊΡ‚ΠΈΡ‡Π½Ρƒ Π΅Ρ„Π΅ΠΊΡ‚ΠΈΠ²Π½Ρ–ΡΡ‚ΡŒ високоолСїнової ΡΠΎΠ½ΡΡˆΠ½ΠΈΠΊΠΎΠ²ΠΎΡ— ΠΌΠ°ΠΊΡƒΡ…ΠΈ Ρƒ Ρ‰ΡƒΡ€Ρ–Π² Π· Π΅ΠΊΡΠΏΠ΅Ρ€ΠΈΠΌΠ΅Π½Ρ‚Π°Π»ΡŒΠ½ΠΈΠΌ дисбіозом. ΠœΠ°Ρ‚Π΅Ρ€Ρ–Π°Π»ΠΈ Ρ– ΠΌΠ΅Ρ‚ΠΎΠ΄ΠΈ: використовували ΠΌΠ°ΠΊΡƒΡ…Ρƒ Π· насіння високоолСїнового ΡΠΎΠ½ΡΡˆΠ½ΠΈΠΊΡƒ Ρ– ΠΌΠ°ΠΊΡƒΡ…Ρƒ Π· насіння Π·Π²ΠΈΡ‡Π°ΠΉΠ½ΠΎΠ³ΠΎ (високолінолСвого) ΡΠΎΠ½ΡΡˆΠ½ΠΈΠΊΡƒ. Π•ΠΊΡΠΏΠ΅Ρ€ΠΈΠΌΠ΅Π½Ρ‚Π°Π»ΡŒΠ½ΠΈΠΉ дисбіоз Π²Ρ–Π΄Ρ‚Π²ΠΎΡ€ΡŽΠ²Π°Π»ΠΈ Ρƒ Ρ‰ΡƒΡ€Ρ–Π² Π·Π° допомогою Π»Ρ–Π½ΠΊΠΎΠΌΡ–Ρ†ΠΈΠ½Ρƒ. ΠœΠ°ΠΊΡƒΡ…Ρƒ Π²Π²ΠΎΠ΄ΠΈΠ»ΠΈ Π΄ΠΎ складу ΠΊΠΎΠΌΠ±Ρ–ΠΊΠΎΡ€ΠΌΡƒ Π² ΠΊΡ–Π»ΡŒΠΊΠΎΡΡ‚Ρ– 10 %. Π’Ρ€ΠΈΠ²Π°Π»Ρ–ΡΡ‚ΡŒ Π³ΠΎΠ΄Ρ–Π²Π»Ρ– становила 18 Π΄Π½Ρ–Π². Π’ сироватці ΠΊΡ€ΠΎΠ²Ρ– Π²ΠΈΠ·Π½Π°Ρ‡Π°Π»ΠΈ наступні Π±Ρ–ΠΎΡ…Ρ–ΠΌΡ–Ρ‡Π½Ρ– ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΠΈ: Π°ΠΊΡ‚ΠΈΠ²Π½Ρ–ΡΡ‚ΡŒ ΡƒΡ€Π΅Π°Π·ΠΈ, Сластази, Π»Ρ–Π·ΠΎΡ†ΠΈΠΌΠ°, ΠΊΠ°Ρ‚Π°Π»Π°Π·ΠΈ, вміст ΠœΠ”Π. Π ΠΎΠ·Ρ€Π°Ρ…ΠΎΠ²ΡƒΠ²Π°Π»ΠΈ Π·Π° ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΠ°ΠΌΠΈ ΠΊΠ°Ρ‚Π°Π»Π°Π·ΠΈ Ρ– ΠœΠ”Π антиоксидантно-прооксидантний індСкс ΠΠŸΠ†, Π° Π·Π° ΡΠΏΡ–Π²Π²Ρ–Π΄Π½ΠΎΡˆΠ΅Π½Π½ΡΠΌ відносних активностСй ΡƒΡ€Π΅Π°Π·ΠΈ Ρ– Π»Ρ–Π·ΠΎΡ†ΠΈΠΌΠ° Ρ€ΠΎΠ·Ρ€Π°Ρ…ΠΎΠ²ΡƒΠ²Π°Π»ΠΈ ΡΡ‚ΡƒΠΏΡ–Π½ΡŒ дисбіозу. ΠŸΠ°Ρ‚ΠΎΠ³Π΅Π½Π½Ρƒ Π΄Ρ–ΡŽ дисбіозу Π²ΠΈΠ·Π½Π°Ρ‡Π°Π»ΠΈ Π·Π° ΡΡƒΠΌΠΎΡŽ Π²Ρ–Π΄Ρ…ΠΈΠ»Π΅Π½ΡŒ (Π² %) Π±Ρ–ΠΎΡ…Ρ–ΠΌΡ–Ρ‡Π½ΠΈΡ… ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΡ–Π² Π²Ρ–Π΄ ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΡ–Π² ΠΊΠΎΠ½Ρ‚Ρ€ΠΎΠ»ΡŽ, Π° Π»Ρ–ΠΊΡƒΠ²Π°Π»ΡŒΠ½Ρƒ Π΄Ρ–ΡŽ – ΠΏΠΎ сумі Π²Ρ–Π΄Ρ…ΠΈΠ»Π΅Π½ΡŒ Ρ†ΠΈΡ… ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΡ–Π² Π²Ρ–Π΄ ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΡ–Π² Ρƒ Ρ‰ΡƒΡ€Ρ–Π² Π· дисбіозом. Π Π΅Π·ΡƒΠ»ΡŒΡ‚Π°Ρ‚ΠΈ: встановлСно підвищСння рівня ΡƒΡ€Π΅Π°Π·ΠΈ, Сластази, ΠœΠ”Π Ρ‚Π° зниТСння рівня Π»Ρ–Π·ΠΎΡ†ΠΈΠΌΠ° Ρ– ΠΊΠ°Ρ‚Π°Π»Π°Π·ΠΈ Ρƒ Ρ‰ΡƒΡ€Ρ–Π² Π· дисбіозом. БпоТивання високоолСїнової ΠΌΠ°ΠΊΡƒΡ…ΠΈ Π·Π½ΠΈΠΆΡƒΠ²Π°Π»ΠΎ Ρ€Ρ–Π²Π΅Π½ΡŒ ΡƒΡ€Π΅Π°Π·ΠΈ, Сластази, ΠœΠ”Π Ρ‚Π° ΠΏΡ–Π΄Π²ΠΈΡ‰ΡƒΠ²Π°Π»ΠΎ Ρ€Ρ–Π²Π΅Π½ΡŒ Π»Ρ–Π·ΠΎΡ†ΠΈΠΌΠ° Ρ– ΠΊΠ°Ρ‚Π°Π»Π°Π·ΠΈ. ΠœΠ°ΠΊΡƒΡ…Π° Π· насіння Π·Π²ΠΈΡ‡Π°ΠΉΠ½ΠΎΠ³ΠΎ ΡΠΎΠ½ΡΡˆΠ½ΠΈΠΊΡƒ Π²ΠΏΠ»ΠΈΠ²Π°Ρ” Π½Π° Ρ†Ρ– ΠΏΠΎΠΊΠ°Π·Π½ΠΈΠΊΠΈ Π² Π·Π½Π°Ρ‡Π½ΠΎ ΠΌΠ΅Π½ΡˆΡ–ΠΉ ΠΌΡ–Ρ€Ρ–. Π—Π°ΠΊΠ»ΡŽΡ‡Π΅Π½Π½Ρ: ввСдСння Π² ΠΎΡ€Π³Π°Π½Ρ–Π·ΠΌ Π»Ρ–Π½ΠΊΠΎΠΌΡ–Ρ†ΠΈΠ½Ρƒ Π²ΠΈΠΊΠ»ΠΈΠΊΠ°Ρ” Ρ€ΠΎΠ·Π²ΠΈΡ‚ΠΎΠΊ дисбіотичного синдрому, який ΠΌΠΎΠΆΠ½Π° Π² Π·Π½Π°Ρ‡Π½Ρ–ΠΉ ΠΌΡ–Ρ€Ρ–ΠΏΠΎΠΏΠ΅Ρ€Π΅Π΄ΠΈΡ‚ΠΈ споТиванням високоолСїнової ΡΠΎΠ½ΡΡˆΠ½ΠΈΠΊΠΎΠ²ΠΎΡ— ΠΌΠ°ΠΊΡƒΡ…ΠΈ.The aim: to determine the therapeutic and prophylactic efficacy of high oleic sunflower oilcake in rats with experimental dysbiosis. Materials and methods: oilcake from seeds of high oleic sunflower and oilcake from seeds of ordinary (high linoleic) sunflower were used. Experimental dysbiosis was reproduced in rats using the antibiotic lincomycin. Oilcakes were added to the composition of mixed fodders in the amount of 10%. The duration of feeding was 18 days. In the blood serum, the activity of urease, elastase, lysozyme, catalase and the content of MDA were determined. The antioxidant-prooxidant index of API was calculated from the indicators of catalase activity and MDA content, and the degree of dysbiosis was calculated from the ratio of the relative activities of urease and lysozyme. The pathogenic effect of dysbiosis was determined by the sum of the deviations (in %) of the markers from the control indicators. The therapeutic effect was determined (in %) by the sum of deviations from the indicators in rats with dysbiosis. Results: there was an increase in the level of urease, elastase, MDA and a decrease in the level of lysozyme and catalase in animals with dysbiosis. Consumption of high oleic oilcake reduced the level of urease, elastase, MDA and increased the level of lysozyme and catalase. Consumption of oilcake from ordinary sunflower seeds had little effect on biochemical parameters. Conclusion: the introduction of lincomycin into the body causes the development of a dysbiotic syndrome, which can be largely prevented by the consumption of high oleic sunflower oilcake.ЦСль: ΠΎΠΏΡ€Π΅Π΄Π΅Π»ΠΈΡ‚ΡŒ Π»Π΅Ρ‡Π΅Π±Π½ΠΎΠΏΡ€ΠΎΡ„ΠΈΠ»Π°ΠΊΡ‚ΠΈΡ‡Π΅ΡΠΊΡƒΡŽ ΡΡ„Ρ„Π΅ΠΊΡ‚ΠΈΠ²Π½ΠΎΡΡ‚ΡŒ высокоолСинового подсолнСчного ΠΆΠΌΡ‹Ρ…Π° Ρƒ крыс с ΡΠΊΡΠΏΠ΅Ρ€ΠΈΠΌΠ΅Π½Ρ‚Π°Π»ΡŒΠ½Ρ‹ΠΌ дисбиозом. ΠœΠ°Ρ‚Π΅Ρ€ΠΈΠ°Π»Ρ‹ ΠΈ ΠΌΠ΅Ρ‚ΠΎΠ΄Ρ‹: использовали ΠΆΠΌΡ‹Ρ… ΠΈΠ· сСмян высокоолСинового подсолнСчника ΠΈ ΠΆΠΌΡ‹Ρ… ΠΈΠ· сСмян ΠΎΠ±Ρ‹Ρ‡Π½ΠΎΠ³ΠΎ (высоколинолСвого) подсолнСчника. Π­ΠΊΡΠΏΠ΅Ρ€ΠΈΠΌΠ΅Π½Ρ‚Π°Π»ΡŒΠ½Ρ‹ΠΉ дисбиоз воспроизводили Ρƒ крыс с ΠΏΠΎΠΌΠΎΡ‰ΡŒΡŽ Π°Π½Ρ‚ΠΈΠ±ΠΈΠΎΡ‚ΠΈΠΊΠ° Π»ΠΈΠ½ΠΊΠΎΠΌΠΈΡ†ΠΈΠ½Π°. Π–ΠΌΡ‹Ρ…ΠΈ Π²Π²ΠΎΠ΄ΠΈΠ»ΠΈ Π² состав ΠΊΠΎΠΌΠ±ΠΈΠΊΠΎΡ€ΠΌΠΎΠ² Π² количСствС 10 %. ΠŸΡ€ΠΎΠ΄ΠΎΠ»ΠΆΠΈΡ‚Π΅Π»ΡŒΠ½ΠΎΡΡ‚ΡŒ кормлСния составила 18 Π΄Π½Π΅ΠΉ. Π’ сывороткС ΠΊΡ€ΠΎΠ²ΠΈ опрСдСляли Π°ΠΊΡ‚ΠΈΠ²Π½ΠΎΡΡ‚ΡŒ ΡƒΡ€Π΅Π°Π·Ρ‹, эластазы, Π»ΠΈΠ·ΠΎΡ†ΠΈΠΌΠ°, ΠΊΠ°Ρ‚Π°Π»Π°Π·Ρ‹ ΠΈ содСрТаниС ΠœΠ”Π. По показатСлям активности ΠΊΠ°Ρ‚Π°Π»Π°Π·Ρ‹ ΠΈ содСрТания ΠœΠ”Π рассчитывали антиоксидантно-прооксидантный индСкс АПИ, Π° ΠΏΠΎ ΡΠΎΠΎΡ‚Π½ΠΎΡˆΠ΅Π½ΠΈΡŽ ΠΎΡ‚Π½ΠΎΡΠΈΡ‚Π΅Π»ΡŒΠ½Ρ‹Ρ… активностСй ΡƒΡ€Π΅Π°Π·Ρ‹ ΠΈ Π»ΠΈΠ·ΠΎΡ†ΠΈΠΌΠ° рассчитывали ΡΡ‚Π΅ΠΏΠ΅Π½ΡŒ дисбиоза. ΠŸΠ°Ρ‚ΠΎΠ³Π΅Π½Π½ΠΎΠ΅ дСйствиС дисбиоза опрСдСляли ΠΏΠΎ суммС ΠΎΡ‚ΠΊΠ»ΠΎΠ½Π΅Π½ΠΈΠΉ (Π² %) ΠΏΠΎΠΊΠ°Π·Π°Ρ‚Π΅Π»Π΅ΠΉ ΠΌΠ°Ρ€ΠΊΠ΅Ρ€ΠΎΠ² ΠΎΡ‚ ΠΏΠΎΠΊΠ°Π·Π°Ρ‚Π΅Π»Π΅ΠΉ контроля. Π›Π΅Ρ‡Π΅Π±Π½ΠΎΠ΅ дСйствиС опрСдСляли (Π² %) ΠΏΠΎ суммС ΠΎΡ‚ΠΊΠ»ΠΎΠ½Π΅Π½ΠΈΠΉ ΠΎΡ‚ ΠΏΠΎΠΊΠ°Π·Π°Ρ‚Π΅Π»Π΅ΠΉ Ρƒ крыс с дисбиозом. Π Π΅Π·ΡƒΠ»ΡŒΡ‚Π°Ρ‚Ρ‹: установлСно ΠΏΠΎΠ²Ρ‹ΡˆΠ΅Π½ΠΈΠ΅ уровня ΡƒΡ€Π΅Π°Π·Ρ‹, эластазы, ΠœΠ”Π ΠΈ сниТСниС уровня Π»ΠΈΠ·ΠΎΡ†ΠΈΠΌΠ° ΠΈ ΠΊΠ°Ρ‚Π°Π»Π°Π·Ρ‹ Ρƒ ΠΆΠΈΠ²ΠΎΡ‚Π½Ρ‹Ρ… с дисбиозом. ΠŸΠΎΡ‚Ρ€Π΅Π±Π»Π΅Π½ΠΈΠ΅ высокоолСинового ΠΆΠΌΡ‹Ρ…Π° сниТало ΡƒΡ€ΠΎΠ²Π΅Π½ΡŒ ΡƒΡ€Π΅Π°Π·Ρ‹, эластазы, ΠœΠ”Π ΠΈ повысило ΡƒΡ€ΠΎΠ²Π΅Π½ΡŒ Π»ΠΈΠ·ΠΎΡ†ΠΈΠΌΠ° ΠΈ ΠΊΠ°Ρ‚Π°Π»Π°Π·Ρ‹. ΠŸΠΎΡ‚Ρ€Π΅Π±Π»Π΅Π½ΠΈΠ΅ ΠΆΠΌΡ‹Ρ…Π° ΠΈΠ· сСмян ΠΎΠ±Ρ‹Ρ‡Π½ΠΎΠ³ΠΎ подсолнСчника ΠΌΠ°Π»ΠΎ влияло Π½Π° биохимичСскиС ΠΏΠΎΠΊΠ°Π·Π°Ρ‚Π΅Π»ΠΈ. Π—Π°ΠΊΠ»ΡŽΡ‡Π΅Π½ΠΈΠ΅: Π²Π²Π΅Π΄Π΅Π½ΠΈΠ΅ Π² ΠΎΡ€Π³Π°Π½ΠΈΠ·ΠΌ Π»ΠΈΠ½ΠΊΠΎΠΌΠΈΡ†ΠΈΠ½Π° Π²Ρ‹Π·Ρ‹Π²Π°Π΅Ρ‚ Ρ€Π°Π·Π²ΠΈΡ‚ΠΈΠ΅ дисбиотичСского синдрома, ΠΊΠΎΡ‚ΠΎΡ€Ρ‹ΠΉ ΠΌΠΎΠΆΠ½ΠΎ Π² Π·Π½Π°Ρ‡ΠΈΡ‚Π΅Π»ΡŒΠ½ΠΎΠΉ стСпСни ΠΏΡ€Π΅Π΄ΡƒΠΏΡ€Π΅Π΄ΠΈΡ‚ΡŒ ΠΏΠΎΡ‚Ρ€Π΅Π±Π»Π΅Π½ΠΈΠ΅ΠΌ высокоолСинового подсолнСчного ΠΆΠΌΡ‹Ρ…Π°
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